Episode 31

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Published on:

2nd Aug 2025

Dr. Jennifer Rodger - #31 - August 2, 2025

Show Notes: The Neurostimulation Podcast – Episode #30 with Dr. Jennifer Rodger

Guest: Dr. Jennifer Rodger, Professor at the University of Western Australia and Head of the Brain Plasticity Research Group at the Perron Institute

Release Date: August 2, 2025

Episode Overview:

In this episode, host Michael Passmore sits down with Dr. Jennifer Rodger, a leading neuroscientist whose lab is pioneering research into the mechanisms and safety of low-intensity, repetitive transcranial magnetic stimulation (rTMS), especially in the developing brain.

Dr. Rodger shares her unique journey from biochemistry to neuroscience, her initial skepticism about TMS, and how her team’s animal model research is helping to unravel the effects and potential of rTMS in both clinical and research settings. The conversation covers:

The challenges and breakthroughs in miniaturizing TMS coils for animal studies

Key findings from recent studies on rTMS in adolescent mice, including effects on brain plasticity and behavior

The translational bridge between animal research and human clinical applications, especially for youth and neurodevelopmental disorders

The importance of safety, evidence-based innovation, and publishing negative results in scientific research

The future of tailored neurostimulation protocols and the need for collaboration across labs and disciplines


Key Takeaways:

rTMS shows promise for treating neuropsychiatric conditions in youth, but careful, long-term research is essential to ensure safety and efficacy.

Animal models provide valuable insights into the mechanisms and potential risks of neurostimulation, especially during critical developmental windows.

Publishing negative results is crucial for scientific progress and helps guide future research directions.

The field of neurostimulation is rapidly evolving, with opportunities for more personalized and integrated treatment approaches.


Resources & Links:

Dr. Rodger’s lab and research group:

https://brainplasticitylab.org/

https://www.perroninstitute.org/research/research-groups/jennifer-rodger/

https://www.perroninstitute.org/research/our-focus-areas/brain-plasticity/


Recent publications and studies discussed:

Our first low intensity rTMS paper is:

Rodger J, Mo C, Wilks T, Dunlop SA, Sherrard RM. Transcranial pulsed magnetic field stimulation facilitates reorganization of abnormal neural circuits and corrects Behavioral deficits without disrupting normal connectivity. FASEB J. 2012 Apr;26(4):1593-606. https://pubmed.ncbi.nlm.nih.gov/22223750/


Description of miniaturised coil design:

Tang AD, Lowe AS, Garrett AR, Woodward R, Bennett W, Canty AJ, Garry MI, Hinder MR, Summers JJ, Gersner R, Rotenberg A, Thickbroom G, Walton J, Rodger J. Construction and Evaluation of Rodent-Specific rTMS Coils. Front Neural Circuits. 2016 Jun 30;10:47. https://pubmed.ncbi.nlm.nih.gov/27445702/


An exhaustive recent review of low intensity rTMS:

Moretti J, Rodger J. A little goes a long way: Neurobiological effects of low intensity rTMS and implications for mechanisms of rTMS. Curr Res Neurobiol. 2022 Feb 23;3:100033. https://pubmed.ncbi.nlm.nih.gov/36685761/


The work exploring rTMS and endogenous brain activity:

Poh EZ, Green C, Agostinelli L, Penrose-Menz M, Karl AK, Harvey AR, Rodger J. Manipulating the Level of Sensorimotor Stimulation during LI-rTMS Can Improve Visual Circuit Reorganisation in Adult Ephrin-A2A5-/- Mice. Int J Mol Sci. 2022 Feb 22;23(5):2418. https://pubmed.ncbi.nlm.nih.gov/35269561/


The recent paper about rTMS in adolescent mice is:

Tomar M, Pow JJ, Penrose-Menz MA, Beros JL, Miljevic A, Meloni B, Rodger J. Low intensity rTMS in adolescent mice affects visuomotor behaviour with no impact on visual topography. Brain Stimul. 2025 May-Jun;18(3):965-974. https://pubmed.ncbi.nlm.nih.gov/40306617/


NB: All research involving animal models was conducted with institutional research ethics board review and approval.


Additional reading on rTMS and neurostimulation:

https://www.mayoclinic.org/tests-procedures/transcranial-magnetic-stimulation/about/pac-20384625

https://my.clevelandclinic.org/health/treatments/17827-transcranial-magnetic-stimulation-tms


Connect with Us:

If you enjoyed this episode, please like, subscribe, and leave a review. Share your questions or comments below, and check out the show notes for links to Dr. Rodger’s work and related resources.

Stay tuned for more conversations at the intersection of neuroscience, innovation, and clinical practice!

The Neurostimulation Podcast – Exploring the science, therapies, and future of brain health.

Transcript
Mike:

Welcome back to the Neurostimulation Podcast, where we dive into the

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science, innovation, and clinical

frontiers of neurostimulation.

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I'm Michael Passmore, and today we're

going to be having a great conversation.

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I'm thrilled to be speaking with Dr.

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Jennifer Rodger, professor at the

University of Western Australia, and

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head of the Brain Plasticity Research

Group at the Perron Institute.

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Dr.

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Rodger's lab is pioneering research

into the mechanisms and safety of low

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intensity, repetitive transcranial

magnetic stimulation or rTMS,

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particularly in the developing brain.

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So we're going to be discussing, among

other things, a recent study that explored

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the effects of rTMS on adolescent mice,

what it reveals about brain plasticity

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during critical developmental windows,

and perhaps the broader implications

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for using neuromodulation in younger

humans as well for clinical purposes and

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also other types of research endeavors.

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Dr.

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Rodger, thank you so much for joining us.

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It's really a pleasure, to

meet you and I'm really looking

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forward to the conversation today.

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Jenny: Thank you, Michael, me as well.

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Mike: Great.

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So maybe, if you don't mind, taking

a few minutes just to introduce

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yourself to us and help the audience

to understand, a bit more about you,

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your work and your experience and what

your lab is focusing in on these days.

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Jenny: Yeah.

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Thank you.

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Please call me Jenny.

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I'm a neuroscientist and I'm

based in Western Australia, in the

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city of beautiful city of Perth.

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And I suppose my background's a little

bit unusual because I come from a

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biochemistry background, so I studied

organic chemistry and biochemistry

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and molecular biology, but I always

wanted to get into neuroscience.

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And, over the years I've studied

a range of different animal models

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of neuroscience, so I've always

had an interest in development.

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Brain plasticity, how the

brain repairs after injury.

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and as you know, I developed my own

research stream emerging through postdocs

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and, various different lab experiences.

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rTMS was a sort of mystery to me,

and I, I have to admit that I was

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a TMS skeptic when I first started

working in this, in this field.

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And I had a number of people around

me who were saying, it's amazing.

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It changes the brain, we can use

it to treat all of these things.

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And I was very skeptical.

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And when, a colleague challenged me

and said, well, what would it take

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for you to believe in, in TMS to

really believe that it, it works?

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I said, well, you know, we, we should

look in animal models because we can

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actually then get inside the brain and

look at pathways and look at cells and

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see the effects of TMS on the brain.

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And, that would convince me

if we could see things and.

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So we applied for a grant and we got the

grant, and that's where my, research focus

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now is based around TMS understanding

how it works, how it can be applied,

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and that all stems from that initial

argument and, and that grant application

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to, to convince myself that our TMS was

actually having an effect on the brain.

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So now my research extends not only

in the mechanisms, but we started

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working in translational neuroscience,

trying to find ways to translate

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basic findings into human practice.

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It's, it's challenging.

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I can't say we've had any major

successes yet, but it's been really

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fascinating journey and I look forward

to talking, about lots of different

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aspects of this with you today.

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Mike: Yeah.

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Fantastic.

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That's so interesting.

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Thanks so much for explaining that.

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I think it's.

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Yeah, I've talked to so many people

who, myself included, who, have been

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skeptical about neurostimulation.

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And I think part of what's interesting

is because I'm thinking of this, I'll

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put it up, I, I'll show this picture

that I'm thinking of, but it has to do

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with the history of magnetism and, and

how, a hundred years ago people were

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doing things putting magnets towards the

head and, and, and so it does engender a

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sense of skepticism and that's it lends

people understandably to wonder to what

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extent this is a scam or there's snake

oil kinds of clinical applications.

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And I think even currently there's,

there's this potential for, unscrupulous

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people to be producing devices that are

nothing more than sham But now 20 years

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on after, really it's been starting to

kind of catch on clinically, there's

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so much evidence and understanding

more about the basic research, that,

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that you and your team are, are

involved with is extremely interesting.

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Yeah.

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So I'm looking forward

to talking about it also.

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Jenny: Thank you.

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Yeah.

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I think it's also TMS is unusual, as

you pointed out, that it sort of, it

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happened and the medical device suddenly

became used and employed everywhere.

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And unlike a, a drug or, you know,

most common interventions, there

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hasn't been that body of evidence

built up before translating to humans.

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So it's almost working backwards.

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And now we've got something that works

sort of most of the time or some of

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the time, uh, going backwards and

trying to understand why it works and

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why it doesn't work in some cases.

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I think it's, it's, it's

a really interesting area.

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Mike: Yeah.

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Yeah.

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And, and just thinking about, this

particular study in terms of the animal

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model, it does bring back memories.

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I did some work study kinds of,

terms in, in undergrad in animal

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biology lab at UBC in Vancouver here.

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And so I, I can recognize the value

of this kind of research, and I'm

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particularly curious about the

logistics of developing miniature

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TMS coils, rodent sized coils.

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So help, help me understand

how that all worked.

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That must have been an

interesting journey.

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Jenny: It was a very interesting journey.

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I, I have, when, when I give talks, I

have a slide where I show a human head

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with a human TMS coil and saying, and

so, you know, I got this grant and we

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were funded to do TMS in, and I put up

a, a mouse to scale with the human head.

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And everybody laughs because you see how

huge the coil is relative to the mouse.

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And there's no way that we could use

a human coil, at least in my opinion.

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And having spoken with a lot of

other people, the whole, the strength

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I think of human TMS is that it

delivers focal stimulation to a

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particular place in the brain so that

you can target particular networks

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and, you know, alter connectivity.

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And that as we know more

about it, we think that that

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vocality is really important.

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But when you try and do that in

a mouse with a big coil, you're

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stimulating the whole animal.

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So it was really important for us to try

and find a way to miniaturize the coils.

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And two people really

were instrumental in that.

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A colleague, professor Rachel

Sherrod, who works in Paris, she

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was the one who actually said, we

need to miniaturize these coils.

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And she developed some prototypes and.

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Had lots of long chats and arguments

about it, but then I had an amazing PhD

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student, Alex Tang, who's now got his own

lab in TMS and brain aging particularly.

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And for his PhD he worked with the

physics department at our university

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in wound coils on a proper coil

wounder, and developed some modeling

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skills using the electromagnetic

field modeling programs like console.

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It was before things

like Simin nibs existed.

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So it was, it was really hardcore

physics and, electromagnetism

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theory that we got into.

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And it took him, the best part of

a year to get a working prototype.

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We had to buy power supplies, we had

to buy waveform generators, look at

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the different shapes of the pulses.

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and yeah, it was, it was quite a journey.

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But those small coils.

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Fantastic because they can stimulate

a quarter of a, a mouse brain, which

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I think is, it's not as good as

in humans, but it's getting there.

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The only disadvantage is that because

the coils are small, the intensity

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of the magnetic field is very weak,

so that means that we can't replicate

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motor evoked potentials that are such,

classic conventions in human TMS.

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We can't deliver stimulation at the

intensities that are clinically relevant.

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So that's led us to take a

number of, different pathways.

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In the study that you spoke about looking

at developing brains, we've had to focus

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on that concept of peri focal stimulation

because even though you have a core of

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high intensity stimulation at the hotspot.

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There's a surrounding, I don't want

to say aura, but lower intensity

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emanation of magnetic field around

that hotspot, which is still activating

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brain cells and having an impact.

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So from that point of view, I

think the coils can be useful in

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understanding some aspects of TMS,

but it's clearly not a perfect model.

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But then no model's perfect.

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Mike: Right?

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Yeah.

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Well it's, it's interesting just

by itself in terms of what affects

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that type of magnetic field.

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And what the observations are and how

those changes might then be relevant

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in terms of clinical applications.

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Jenny: Exactly.

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I hope that it's contributing.

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Sometimes I ask myself, how relevant these

models really are, but then you there,

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if we can get effects with low intensity

magnetic fields, then do we really

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need high intensity magnetic fields?

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Are there opportunities to change

the parameters and explore other

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mechanisms that might have.

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More impact in other disorders or have

different effects on brand cells, mm-hmm.

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Again, I think all of that

discovery is important.

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Mike: Yeah, for sure.

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And I think it makes sense just

in terms of understanding the

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emerging breadth of potential.

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Neurostimulation applications, that

are coming out, whether it's tDCS or

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transcranial focused ultrasound or so.

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So it's clearly not just limited

to, the specificity of focal, High

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frequency or low frequency rTMS in a

human model, So it's super interesting.

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So then, given what you were just saying,

what kinds of, I guess, maybe if it's

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presumptuous to ask or if we're not quite

there yet, but what do you envision then

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as perhaps a potential translational

bridge between what you've learned with

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the rodent studies and potential clinical

applications for humans down the road?

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Jenny: Well, I suppose the most advanced,

example of that is work that we've

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done with Kaylene Young, a colleague

in Tasmania at the Menzies Institute.

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And a few years ago we started working

out what is TMS doing not only to

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neurons, but also to other brain cells.

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and the brain isn't

just made up of neurons.

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They're astrocytes, they're

oligodendrocytes, but all the

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blood vessels, microglia and their,

colleagues in Germany who are doing

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a lot of work around microglia.

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But the work with Kaylene was

interesting 'cause we focused

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particularly on oligodendrocytes.

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Her lab is expert in multiple sclerosis

research, and she found that the low

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intensity stimulation would improve

the survival of oligodendrocytes.

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And in mouse models of multiple sclerosis,

it will improve, remyelination, it

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will increase the amount of myelin that

they produce, that the cells produce.

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So it's actually a completely unexpected

outcome of rTMS Electromagnetic

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stimulation of the brain has the potential

to improve myelination and then we've

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translated the circular coils and mice,

stimulating large areas of the brain in

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humans, we've measured equivalent magnetic

fields so that the, the cortex of the

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mouse was receiving a certain intensity.

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And we've matched that in humans

through, again, a lot of modeling and

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back of the envelope, calculations.

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And we're in, phase two clinical trials

now, looking at efficacy of that.

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So for us, for me, it's not really

my story, it's Kaylene's story, but

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it's been a great privilege to be

involved in that and see how some

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really basic questions that our devices

help to ask have actually led to some

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new innovations in, in human trials.

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So I'm hoping that for things

like depression and anxiety,

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our work will again, contribute

to that in, in the future.

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But I think there's a lot of potential

for it, for there to be a strong

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translational pipeline between

the animal models and the human.

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Mike: Mm-hmm.

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Yeah.

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Yeah.

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Absolutely.

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That's fascinating.

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I think that's really interesting to

think about how these technologies are

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affecting systems in the brain, aside

from the neuronal systems and pathways

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and connectivity and neuroplasticity,

these, the glial cells are often just

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underrecognized in terms of their

importance I'm sure it's just a limitless

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kind of area for, for investigating

with these kind of technologies

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. So the other part of it that I

was fascinated by, is just this

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idea of the, the impact of the

TMS on the, the developmental

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piece, you know, the, the, the

neurodevelopmental sort of change there.

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So I'm just curious if you don't

mind, you know, that particular study,

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so as I understand it was targeting

visual cortex during an important

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period of the mouse development.

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So can you tell us a little bit

about that and what, what the study

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basically yielded in terms of findings?

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Jenny: Yeah.

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That, that's the study that we're, we're

particularly interested in at the moment.

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you know, TMS is approved in adults for

treating major depressive disorder and one

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of the real attractions I think of TMS is

that there are very few side effects and

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we know that young people who experience

depression and anxiety are, they really

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don't respond to medications very well.

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The medications are often developed in

adults, they're not well adapted to use.

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There's a lot of side effects.

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youth themselves feel a little bit

disempowered when they just get given a

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pill and told to go away and get better.

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So there's a lot of interest in

trying to find new treatments.

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And TMS is, has been

trialed in young people.

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There's reasonable, I'd say

actually very good safety evidence

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that there are no side effects

beyond what you see in adults.

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And the young people tolerate it well

and they seem to respond reasonably well.

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The efficacy, I think, is

still not particularly.

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There's not a lot of evidence yet

for the efficacy, but because the,

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the developing brain in humans,

the brain continues to develop, to

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develop until roughly the age of 25.

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So if you're stimulating the brain in a

young person, it, it is an opportunity

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that, could be fantastic because the

brain is very plastic in a teenager.

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Or in a child.

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So you have great potential to modify

it and to, repair anything that

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might be, abnormal circuitry or neuro

develop neurodevelopmental disorders.

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But you also have a big risk

that any changes you make in

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that period have the potential to

affect lifelong brain functioning.

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And in humans, we've had

TMS in the population for

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probably more than 20 years.

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So I think there's a lot of

confidence in adults that we're not.

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Predisposing people to neurodegenerative

conditions, and we're not causing

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lesions, and we're not altering

DNA or giving people cancer.

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So we're confident about that for adults.

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But children really are, I don't want to

say vulnerable, but susceptible to change.

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And one of the questions that we've

had from speaking to young people

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with anxiety and depression is we

love the idea of TMS, but what am,

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what's my brain going to look like in

20 years or in 30 years when I'm 80?

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Is it going to impact, who I am

and, and how my brain works later?

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So we thought, well we can't

do that in people 'cause it's,

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nobody's gonna fund us for 50 years.

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Much as we would love to

get funded for 50 years.

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It's not going to happen.

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So we thought animal models are

a perfect way to look at this.

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We can take a young mouse.

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the adolescent period is

roughly up to about 40 days.

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give the animal TMS during that

period and then just see what happens.

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And the paper that you mentioned that we

published in brain stimulation last month

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really describes that short term outcome.

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So we did the very simple experiment.

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We gave the animal our low intensity

stimulation, arguing again, that we're

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looking because we can't deliver the focal

stimulation to the prefrontal cortex mass,

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we can still deliver the peri focal, the

low intensity that a child would receive.

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And we stimulated the visual cortex

because in mice it's very difficult to

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measure things like mood and depression,

and those models are quite controversial.

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Whereas in the visual system,

you've got a great readout of, the

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organization of the visual system

connectivity, because there's a point

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to point mapping between the retina

and all of the visual brain centers.

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So the actual connectivity

is easy to measure.

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You then also have a behavioral readout.

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Can the animal still see, can

it respond to visual stimuli?

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So although it does abstract the

model away from humans, it's actually

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a really powerful model because it

allows us to examine the anatomy, the

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cellular composition and the behavior.

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I suppose in the reverse order.

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You look at the behavior first,

and then in those same animals,

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you can euthanize the animals and

then examine the brain structure.

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So that was the idea behind the study that

we wanted a really clear readout of the

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structure and function of the brain after

it had received TMS during development.

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So we were the results are compelling and

we were still there's a lot more to do

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in a nutshell, there were no, there was

no impact that we could find on any of

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the anatomical organization of the brain.

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There were no changes to any of

the neurotransmitter markers,

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but I'll come back to that later.

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There didn't seem to be any inflammation.

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We used some fairly broad tools to look

at that, but there was a behavioral,

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change and that really puzzled us

because we didn't expect to see that.

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And the behavioral

change was very specific.

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It was, visual motor integration.

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So when you, the test that we use is

called, an optic kinetic nystagmus test.

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And all that means is it's basically

your eye tracking movement.

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So when you sit in a train or a car and

you're looking out the windows, your eyes

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flick back and forth, as the landscape

passes by, because it's, it's a reflex,

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we can't really control it that well.

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but our eyes follow moving objects.

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And you can do this in mice.

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You put them in a, a moving circular drum.

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As the stripes move past the

animal, their heads and eyes track

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the stripes and you can count the

number of times that they do that.

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So after TMS, we found that

the mice did less tracking.

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They essentially didn't follow moving

stripes as often as control mice did.

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And so we went back to the anatomy and

we looked at the different regions we had

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traced and found absolutely no change.

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And there.

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You know, though we looked

at the main visual pathways,

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:

but there are always more.

318

:

So we can't rule out that other visual

pathways might be disorganized, but

319

:

because the deficit involved both vision

and movement, I think it's actually a

320

:

really interesting idea to think that

TMS might have compromised some of

321

:

that sensory motor integration pathway.

322

:

So it's not just about vision, it's about

how vision integrates with movement.

323

:

In development, those

processes are really complex.

324

:

They're still developing, and it's

possible that by providing stimulation

325

:

and providing additional activity,

TMS essentially increases the

326

:

electrical activity in the brain.

327

:

we could have compromised the development

328

:

Mike: pathways.

329

:

Jenny: So is that important?

330

:

does that strike fear into

my heart for TMS in young,

331

:

people, it, it honestly doesn't.

332

:

Partly because we're looking at

a model that's very abstract.

333

:

we're looking at a visual system.

334

:

We're looking at sensory pathways,

sensory motor pathways, and the

335

:

deficit was very small and the deficit

happened immediately after TMS.

336

:

So we're thinking probably if we stopped

TMS and let the animals just live

337

:

normally for a couple of weeks, the brain

would probably restore normal function

338

:

because that's what the brain does, and

especially in young people where the

339

:

brain remains plastic for a long time.

340

:

also we don't really know what

would happen in an abnormal brain.

341

:

So a brain that had, connectivity related

to depression or anxiety like symptoms.

342

:

But what is the equivalent of

sensory motor integration in those

343

:

brain regions involved in mood

regulation and emotional processes?

344

:

So I think it's interesting.

345

:

It raises questions and it certainly

raises, Just concerns that there

346

:

is something going on in the young

brain that doesn't probably happen in

347

:

the same way in, in an adult brain.

348

:

Mike: Mm-hmm.

349

:

Yeah, that's really interesting.

350

:

I mean, it's certainly reassuring

that there were no concerning

351

:

findings on the cellular and

neurotransmitter and inflammation side.

352

:

Yeah.

353

:

Mm-hmm.

354

:

I can see how there's caution that's

required in terms of interpreting

355

:

those behavioral findings in terms of

the applicability to humans For sure.

356

:

Jenny: Yeah, I think the, the

neurotransmitter question was tricky.

357

:

We, we did additional experiments

in response to reviewer comments

358

:

on the paper saying, well, if

it's not anatomy, what is it?

359

:

You have to have an explanation.

360

:

So we went back and looked at the ex

and inhibitory balance in the brain.

361

:

But again, animal experiments are

quite tricky because we wanted to

362

:

use the same animals for everything.

363

:

So we have the behavioral

outcomes in the animals.

364

:

We have the anatomical tracing, and

then in the same brains we actually

365

:

studied the neurotransmitter and,

inhibitory excitatory balance.

366

:

But after TMS has stopped, by the time

you've done the behavioral experiments

367

:

and the anatomical tracing, it takes

about a week to 10 days to do all of that.

368

:

So the effects of TMS are already

starting to wear off at the time that

369

:

you euthanize the animals and start to

look at the neurotransmitter profiles.

370

:

So.

371

:

No, we, we were really limited in

how much we could interpret that

372

:

because so much time had gone by.

373

:

So at the moment we're, you

know, continuing on from,

374

:

from those experiments.

375

:

We're hoping to do some long-term

studies, not even, three months

376

:

after the TMS, but animals live

for roughly 18 months to 24 months.

377

:

So that is within the capacity of

a funding body where we can have

378

:

studies that TMS mice in youth and

study them all the way into old age.

379

:

And that will give us a much more

detailed time course of what's going on.

380

:

And we have the capacity also to

take different cohorts of animals to

381

:

specifically address questions like

excitatory and inflammatory balance, as

382

:

well as, putting them in the MRI machine

scanning, brain connectivity, and, and

383

:

getting much bigger picture of what's.

384

:

Mike: Yeah.

385

:

That's fascinating.

386

:

I mean, that totally makes sense

in terms of the next steps and how

387

:

to sort out all of these questions.

388

:

For sure.

389

:

And I think it's, I certainly

feel reassured as well.

390

:

I'm glad to hear that

you're, you're being, right.

391

:

Immersed in, in this work or are

also reassured around the likelihood

392

:

that this is gonna be a safe.

393

:

Clinical application in, in

children and adolescents.

394

:

And I guess just thinking about the recent

FDA approval of rTMS in adolescents with

395

:

major depressive disorder, I think that,

as you said, not only the, the long now

396

:

20 plus year history of effectiveness

and safety in adults is, is reassuring.

397

:

But I also think, maybe this is

more of a general speculation

398

:

based on the idea that.

399

:

Young brains are more plastic in general.

400

:

It would strike me that, that then would

by itself be a reassuring factor in terms

401

:

of, well, if we're, if we're, imposing

this energetic change on the brain in a

402

:

therapeutic sense, then hopefully the.

403

:

The baseline neuroplasticity of the

developing brain is, is is almost a buffer

404

:

that would help to guard against any

long term side effects or, or, or, yeah.

405

:

Other morbidity issues that might

some level be conceivably related

406

:

to the short term application

of the, of the magnetic field.

407

:

Jenny: Yeah, I completely

agree and I think.

408

:

Also we, you know, this is a whole

other question, but we don't know

409

:

if the same parameters that work in

adults are also effective in humans.

410

:

We have a fairly limited, um, well,

the parameters with TMS are unlimited.

411

:

You know, any combination of frequency

and intensity and number of pulses, it's

412

:

a, it's a bit of a scary, uh, area to go

into 'cause there's so much possibility.

413

:

In adults, we've sort of narrowed it

down to maybe two or three frequencies

414

:

that we think are effective and that

seem to give good outcomes, whether

415

:

those work in children or whether

it's worth actually re-exploring some

416

:

of those stimulation parameters to

try and find some, find something

417

:

that's more specific to children.

418

:

I wouldn't even know how to start

going about that, um, apart from

419

:

attacking that huge parameter space.

420

:

But I think that it's a bit like

with drugs, we can't just assume

421

:

that children are small adults.

422

:

You know, they're, they have

different brain chemistry, they

423

:

have different brain structure.

424

:

Neuroplasticity is hugely

significant at that stage.

425

:

So I think, it's important to think

carefully and make sure that we,

426

:

we do TMS properly in young people.

427

:

Mike: Mm-hmm.

428

:

Yeah, it makes sense.

429

:

And I think it also makes sense in

terms of what I hear a lot of people

430

:

talking about, and it makes perfect

sense, is just this idea of tailoring

431

:

protocols to, to an individual's needs.

432

:

So whether it's age on, on the young

end or even on the later life end or

433

:

other, other aspects of, of particular

neuropsychiatric disorder or other.

434

:

I'm not sure.

435

:

I mean anything just as, as a

medication, I think probably this is

436

:

a limitation of the legacy medication.

437

:

I think obviously psychotherapy,

there's more room for tailoring

438

:

necessary obviously, but on the

medication side, perhaps not.

439

:

Right?

440

:

So maybe with a multimodal approach

to treatment with tailored protocols,

441

:

depending on what the research shows

across the age spectrum, that it

442

:

makes sense that this is the sort

of work that would help to inform

443

:

those eventual clinical guidelines

and protocols being accepted.

444

:

Jenny: No, absolutely.

445

:

And TMS is, is actually really well set up

for TA for being tailored because there's,

446

:

choice not only around the region that's

being targeted, but also all of that.

447

:

Then sort of electromagnetic parameters

with the pulses and the intensities.

448

:

And I think we've seen with things like

the Saint Protocol coming out, that there

449

:

is a lot of opportunity for tailoring.

450

:

There's quite a lot of excitement

around even just very simple.

451

:

Targeted, tailoring brain regions

based on connectivity patterns.

452

:

So I think there's, you know, we've

taken the first steps and it's now

453

:

open to, to a lot of opportunities.

454

:

As you mentioned, I think the combinations

as well, TMS combined with medication, TMS

455

:

combined with psychotherapy, those sorts

of, really integrated treatments are, are

456

:

really exciting and for youth where we

know, they really want to be involved.

457

:

Well, the youth that we've spoken to

in, in Australia, they really want

458

:

to be involved in their treatment.

459

:

They want to feel like they're empowered

to be part of the decision making process.

460

:

And I think the opportunity to tailor

treatments and to get them engaged in

461

:

making decisions around that is, is gonna

be really powerful because that will

462

:

also support their own mental wellbeing.

463

:

Mike: Definitely.

464

:

Yeah, definitely.

465

:

I think that's a part of the issue

historically with the legacy approaches

466

:

is, is exactly as you say, it's that

it's the way that clinicians kind of get

467

:

sucked into the whole pharmaco industrial

complex and they're only insured for a

468

:

limited amount of time, which makes it.

469

:

Easier, shall I say, to write a

prescription and, and then, book

470

:

an appointment in a few weeks time

thing, and I can see how already.

471

:

Younger, younger folks would be already

disinclined to come in the first place.

472

:

And then if that's the sort of

approach, then, they're justified

473

:

in having a skepticism around that.

474

:

So hopefully these kinds of novel

treatment approaches and more ability

475

:

to ask questions and be interested

in the technology that will help

476

:

to foster a sense of agency and

involvement with their own treatment.

477

:

Definitely.

478

:

It's fascinating.

479

:

The other thing that's interesting

that I was thinking just now is the

480

:

potential for perhaps the tailoring to

involve not only as you were saying,

481

:

a given neurostimulation option, plus

medication, plus psychotherapy, but.

482

:

Of neurostimulation options like

TMS and then maybe something like

483

:

TDCS for maintenance treatment,

something along those lines.

484

:

and it's also interesting to think

about, I'm wondering a bit about whether,

485

:

whether you're, based, it's probably too

early to say, but if, if, in terms of

486

:

thoughts that you and your team had about

future directions to explore with this

487

:

kind of research or potential clinical

implications, was there any sense that

488

:

there might be some applicability for.

489

:

Purely considered neurodevelopmental

disorders, like along the lines

490

:

of, say, autistic spectrum

disorder or those sorts of things.

491

:

Jenny: Yeah.

492

:

We, we've spoken to, there's obviously

a lot of interest in using TMS for

493

:

things like autism and A DHD as well

is, is a question that we get a lot and

494

:

speaking to clinicians, they say, but,

TMS alters dopamine and it targets these

495

:

brain regions and we know from the MRI

studies it, it activates these pathways.

496

:

Why aren't you using it for a DHD?

497

:

And it, you know, I don't, I

don't know the answer to that.

498

:

I think the, again, it's this sort of

clinical trial versus animal models

499

:

and, sequence that, we haven't got the

animal, we, there are animal models

500

:

for things like autism and A DHD, but.

501

:

Again, they don't always model all

the different aspects of, of the human

502

:

disorder and treating people with

autism and A DHD is, especially, a

503

:

lot of them tend to be young people.

504

:

The ethical considerations around

that are are quite complex.

505

:

So I think there are a lot of

difficulties in moving into that

506

:

space and getting TMS approved for

youth with depression is probably a

507

:

first step in moving towards that.

508

:

It's the easy way in that population.

509

:

Certainly clinicians that we've spoken

to are really excited about possibility

510

:

and, parents and children as well.

511

:

You know, the people need, I think,

better treatments overall for those

512

:

neurodevelopmental disorders, and

TMS certainly has the capacity

513

:

to modify the developing brain.

514

:

As you know, a lot of people have

shown we're not the only people

515

:

who have done work in development

as a lab in, in Germany that did

516

:

some work in developing rodents.

517

:

looking particularly at the critical

period and they showed some really

518

:

interesting effects around the inhibitory

excitatory balance, particularly

519

:

paval parvalbumin into neurons.

520

:

Alia Benal in class, Funke did some great

work on, characterizing changes in those

521

:

in neurons that we know are involved

in autism and regulating activity.

522

:

Brain pathways.

523

:

So there's a little bit of preclinical

evidence, but translating that.

524

:

Complex and you want to get it right.

525

:

I think particularly for something like A

DHD where balance, it's all about balance.

526

:

Autism probably as well, and, and

it's important to get it right.

527

:

Mike: Mm-hmm.

528

:

Mm-hmm.

529

:

Yeah.

530

:

I'm curious in terms of follow up

studies or ideas based on, the, the

531

:

study that we're talking about with

the visual cortex development mm-hmm.

532

:

would it be feasibly something to

think about in terms of potential for a

533

:

follow up study that looks at perhaps.

534

:

Such as auditory processing

or executive function.

535

:

Thinking about o other aspects of brain

function that are critical for, say,

536

:

learning and, and, and success in,

in, in academia or social settings?

537

:

Jenny: Mm.

538

:

That, that's a great question.

539

:

We've, I work with a colleague who's,

an auditory physiologist and we've done

540

:

some work on tinnitus and, and TMS.

541

:

And I've spoken to her about some way

that we could use the auditory system.

542

:

there are techniques like, mismatch

negativity and oddball paradigms

543

:

where you can measure the brain's

response to different auditory stimuli.

544

:

so we we're we've spoken

about that a little bit.

545

:

but you're right.

546

:

It's the idea of, of looking at.

547

:

More cognitive and emotional type

tasks around executive function

548

:

and, social interactions as well.

549

:

we're starting to develop

those paradigms in lab.

550

:

we're almost spoiled for choice.

551

:

I can't say, you know, we've, we've

gone in the direction of extending

552

:

the timeframe of the studies, as

I said, for a couple of years, and

553

:

we've focused in that long-term study

on a particular model of anxiety.

554

:

Which is a prenatal stress model.

555

:

So the animals that we're taking out two

years with TMS do actually have altered

556

:

behavior in things like, the elevated

plus maze where you measure anxiety.

557

:

The amount of time that rodents spend

in open spaces indicates anxiety.

558

:

And we're also looking at social

interaction in those animals.

559

:

So how much time they spend with familiar

or novel, conspecifics, so animals, other

560

:

mice that the mice have never met before.

561

:

So we're, trying to build in a wider

range of behavioral tests that are

562

:

more relevant to, mood disorders.

563

:

and again, I think once we have a

better idea of what's happening over

564

:

this two year period, we can then go

back in again and focus on expanding

565

:

particular areas or focusing on

a particular time point as well.

566

:

And the big question that

everybody asks us is, how about

567

:

maintenance TMS maintenance?

568

:

How are you going to give the mice

maintenance TMS at six months?

569

:

Oh no, you've just added another

6,000 million mice to our experiment.

570

:

It's just, there's only so much

that we can do, and there's

571

:

so many questions to answer.

572

:

Mike: Mm-hmm.

573

:

Yeah.

574

:

There must be a challenge to think

about in some ways how to balance

575

:

the focusing on the safety with.

576

:

Changes that might correlate with

effectiveness in human clinical models.

577

:

Jenny: And I think that the

safety, the safety issue, we're

578

:

really confident that TMS is safe.

579

:

the changes in behavior that

we've identified were, we're

580

:

hoping that we'll be able to show

that they spontaneously revert.

581

:

if not, I think the sorts of

changes around integration in

582

:

sensory motor brain function.

583

:

We know that there are very good

physiotherapy type interventions

584

:

that can act on those things.

585

:

So if we do need to combine TMS with some

sort of rehabilitation therapy afterwards

586

:

to make sure that those pathways are

restored, I think that's very feasible.

587

:

'cause there's a good background

on those sorts of interventions.

588

:

so the safety I think.

589

:

we're confident that there's not

going to be any major problems.

590

:

it's just making sure that the

efficacy is really targeted.

591

:

I think that's one of the

big goals of the lab moment.

592

:

Mike: Mm-hmm.

593

:

So would you say that, that there's some,

there's some validity in the notion that

594

:

then perhaps the less focused magnetic

field might be almost more akin to TDCS,

595

:

where there's, there's perhaps more of a.

596

:

Priming.

597

:

So that, and concurrent kind of activity,

as you say with the physiotherapy

598

:

or behavioral therapy or some sort

of active enrichment paradigm is, is

599

:

gonna be where there's Yeah, there's

kind of a synergistic effect for, for,

600

:

in like a positive therapeutic sense.

601

:

Jenny: Yeah, that's a

really good question.

602

:

And we've had the low intensity

TMS compared to TDCS or TACS.

603

:

The transcranial, alternating current,

in a number of, conferences and

604

:

discussions, reviews that we've had.

605

:

So I think that's a

really interesting point.

606

:

And, it comes back to how much, how

much do we actually need to stimulate

607

:

the brain when we are delivering TMS

and, activating motor of potentials

608

:

and triggering action potentials.

609

:

Is that overkill?

610

:

Are we actually.

611

:

Activating the brain so much

that you then call up homeostatic

612

:

mechanisms, might try and reverse that

plasticity because we've gone too far.

613

:

So the low intensity stimulation from

that point of view of priming and

614

:

raising the capacity of the brain to

respond in a more sensitive way to

615

:

stimuli is a really tempting way to

look at those mechanisms, I think.

616

:

And homeostatic plasticity

is, is very complicated.

617

:

I don't think I really

understand it still.

618

:

And we, it would be wonderful

to think of TMS as a primer.

619

:

And we've done some work in

animal models where we deliver TMS

620

:

concurrently with a learning paradigm,

concurrently with wheel running.

621

:

So exercise.

622

:

And, we also have delivered TMS to

the visual system in the dark so the

623

:

animals aren't getting concurrent light

stimulation while they're getting the TMS.

624

:

And they're really, I

think they're really.

625

:

I'm very proud of that work.

626

:

I think it's really, really

interesting work because by

627

:

playing with the, endogenous brain

activity at the same time as you're

628

:

delivering TMS, we could identify,

you can have too much activation,

629

:

but you can also have too little.

630

:

And it's that goldilocks bit where

you get the right amount of endogenous

631

:

activity combined with the right

amount of TMS, in order to repair brain

632

:

circuits in the best possible way.

633

:

Mike: Yeah, that's fascinating.

634

:

And so much of what we know about the

brain and, and how you know that the

635

:

tried and true treatments work, it, it

does really reinforce this idea of just

636

:

trying to restore homeostasis and balance.

637

:

And so that makes total sense.

638

:

Yeah.

639

:

Just also trying to, just trying to

not interfere too much with, with

640

:

what our body does naturally to try

and maintain its own equilibrium.

641

:

Yeah, definitely.

642

:

so I'm just curious, like as far as,

you've mentioned, you know, a few

643

:

times, understandably, certain kinds of

limitations around things funding and

644

:

that, and so I guess just in an imaginary

world, if you had unlimited funding and

645

:

no barriers, what ambitious experiment do

you think you'd be interested in doing?

646

:

Or, you know, what would be

something that you maybe would,

647

:

would wanna try and pursue based on

what the, the lab has found so far?

648

:

Jenny: Yeah, that's, that's

a really good question.

649

:

And I love those open-ended questions.

650

:

Wow, what would I do?

651

:

And I'm actually the two year study,

the long-term lifespan study in, in mice

652

:

that I've described a few times today.

653

:

That was really my, my dream

experiment that I would do, and

654

:

I'm very fortunate we received a,

a large grant to, to do that work.

655

:

And it's, it's an exceptional

opportunity, I think, for us to answer

656

:

that big question of, of the lifespan.

657

:

It's, it's not a small undertaking,

but even, you know, bigger than

658

:

that, it was, it was interesting.

659

:

I was at, a conference at the end of last

year where we had a TMS symposium with

660

:

researchers, from various labs in the us.

661

:

They very kindly invited me

to, to join in that symposium.

662

:

And the, the impression I took

away from that was that we're all

663

:

doing very different experiments.

664

:

So some people are using optogenetics

to trigger activation of neurons in the

665

:

brain to study, particular frequencies.

666

:

And other researchers have, done

similar to what we've done, miniaturize

667

:

the coil, but managed to engineer it

in such a way that they get a much

668

:

higher intensity, magnetic field.

669

:

And they're, they're looking at

the processes involved in that.

670

:

There are other groups that are using

electrical stimulation, so bypassing the

671

:

magnetic field altogether in animal models

and, and activating neurons directly.

672

:

And all of the talks were just so

fascinating because they addressed a

673

:

particular question in so much detail that

they, they, nobody's solved any problems,

674

:

but they're really increasing knowledge.

675

:

And I think at the moment, what's

so exciting about the TMS field is

676

:

that everybody's doing different

models and different approaches and.

677

:

In a few years.

678

:

I, I'm really hoping all

of that will come together.

679

:

And the big experiment that I would

like to do almost is to regularly get

680

:

these preclinical animal researchers

together and make sure that we're

681

:

doing things in a way that we can

share that information across models.

682

:

because it's, I think all of the

models have value you if you're

683

:

asking a question there is.

684

:

A model that will answer that particular

question in the best possible way.

685

:

But we all have different questions,

so we're all using different models.

686

:

But you know, it would be wonderful

to just put all of that together

687

:

in a way that we could then make

sense of the bigger picture based

688

:

on those individual puzzle pieces.

689

:

it, I think the TMS field at

this point is, it's a bit wild.

690

:

Everybody's doing their own thing, but.

691

:

It will come together.

692

:

And I think maintaining that communication

across labs and facilitating travel

693

:

and exchange and collaboration will,

will really move the field forward.

694

:

I don't have a big vision yet.

695

:

I think that vision will emerge,

but I'd love to be part of

696

:

bringing that vision together.

697

:

Mike: Yeah.

698

:

It, uh, makes, that makes perfect sense.

699

:

And it makes me think that one of the

things you said earlier about how the

700

:

evolution of TMS has almost kind of

gone backwards, where, you know, it was

701

:

just sort of devised as the device, you

know, initially when 25 odd years ago,

702

:

and then just trialed on people and then

the research has kind of gone backwards.

703

:

Right.

704

:

And so now I could, mm-hmm.

705

:

That kind of time course makes sense

in terms of how then there's this

706

:

sort of perhaps somewhat disorganized

kind of scattershot of approaches

707

:

in terms of other technologies

or variations on theme of PMS.

708

:

But you know, hopefully, I think the

more, obviously the more information

709

:

that we have about these therapies,

these technologies, then the

710

:

better we're better off we all are.

711

:

We can just, the synthesis of it, I

think, as you say, is really important.

712

:

Separating the wheat from the chaff,

I guess, and then figuring out how

713

:

then to best apply that in clinical

terms to get people well as quickly

714

:

as possible for as long as possible.

715

:

Yep,

716

:

Jenny: yep.

717

:

I think also there's the temptation in

TMS to dive into that parameter space

718

:

where you can test infinite numbers

of frequencies and pulses, and I don't

719

:

think we have enough time to do that.

720

:

Literally.

721

:

I think it would take just

a ridiculous amount of time.

722

:

So every so often we sit down in

the lab and discuss, how could we

723

:

design an experiment or how could we

use, the tools like AI and modeling

724

:

to work out what parameters are

the most likely to be effective.

725

:

And I think that's more

strategic, thinking around what

726

:

are the best experiments to do.

727

:

it's important to do that from

a translational point of view.

728

:

'cause it's so easy to

get lost in all of these.

729

:

Very complicated parameters.

730

:

And as you mentioned before, there are

a number of stimulation modalities.

731

:

You've got the TDCS and TACS

ultrasound is becoming, is the

732

:

latest, exciting, new, new tool.

733

:

are we back again to this, device that's

going to start being used in, in people

734

:

without having the research to back it up.

735

:

So I think also there's cautionary

tales there moving forward, if

736

:

we have got new technologies that

can stimulate the brand, let's.

737

:

Maybe just take a step back and do some

of the basic safety and, and mechanisms

738

:

so that we know what we're doing.

739

:

Mike: Yeah.

740

:

No, well congratulations to you and

your team for that because I think

741

:

it's extremely important to just

guard against the, the potential for

742

:

there to be excesses and people to be

perhaps, taking advantage of, if it's

743

:

some, someone that's maybe un or maybe

just overly excited and developing.

744

:

Are not necessarily regulated

or, or perhaps as evidence

745

:

based as they should be.

746

:

And then, so having research like yours

that is, is obviously solid and is just

747

:

gonna add to the body of work that shows

that there is an evidence based, not only

748

:

kind of clinical underpinning based on

population based studies, but the, the

749

:

basic science is also aligned in terms

of the evidence, not only in terms of the

750

:

effectiveness, but the safety, especially.

751

:

Jenny: Thank you that that means

a lot to me and I'm sure my team

752

:

will appreciate that as well.

753

:

The other thing I, I want to mention is

that we publish a lot of negative results,

754

:

and that I think is also really important.

755

:

It's always a bit of a struggle to get

those results published and the students

756

:

often who lead those studies often feel

a little bit disappointed, but it's

757

:

really important to point out when things

don't work or don't have an effect.

758

:

and I think that.

759

:

Something that, again, we're really

proud of, of publishing as much negative

760

:

results as we can when possible.

761

:

Mike: Yeah, that's a

really important point.

762

:

Maybe for listeners, like viewers

and listeners, can you just explain

763

:

a little bit about what that means?

764

:

Negative studies and maybe if you have

a couple of examples from your lab.

765

:

Jenny: Yes.

766

:

so I have plenty of examples.

767

:

The, well, I suppose the, the

recent study, the adolescent

768

:

mouse TMS study really.

769

:

Initially we thought that that was going

to be a completely negative result study.

770

:

So we, when we stimulated the mice

and didn't see any changes in the

771

:

anatomy, didn't see any changes in

the cellular components, but only

772

:

a very small behavioral change.

773

:

Now that was essentially, most

of that study was negative.

774

:

And what that tells us is that TMS is

probably not having massive effects

775

:

on certain things, which in our

context was a good result in safety.

776

:

We've had other, studies, for example,

where we've given stimulation during

777

:

a, sorry, I'm thinking of the task.

778

:

It's a, it's a lever pressing

task where you train, mice to

779

:

press a lever to get a reward.

780

:

And we thought that because.

781

:

Generally TMS is thought to

increase dopamine levels and

782

:

might affect the reward pathway.

783

:

We thought, this is a great model

to look at so that we might be able

784

:

to see that delivering TMS during

leaving lever presser might reinforce,

785

:

those compulsive or addictive

behaviors or it might prevent them.

786

:

And that was a study that was negative.

787

:

so that allowed us to say, well,

in our models with our TMS, we're

788

:

not going to waste any more time

looking at addiction or looking at.

789

:

compulsive behaviors because

our particular tools don't work.

790

:

It doesn't mean that, human TMS

doesn't work, but in our models we

791

:

cannot use that to study addiction.

792

:

mm-hmm.

793

:

So those sorts of examples

I think are really useful.

794

:

Mike: Yeah, definitely.

795

:

No, again, congratulations.

796

:

I think it's just, it's really

impressive and, you know, it's, it's,

797

:

it's very exciting just in terms of,

I'm just sort of dipping my toe into

798

:

understanding more and more about the

basic research, the animal models.

799

:

And I think it's just endless

in terms of the potential and

800

:

it's extremely interesting.

801

:

well maybe before we wrap up, was

there anything else that you wanted

802

:

to share about, you know, your,

your work, your lab's work and yeah.

803

:

Anything that you thought

that might be important?

804

:

Jenny: No, thank you very much.

805

:

I just like to acknowledge that, you know,

I've spoken a lot about myself and as if

806

:

it's my, my work, but, obviously it's,

it's, the work of many, many students.

807

:

Very talented, honors and PhD and

master's students and postdocs

808

:

in my lab over the years.

809

:

And, also in, in research, people

bring their own interests to the

810

:

team and it's really been through

students asking particular questions

811

:

and their own interests that.

812

:

We've gone off on little side tangents and

found some really interesting findings.

813

:

So being in science is really

exciting and the opportunity to

814

:

do these experiments and ask these

questions is a real privilege.

815

:

thank you for letting me talk about it.

816

:

Mike: Oh, that's great.

817

:

Thank you so much for,

for talking to us today.

818

:

I really appreciate it.

819

:

And yeah, again, congratulations to you

and your colleagues, students, everyone

820

:

think it's just a fantastic, fantastic,

projects that, that you spearheaded.

821

:

And I think that hopefully we'll find

out more in the coming months and

822

:

years about the upcoming results,

especially of the two year study.

823

:

I think it's gonna be very

interesting to see how that goes.

824

:

So myself posted on that.

825

:

Jenny: Thank you.

826

:

I'm excited as well.

827

:

Mike: Okay.

828

:

Well thanks again, Jenny.

829

:

Really, really appreciate your time

and such an interesting conversation.

830

:

So all the best and yeah, hopefully

maybe we'll bump into you at some

831

:

point conference or, have another

podcast at some point in the future.

832

:

Maybe we can plan to talk a bit about

the results of the, the long-term

833

:

study, when those are available.

834

:

Jenny: Love to, that would

be fantastic, Michael.

835

:

Thank you.

836

:

Mike: Okay.

837

:

Yeah, thanks.

838

:

So that brings us to the end of

today's conversation with Dr.

839

:

Jenny Rodger.

840

:

Her research offers crucial insights

into how low intensity rTMS interacts

841

:

with the developing brain, and it really

reminds us of the importance of cautious

842

:

evidence-based innovation as we expand

neurostimulation into younger populations.

843

:

If you've enjoyed this episode,

please be sure to like and subscribe.

844

:

Leave a review or ask questions in the

comment section below and share it with

845

:

anyone that you think might be interested.

846

:

I'm going to add links to Dr.

847

:

Rodger's labs, information and

contacts and just, the relevant papers.

848

:

I'll leave links to all of

that in the show notes below,

849

:

so please do check those out.

850

:

if you're interested in diving deeper

into this really important subject.

851

:

Thanks again for your time, your

interest and your attention.

852

:

I really appreciate, the fact that

you've watched or listened to the

853

:

podcast and we'll see you next time

on The Neurostimulation Podcast.

854

:

Thanks so much.

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About the Podcast

The Neurostimulation Podcast
Welcome to The Neurostimulation Podcast, your go-to source for the latest in clinical neurostimulation! Here, we dive deep into the revolutionary techniques that are shaping the future of health care.

Whether you're a healthcare professional, a student, or simply passionate about neuroscience, this podcast will keep you informed, inspired, and connected with the evolving world of neurostimulation.

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About your host

Profile picture for Michael Passmore

Michael Passmore

Dr. Michael Passmore is a psychiatrist based in Vancouver, BC, with expertise in neurostimulation therapies. Having completed specialized training in multiple neurostimulation modalities, including electroconvulsive therapy at Duke University and transcranial magnetic stimulation at Harvard University, Dr. Passmore brings a robust clinical and academic background to his practice. Formerly the head of the neurostimulation program in the department of Psychiatry at Providence Health Care, Dr. Passmore now serves as a clinical associate professor at the University of British Columbia’s Department of Psychiatry. From his clinic, ZipStim Neurostimulation (zipstim.com), Dr. Passmore offers private, physician-supervised, home-based transcranial direct current stimulation (tDCS) treatments tailored to clients across Canada.​