Episode 35

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Published on:

6th Nov 2025

Brainwaves & Breakthroughs: tACS in Psychiatry - A Conversation with Dr. Elyamani - #35 - Nov 1, 2025

Exploring tACS: Current Research and Future Potentials in Neuropsychiatry

In this episode of the Neurostimulation Podcast, Dr. Michael Passmore hosts Dr. Osama Elyamani, a psychiatrist and neuroscientist. They discuss the emerging applications of transcranial alternating current stimulation (tACS) in psychiatry, including its potential as a research tool and therapeutic intervention. They delve into the science of brain oscillations, the clinical evidence surrounding tACS, and future prospects in the field. Particular attention is given to the distinctions between tACS, TMS, and tDCS, as well as the limitations and safety considerations of these neurostimulation techniques. The conversation also touches on the significance of symptom-based approaches in psychiatric treatment and the potential for tACS to aid in diagnosing and treating disorders like depression and schizophrenia. Dr. Elyamani provides insights into ongoing research, future directions, and offers advice for young researchers entering the field.

Dr. Osama Elyamany (PhD) is currently a postdoctoral researcher and resident psychiatrist at the Centre of Psychiatry at Justus Liebig University Giessen.

He is working on research projects investigating brain oscillations in psychiatric disorders using EEG and fMRI, aiming to develop targeted therapies through pharmacological substances and neurostimulation techniques like tACS and TMS.

Email Address: osama.elyamany@psychiat.med.uni-giessen.de

Website: https://www.ukgm.de/ugm_2/deu/ugi_psy/ugi_psy_team.php

LinkedIn: https://www.linkedin.com/in/osama-elyamany/

00:00 Introduction and Guest Welcome

01:39 Dr. Elyamani's Background and Research Focus

02:54 Understanding Brain Oscillations and tACS

07:31 Comparing tACS with Other Neurostimulation Techniques

11:12 Potential Therapeutic Applications of tACS

20:42 Challenges and Future Directions in tACS Research

35:20 Safety and Practicality of tACS

41:10 Closing Remarks and Future Outlook

Transcript
Mike:

Welcome back to the Neurostimulation Podcast.

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I'm your host, Dr.

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Michael Passmore, and

today I'm joined by Dr.

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Osama Elyamani, a psychiatrist and

neuroscientist whose work is helping to

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shape our understanding of transcranial

alternating current stimulation or tACS

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as both a research tool and a potential

therapeutic intervention in psychiatry.

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His group has published influential

reviews and clinical research exploring

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how brain oscillations might be modulated

to improve psychiatric outcomes.

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We'll be diving into the science,

the clinical evidence, and where

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this field might be headed.

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So stay tuned.

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It's gonna be a really interesting

conversation and I think you're

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really gonna get a lot out of it.

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Dr.

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Elyamani, thanks so much

for joining us today.

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We're really looking forward to

this conversation and just really

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interested in your work and appreciate

that you're taking the time out

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of your busy schedule to share all

of this information with us today.

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So thanks very much.

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Osama: Thank you very

much for the invitation.

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I'm pretty excited

actually to be with you.

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at your YouTube channel and it's

really interesting, to share

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the stuff with the audience and

hopefully we get a nice feedback.

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Mike: Definitely.

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Yeah.

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Thanks.

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Thanks again.

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Maybe we can start by you, providing

a little introduction yourself,

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your background, where you're

located, and a little bit about what

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your lab is currently working on.

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Osama: Yeah, with pleasure.

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my name is Osama Elyamani, I'm a postdoc.

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I have just finished my PhD dissertation.

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I'm pretty excited for sure to share

this piece of information with you.

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Just finished it in July 20 25.

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I'm working on neurostimulation,

especially tACS and TMS in the

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context of psychiatric diseases,

more specifically schizophrenia.

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And we try to record with EEG and

MRI, the activity of the brain and

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accordingly target, the specific activity

associated with psychiatric disorders

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and psychiatric symptoms and modulate

them in order to normalize them.

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And hopefully we help

patients with these disorders.

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I'm located right now in Germany,

Liebig University in Giessen and,

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supervised by Professor Christoph Mulert.

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He has a lot of work done in this field.

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Thank you.

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Mike: Yeah, that's great.

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Well, it's really exciting to, just kind

of get involved in all of this and venture

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out and try and explore these ideas that

you've got passion for and interest in.

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And I'm curious in terms of that,

what would you say first drew you

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to investigate this particular topic

of brain oscillations and, tACS, TMS

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in applications in neuropsychiatry?

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Osama: Well, it's a very hard

question to start with, to be honest,

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the point is, we try to find, the

fingerprints of, the psychiatric

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disorders and the psychiatric symptoms.

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And, as you might know, it's, it's

really limited in patients with

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schizophrenia or psychiatric disorder,

or even in, nonclinical populations.

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we don't have access to

brains in comparison to

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rodents or monkeys whatsoever.

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So we have to depend on the status quo

of methodologies or methods we have.,

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usually we have electrically or

magnetically related methods like

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EMG, EEG or imaging tools MRI and

including for sure functional MRI.

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And if we look at these, we tend to

have patterns of activities in the

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brain, either indirectly with MRI or

directly with EEG: I'm recording the

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electrical activity of the brain.

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And that's why, we have chosen, to

focus on the electrical activity.

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'cause it's a direct measure of

what, what's happening in the brain.

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Although it's really limited in

terms of its, spatial resolution.

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But it gives us a, a very

good temporal resolution.

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And that's why we are interested in this.

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And our work is pretty related to

the association of brain oscillations

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and how we could target these.

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Are they causally related to

the different brain states?

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And in our case it would be the

psychiatric symptoms and in that case

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we could try to modulate them and that's

why we have chosen this pathway in

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order to, to prove this causality or

this causal nature of the electrical

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activity that we could measure with

EEG, for example, and to modulate

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them accordingly with, stimulation

techniques, and in our case, tACS.

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Why tACS?,

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Because it, it tries to simulate

the electrical activity of the

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brain sending alternating current,

alternating waves to simulate these

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coming from the brain that we measure

and hopefully we could, modulate them.

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In terms of potentiation or even

decreasing them, and in order to

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modulate the, the corresponding

functional, or functions of the brain.

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Mm-hmm.

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And sure the symptoms which are

main goal, at the end of the day.

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Mike: Yeah, no, thank you for that.

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That's a, a really succinct way of

explaining a very complicated premise.

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So, so I think one of the key things, as I

understand it, is the distinction between.

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The spatial resolution that would

be afforded by imaging techniques

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like MRI in particular, and then

versus the temporal resolution.

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So the real time brain changes

that can be measured by EEG

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and how tACS influences it.

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Is that, am I on, on the

right track with that?

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Osama: I, I think so.

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I think so.

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And, even to add a more, one more

limitation, once we stimulate with TT

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s we are not able anymore, during the

stimulation to record the electro activity

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of the brain because of, the huge amount

of artifacts that we induce in the brain.

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so we kind of like depend

on the EEG oscillation.

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The EEG measures oscillations, and

we try to modulate them, but we

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can't measure the direct action.

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Of, or the direction, mechanism of action,

let's say, or the influence of tACS on

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the brain, because of the artifacts.

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So we have to depend as well on, MRI,

on the other side, MRI gives us like,

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huge or quite, quite, I would say robust

spatial resolution on the other side, we

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have this drawback of temporal resolution.

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We could try to combine both, for sure

but still, we have to have some kind

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of compromise, There are some papers

actually, which try to measure even

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the local field potential inside the

brain, like intracranial recordings.

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I think the, the, this limited amount of

papers gave us as well access to what's

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really happening in the brain electrically

up on stimulate stimulation with tACS.

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Still, we could still, Try

to use MRI in this, regard.

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using the hemodynamically change,

which is indirect, proxy or

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indicator of brain activity.

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Mm-hmm.

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that's, the limited world

that we have right now.

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Mike: Right, right.

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Yeah.

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And it makes sense to be getting

the best of both worlds in terms of

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using the tools that allow for the

spatial resolution and the tools that

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allow for the temporal resolution in

order to get the best understanding.

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So I'll put an image up of a basic tACS

setup, but perhaps you could just briefly

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explain for those who are less familiar

with tACS compared with other clinically

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available technologies like TMS and

tDCS, do you mind just giving a brief

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overview of tACS and how, how that perhaps

differs from those other two modalities?

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Osama: So I would formulate it like this.

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tACS is more or less at its infancy,

in comparison to the other, modalities.

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I think TMS was the one of the

first to be discovered and even

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used in clinical populations.

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It's, it's FDA approved, I

think in, in Canada as well.

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In, EU it's quite approved as well.

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More specifically for depression.

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It sends magnetic fields in order to

stimulate a specific, parts in the brain.

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And, one of the most used regions,

dorsolateral prefrontal cortex because

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it's quite related, a central hub,

for different, connective functions.

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in terms of depression, it's,

we, we could call it that.

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We could, consider supra

threshold stimulation.

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It could.

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induce action potentials at the target

brain region, those sorts of frontal

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cortex and spec with a specific timing,

even specific stimulation protocols

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we could induce, synaptic plasticity.

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that would lead, to different,

consequences in the brain, to ate

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specific, pathways in the brain

that would lead, to the relief.

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Of, depressive symptoms.

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on the other hand, tDCS and tACS,

they use electrical stimulation.

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So we pop some kind of electrodes on the

skull and we try to target specific brain

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region with, with, with these, electrodes.

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but there is a huge difference.

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in terms of both, tDCS, as the

name will say, properly, some

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people might know about, might

not know about the abbreviation.

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Transcranial direct current

stimulation, tACS is transcranial

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alternating current stimulation.

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So tACS since kind of alternating

current, accelerating current in terms

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of waves, tDCS is just, sending at

one electrode like positive activity

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and the other like negative activity.

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So it's kinda constantly inhibiting or

stimulating one region of the brain.

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in comparison to tACS, and that's

the uniqueness of this method since

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alternating, it simulates what's

really happening in the brain.

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Our brain is really oscillating.

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It's all about rhythms, like different

rhythms in different frequencies.

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And that's why we tended to tailor,

the simulation frequency and the

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parameters using tACS in order

to simulate this in the brain.

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And we drive, with our own frequency

what should happen in the brain.

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For sure.

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There are a lot of, complexities

that we try to overcome with this

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method, but this, the concept behind

it that we simulate what's really

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happening in the brain and compress

it to tDCS with direct current,

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constantly inhibiting or stimulating.

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And TMS was ascending, a

specific, magnetic stimulation

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and, causes action potentials.

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in comparison to TMS, both tDCS and

tACS cannot induce, direct, action

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potentials the increase or decrease

accordingly, the probability to fire

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action potentials a specific phase, in

terms of TAS for sure, at the peak, the

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wave goes down and so on and so forth.

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And, I think this is quite important to

consider, is to not induce, this huge

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amount, of stimulation at the target brain

region, but we would tailor, we would

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induce a specific rhythm, in the brain.

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I think this is like at the heart

of that what's really happening.

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Mike: Yeah, no, that, thanks for

explaining that and that that kind of fits

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with my understanding in terms of this

important concept of the entrainment or

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as you say, tailoring, I like that term to

try to entrain or tailor or encourage or

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prime, I suppose the, the oscillations and

not only perhaps in terms of modulating

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brain function, but also in terms of, it's

curious as well this idea about it being

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a potential, application on the diagnostic

measurement side as well as potentially

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on the therapeutic side as well.

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yeah, it's really interesting.

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And I suppose the potential, or I guess,

what would you say the implications

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are that that has bearing on potential

therapeutic properties in terms of

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things like neuroplasticity as well?

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Osama: Yeah.

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I totally agree.

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we, think you have highlighted, a

very important point that we have

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already mentioned in our, systematic

search review, in this review in the

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European archives of, neuroscience.

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we try to encourage other

scientists, to work with this.

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Infant method, which is tACS, to

discover, how the brain would react to

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this oscillating current the brain is

sending on its own, oscillatory, waves.

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And we, if we simulate them,

if we induce our, with our own

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rhythm, what would really happen?

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And this reactivity would really, help

us not only in maybe treating some

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diseases in the future, which we don't

have at the moment with VACS, but also

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maybe for diagnostic purposes or even

prognostic, purposes, how the brain would

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react to this kind of, modulatory action.

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I think, maybe a subpopulation of,

patients might react differently.

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Accordingly, we could,

try to, they ignore them.

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This would be really amazing because

right now in most of the psychiatrist

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disorders or even all of them,

we don't have objective measures.

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if we will ignore Alzheimer, disease where

we have amyloid plaques and tau protein,

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this whole story and schizophrenia,

depression, and the other guys, we don't

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have this, neurobiological correlate.

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we do have a lot of evidence for

sure, that we try to run some

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associations, but we don't have

this direct path, physiology.

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I think, brain installations, might

help decipher, this picture and, this

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reactivity to tACS specifically because

it simulates, again, the brain activity

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might be, one way trying to discover this.

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Mike: Hmm.

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Yeah.

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So I guess on the diagnostic side,

then the idea would be like, as, as

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a, as a, a biomarker kind of tool.

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Yeah,

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Osama: yeah, yeah.

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Sure.

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I think, we are for sure limited

with EEG because, and EEB because the

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tended to record, the surface of the

brain, the, we don't have, huge amount

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of information from deep structures.

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So we're kind of limited, but we still

have a direct, proxy or indicator of

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the electric activity of the brain.

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So we can depend on this and

the activity of this, kind of

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activity again, would be as well,

interesting way to look at the brain.

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Mike: Mm-hmm.

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Yeah.

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Well, I was curious because

in, in the review that you just

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mentioned, your team highlighted.

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Altered oscillations and, and the

importance of, I guess, the oscillatory

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signature or something like that

across a variety of disorders.

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Schizophrenia, depression, OCD, ADHD,

dementia, neurocognitive disorders.

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So I guess I'm curious, and maybe this

is a bit too broad of a question, but

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which, if any of those disorders do you

think perhaps are the most prominent?

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Uh, so, let me see.

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which, yeah, which of those disorders

would you predict maybe are the

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most promising initial targets for

tACS therapeutic interventions?

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Osama: So you mean which

diseases might show hope?

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using this?

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Mike: Yeah, I guess so.

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what, what maybe the most promising, maybe

it's a difficult, we could go disorder

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by disorder and then you could kind

of, or, or if there's one in particular

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that you think lends itself best to

this kind of technology, both in terms

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of the biomarker potential and or in

terms of some therapeutic potential.

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Osama: That's a very important question.

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I think before asking this

question, we could ask ourselves

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in a very other question.

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Mm-hmm.

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Which is, do we think we have to approach

psychiatry, The typical or the classic way

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of doing it, an disease, based approach

or rather with symptom based approach.

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Mike: Mm-hmm.

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Osama: If you do it symptom based approach

or kind of brain estate based approach.

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And, given that, some brain estates

are connected to or societal, the

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specific patterns and the electrical,

finger or electrical fingerprints.

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Hmm.

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I think this would be kind of interesting.

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we, we don't deal with these diseases

depression as, as a whole, but rather

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oppressive symptom or specific symptoms

that might overlap actually in D or,

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these kind of clinical pictures are

kind of overlapping and we have, for

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example, schizoaffective disorders,

which are really overlapping, with

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the huge umbrella of symptoms.

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So I think, especially with DACS, we

might focus on specific brain states,

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specific, associated with this brain

state, and we target them, according

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to what we record with EEG or MEEG.

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so I would say, I think in the future

most of the researcher might focus

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in, in this, in this direction,

like symptom based approach, rather,

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rather than a disease based approach.

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if we were, or if we, we will discover

kind of, electrical fingerprints

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related to the whole disease.

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So we could try to for sure, like with

the classical disease based approach.

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But think, how we.

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How we, what we know about the

brain, that it works, in different

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states, or it has situational,

let say, electrical fingerprints.

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Mm-hmm.

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And we target these, especially

if we could consider kind of like,

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closed loop, stimulation that we, in

real time we target specific brain

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networks with the specific brain

oscillations with TA Cs, for example.

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but back to your question, if I like

to, kind of predict, in which direction,

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or which disease would show most of the

hope, I think it would be the disease that

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has, specific brain networks involved.

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We kind of discover them like the most,

something like depression where we

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have, specific networks implicated in,

in the pathophysiology or something

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like, obsessive compulsive disorder

where we know like specific networks of

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kind of activated or inhibited and they

lead to the symptoms of OCD, these two

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diseases might be like, interesting.

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to, to, to target with the ICS.

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Mike: Mm-hmm.

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Yeah.

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Well thanks, thanks very much for

explaining that first part because

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I think that's extremely important.

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And it was really interesting because

in a recent episode with, doctors Hamel

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and, and, colzato, we talked a bit more

about this idea about how neuromodulation

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technologies are helping to encourage

people to rethink a little bit about how.

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Psychiatric disorder, neuropsychiatric

disorders are characterized in

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terms of the diagnostics, right?

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And perhaps not, not necessarily

being beholden to this legacy,

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although it's important obviously,

for, for consistency of approach.

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And so, in terms of medication approval,

therapeutic approval, research studies,

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all this kind of stuff, obviously there's

importance in having diagnostic criteria.

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And this is not to disrespect the

legacy of the DSM and any of that

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stuff, but I think a lot of us who

have, clinically experience understand

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that there are shortcomings to that

and, and, and all the, the difficulty

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that goes into thinking about having

to pigeonhole patients so-called into

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like specific diagnostic categories.

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So, so combining that, again, it's

a matter of not either or, but the

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getting the best of both, right?

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So combining that legacy diagnostic

approach with, as you say, a symptom-based

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approach that fits more with.

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These kinds of technologies and the

biomarkers, the, the electrical signatures

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that go along with certain brain states

and, and specific symptoms that, that

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cross in between different disorders.

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It's a really important point.

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yeah, and I guess that also makes

perfect sense in terms of those

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disorders specifically that seem

to be correlated with, with, with

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particular network disruption.

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yeah, it's, it's, it's fascinating because

I think part of it as well is that the,

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perhaps the disorders that, these other

ones, the schizophrenia and then the,

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the dementias that seem to be perhaps

well, are, are, all these disorders are

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complex, but the ones perhaps, that are

more complex than others in terms of like

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the global brain state disruption or have

multiple different symptom complexes.

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I mean, I think if, so, if we

take something like schizophrenia,

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I suppose you could conceivably

break it down into those.

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I think you're, we're taught

the three clusters, the positive

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symptoms, the negative symptoms,

and the cognitive symptoms.

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Yeah, it would be interesting to know

a little bit about whether tACS might

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be helpful in terms of modulating.

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'cause I think the medications are,

are, are pretty good about, helping to

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reduce positive symptoms, shall we say.

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Obviously there's shortcomings and

side effects, this and that, but really

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there's historically been a real dearth

of treatment options for the negative

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symptoms and the cognitive symptoms.

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Do you think perhaps that tACS might.

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Show some promise in terms of treating

any particular symptoms of schizophrenia.

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Osama: Okay.

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That's a very hard question, but

especially, talking about schizophrenia,

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me personally, I, I think that

schizophrenia could be, as you

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said, like kind of subclassified or

subgroup into, sub schizophrenias.

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we see a huge amount of variability,

the clinical pictures and, in our

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own, daily psychiatric, activity, we

are, facing every single time kind of,

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new cluster of symptoms, let's say.

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and so it's kind of, a syndrome cluster of

symptoms and that's why, TACS might, jump

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in, to target these specific symptoms.

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And, I think we are still.

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In the phase where we need a lot of,

research to be implemented, first of all,

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to sub classify, these schizophrenias or

to kind of discover them and for sure,

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associate with them specific electrical

fingerprints or signatures, as you said.

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And to target these very, specifically

and hoping to alleviate the symptoms.

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would say, we, in terms of this legacy

problem, as you said, we don't have

353

:

to consider to consider, medications

versus stimulation techniques or

354

:

all or none, fashion or manner.

355

:

which could combine both.

356

:

where we consider antipsychotic, kind of

dirty drugs where we have a lot of, mostly

357

:

a lot of receptors, blocked or, activated,

deactivated and so on and so forth.

358

:

We fine tune the brain.

359

:

there are neuromodulators

somehow with the, with the neuro,

360

:

neurotransmitters being, targeted

like dopamine, serotonin whatsoever.

361

:

Hopefully we can do it in the

future, target dopamine specific

362

:

regions and we, the serotonin, other

regions and so on and so forth.

363

:

But it's not the case.

364

:

We do it, un selectively in the whole

brain with the help of TACS we could

365

:

add this kind of, specialization, this

kind of specification, of targeting.

366

:

so we kind of tailor what we could target

so we could use both, to, dramatically,

367

:

let's say reduce the positive symptoms.

368

:

it's very well known in, all around the

world, but, antipsychotics are very, very,

369

:

important or play a very important rule.

370

:

with, positive symptoms, but with

negative symptoms and, and, cognitive,

371

:

symptoms, et cetera, cognitive domain,

we sometimes even worsen the situation

372

:

with, especially with the older

373

:

antipsychotics.

374

:

I think the a CS has, has now its

rule, to jump in and try to, figure out

375

:

what really happens in the brain and,

to target specifically these works.

376

:

And, the, I think because some of

these cognitive symptoms and negative

377

:

symptoms are being overlapping

for some other disorders, what

378

:

we said in terms of depression.

379

:

Mike: Mm-hmm.

380

:

Osama: We could do kind of trans agnostic

approaches where we recruit, patients

381

:

with depression, schizophrenia, some other

disorders, and all of them might share

382

:

the same, symptom like working disturbance

or cognitive, disturbances or impairment.

383

:

And we stimulate them with DACS.

384

:

I think this could be

kind of, fascinating.

385

:

So we go translate agnostically

and we find something that could,

386

:

target a specific, symptom.

387

:

I would not say that a specific

stimulation would really, improve the

388

:

whole picture of a psychiatric disorder.

389

:

Is like, I think from my side is will

like really naive a story because we're

390

:

targeting a specific, brain network.

391

:

And we don't have like this, holy grain

network, the brain that, that would

392

:

affect the whole condition of patients.

393

:

Mike: Yeah, no, for sure.

394

:

I think it's, again, we've had similar,

we've touched on this in similar,

395

:

conversations in previous episodes, but

this whole idea of personalized treatment,

396

:

so having the TICS as a potential option

just in conjunction with medication

397

:

and psychotherapy, both in terms of

the diagnostics and then therapeutics,

398

:

which is fascinating as well.

399

:

But I guess with, yeah, so with say

like, okay, well, let's maybe move

400

:

away then from talking particularly

about diagnostic categories, but

401

:

if we talk about, say, a depressive

syndrome, put it in those terms.

402

:

It seems that there are some studies

that show perhaps frontal alpha,

403

:

tACS in, in normalizing oscillations,

improving symptoms, but it seems that

404

:

those improvements are short-lived.

405

:

do you think that there's

some kind of promise in terms

406

:

of that type of an approach?

407

:

Osama: Yeah, I think so.

408

:

I think so.

409

:

to be honest, alpha has a lot

to do with, with depression.

410

:

there is this concept like

frontal alpha asymmetry.

411

:

There's no, huge consensus.

412

:

in this regard, some people could, manage

to prove it, manage, some, couldn't,

413

:

find it in the depression patients

or, depression populations, let's say.

414

:

I would say, Those are the prefrontal

cortex specifically, has a lot

415

:

to do in terms of, depression.

416

:

That's what we know from, research

from, MRI, from EEG, techniques,

417

:

but also from interventional

approaches using DMTS, for example.

418

:

So, and that's why, a lot of,

a lot of researcher are pushing

419

:

forward, to the using as well front

as TTCs, to treat, depression.

420

:

Not about Canada, but I think in

Europe it's really advancing and

421

:

trying to get it approved, or even

off-label views and so on and so forth.

422

:

I think, yeah, the frontal alpha

would, would play an important goal.

423

:

I think, there is, a very famous lab

fluffy Lab and, and USA and they are

424

:

doing a lot of research in this regard,

and I think they are achieving quite a

425

:

lot, and we have mentioned this, I think

some of their, of them, of their papers.

426

:

In, our, in our systematic review.

427

:

again, it depends, how we will.

428

:

Tailor it.

429

:

And I think you pointed a very

important point in this regard, tACS

430

:

would be helpful to tailor to further

personalize medicine in general.

431

:

psychiatric approaches because we

target specific brain ulcerations

432

:

or that are, may be unique for this

specific patient or that patient

433

:

Mike: and

434

:

Osama: we could even, further personalize

it, applying closed loop approaches

435

:

real time we, apply a stimulation

according to, the actual, oscillatory

436

:

pattern for specific, patient.

437

:

So, I think, yeah, back to your questions

real, it's very interesting to apply

438

:

this in in a personalized way for sure.

439

:

frontal, for example, frontal

asymetry or frontal activity, in

440

:

the brain and D-L-P-F-C would be a

very fascinating target with this.

441

:

Mike: Yeah.

442

:

Yeah.

443

:

and I think, thanks for explaining

this concept about the importance of

444

:

understanding the personalization piece

and the individual differences in EEG

445

:

activity, brain oscillations in different

states and different individuals.

446

:

it makes me think about how it's well

known that experienced meditators, are

447

:

much more, they shall we say, I don't

know the specifics, but my general sense

448

:

is that they maybe would have a much

stronger propensity to have alpha states

449

:

in general versus someone who doesn't,

and, or that they can have more control

450

:

over that, or something along those lines.

451

:

So that might be an example of, of

this, this type of, depending on

452

:

someone's background and to the degree

to which their, their symptoms maybe

453

:

correlate with what their baseline

oscillatory activity is and, and

454

:

all of that type of consideration.

455

:

Osama: Yeah, sure.

456

:

and I think, alpha is one of

the main reasons in the brain.

457

:

we do see as like an EG analysis

and, MEG, where Alpha is really

458

:

prominent in our atory, pattern.

459

:

once we close the eyes,

we, we do stimulate it.

460

:

we, we do differentiate it,

especially in the occipital activity.

461

:

And I think the default mode network

plays a, a major rule in this, regard.

462

:

And as, as you said, even with

meditation or even, even tiredness.

463

:

we do see it in all laboratory,

on every single day.

464

:

once we record like resting EEG,

before and after a specific paradigm

465

:

or, mental activity, we do see

this, tiring effect, let's say.

466

:

Mike: Mm-hmm.

467

:

Yeah.

468

:

Yeah.

469

:

I'm curious.

470

:

I was, One of the courses I've been

doing online is a recent course

471

:

on, TMS actually, and in one of the

later sessions they talked about

472

:

a study with tACS in, post-stroke

patients who have left he neglect.

473

:

And that was really fascinating.

474

:

And I think in general, I was

understanding that there is some

475

:

emerging evidence that tACS as a

diagnostic kind of biomarker tool might

476

:

be able to help differentiate between.

477

:

Something like mild amnestic,

mild cognitive impairment, and

478

:

mild stage Alzheimer's disease.

479

:

'cause that's a challenging

differentiation often, and I know that,

480

:

it hinges on functional impairment,

but then often there's a, a gray zone

481

:

there and obviously patients are, are

anxious to know one way or the other.

482

:

And the more we can give them as far

as advice with biomarker tools and

483

:

hopefully non-invasive biomarker tools,

'cause you know, there's the LP and

484

:

this and that, but, you know, if there

are other non-invasive diagnostic

485

:

tools, it would be very helpful.

486

:

Do you see tACS as a promising

technology to help with early stage

487

:

diagnostics in neurocognitive disorders?

488

:

Osama: Yeah.

489

:

Yeah.

490

:

I, I, I think so, for sure.

491

:

And I, I think you, you, you have

already seen it, like in one, one

492

:

paper, try to, to use this in our,

the review we, we have published.

493

:

but again, we will refer back to,

the, The nature, let's say, how brain

494

:

oscillations are being developed

or are developed in, in the brain.

495

:

they depend on or the sato,

let's say formulated in this way.

496

:

The brain oscillations are

coming from primal neurons, more

497

:

specifically from layer five, let's

say in, in the cerebral cortex.

498

:

And they're pretty connected.

499

:

There is a huge connection in the brain.

500

:

the whole brain works,

depends on connectivity now.

501

:

the whole, different brain regions and

even within each region we have entin

502

:

neurons of that tended to, inhibit it.

503

:

These prime blood neuros.

504

:

And at the end, if we, consider this

whole collection in like in a specific,

505

:

Serra colon or cortical colon, we

do see rhythms, in, in the brain.

506

:

So imagine if we lose, a neurogenerative

disorder, some of these neurons

507

:

or entering neurons or whatsoever.

508

:

And I think, the ability of this

cortical, colons or these cortical

509

:

colons to produce the same oscillatory

activity would, would differ.

510

:

and it would be like really, really, maybe

compensating or decompensating, mm-hmm.

511

:

I think if we induce, much more current

from, from outside ex externally in ex

512

:

externally injecting current, and seeing

the reactivity, how, how, the, this

513

:

internal rhythm would, would change.

514

:

And upon the stimulation, this would give

us kind of, I think hint what's really

515

:

happening in terms of neurogeneration

this, this is how I, I see it, I look at

516

:

like, like the very basis of these, brain

oscillations and, what's really happening.

517

:

We do know that, these cells, die and,

and neurogenerative disorders, Alzheimer

518

:

whatsoever, and once they die, we, I, I

think we lose some of the rhythms that

519

:

these neurons were responsible for.

520

:

Mike: And,

521

:

Osama: the ability to react to

externally injecting, current,

522

:

I think would differ for sure.

523

:

And building on that, I think we would

use TICS maybe in the future to further

524

:

de diagnose, how much we have of

neurogeneration, for example, or how, how

525

:

much we have kind of impairment and the

function of a, of a specific brain region.

526

:

'cause how I approach it, let's say.

527

:

Mike: Mm-hmm.

528

:

Yeah.

529

:

No, I think that makes sense.

530

:

I mean, and again, kind of going back

to the distinction between spatial

531

:

resolution and temporal resolution,

perhaps it might make sense.

532

:

'cause these days, of course, we, we

would do, typically, we might recommend.

533

:

A sequence of images in someone

whose diagnosis is unclear.

534

:

Maybe, an MRI at baseline, and then

again, the following year or two, and

535

:

then so on and so forth to see if there's

any progression in atrophy, I suppose.

536

:

But then perhaps EEG could similarly

be done at baseline, and then at

537

:

year two and year four, whatever,

and, and noninvasive again, and not

538

:

particularly expensive, I suppose.

539

:

And then that could be perhaps in some

way combined with tACS as, as a way

540

:

of figuring out, okay, well is there a

biomarker signal here that's concerning?

541

:

Osama: yeah, for sure.

542

:

And I think in this regard, I have to

highlight something that, at least we, we

543

:

try to, to, to approach in our laboratory.

544

:

There's source localization, to use

EEG, brain, a scalp activity and try

545

:

to find what's really happening at

the source level within the brain.

546

:

we do have some methods trying to

estimate, the source, activity,

547

:

although they are pretty limited, but

we, we could kind of connect, in a

548

:

very rough estimation, what's really

having an every single gray matter,

549

:

source, hippocampus or whatsoever.

550

:

I, I think they're quite limited.

551

:

I will not highlight their

very, huge importance.

552

:

But we could use this, these techniques

and maybe we could combine them as well

553

:

with something like functional MRI and

we have, two Specific indicators even

554

:

from deep, deep brain s instructions?

555

:

yeah, for sure.

556

:

I do agree that we have, very limited,

spatial resolution, but, if we use

557

:

kind of, MRI based EEG analysis mm-hmm.

558

:

These, those kind of, it would be I

would say for the current states, like

559

:

Holy Grave or the brain activities

that we have like both of them, like

560

:

the spatial resolution from MRI and

the temporal resolution from the EG.

561

:

Mm-hmm.

562

:

That's the best of what we have right now.

563

:

You'd say.

564

:

Mike: Yeah, and I, I don't, I

have this vague recollection.

565

:

I, I don't have any clinical

experience with interpreting EEGs.

566

:

I've never had that training, but I

do recall something around frontal, in

567

:

particular, perhaps there being, some

intranasal electrode placement that

568

:

might help to provide some specific

measurement of frontal function.

569

:

Is that something that maybe

can be, or is being researched

570

:

as part of the tACS protocol?

571

:

Osama: I, I don't know, to be honest,

but I think, I mean, for sure the

572

:

more coverage we have or the head,

the more we could, measure the

573

:

electrical activity of the brain.

574

:

But what I could say here in this regard

that, there are, I'm for sure again, some

575

:

limited intracranial recordings, like

in different, papers already published.

576

:

I mean, with, eucalyps patients, like

most of them, and again, we don't

577

:

have physiologically acting brains.

578

:

I mean, they're not functionally,

normal, to be honest.

579

:

We are looking from, the brains

of epilepsy patients, which more

580

:

or less, Would show, some other

dynamic from an eclipse, population.

581

:

so I have never heard, heard of

it, to be honest, but, I think

582

:

that would be interesting for sure.

583

:

I mean, like, to have the more, the

more we cover the head with clothes

584

:

for sure, the more we would get, like

a glimpse of what's really happening

585

:

with the brain, especially for use or

apply later on source localization.

586

:

Mike: Mm-hmm.

587

:

Yeah.

588

:

Well, it strikes me, just in reviewing

the, the literature that in general

589

:

the safety and tolerability of tACS

is strong, not really concerns about

590

:

side effects or any particular risk of

seizure induction or anything like that.

591

:

Osama: indeed.

592

:

I think tACS maybe one, the

safest or one of the safest

593

:

neuro stimulatory, techniques.

594

:

what we know that TMS because

it's a software threshold, as we

595

:

said, has threshold stimulation.

596

:

It might unfortunately induce some

epileptic, charts or whatsoever,

597

:

or elliptical cases if we do

have risk factors for this.

598

:

we do screen for sure, before

applying it, but still there

599

:

is a huge risk, to development.

600

:

And that's why we try to, to exclude

patients or even participants

601

:

with in risk, to develop.

602

:

eclipse or compulsions, the stimulation

tDCS, it's more or less safer

603

:

than TMS, but still, it has more

adverse events comparison to tACS.

604

:

I think according to the current

literature, tACS, the safest right

605

:

now, even for the, fine tingling

sensation and the local sensation,

606

:

tACS has proven to be the safest.

607

:

To my knowledge, or according

to the best of I know, there is

608

:

no one epileptical case that was

reported with, tACS, for example.

609

:

I think that not to be biasing, one

factor is that we do exclude, in

610

:

advance, patients participants who might

have any risk to develop, epilepsy.

611

:

in a nutshell, it's, much safer than,

tDCS for sure and, TMS, maybe because

612

:

of this oscillatory pattern, because

in tDCS for example, we do have,

613

:

again, sub threshold stimulation.

614

:

We don't induce action potentials,

but we do, constantly induce,

615

:

or increase the probability of

failing action potential with this,

616

:

catho or nodal way of stimulation.

617

:

Mike: Yeah, no, thanks

for explaining that.

618

:

That's, I think that's the, typically

the, well, it makes sense that

619

:

that's one of the major hurdles to

overcome in order to get regulatory

620

:

approval for therapeutic applications.

621

:

So I'm curious to know, what would

you see if you were to look forward

622

:

into the next 5, 10, 15 years?

623

:

does it seem that, based on your research

and your, obviously your expertise in

624

:

this, would you hope that tACS will

become more clinically available for

625

:

biomarker diagnostics and or therapeutic

applications or both, I guess.

626

:

Osama: I'm not the very good

person, to predict what's

627

:

really happening in the future.

628

:

But anyway, tACS is still,

again, it's at its infancy.

629

:

We do have some clinical trials, even some

registers on them if we go to, clinical

630

:

trials, trials I forgot the website.

631

:

clinical trials.gov,

632

:

I think.

633

:

Mike: Okay.

634

:

Yeah, yeah.

635

:

Clinical trials.gov.

636

:

That's right.

637

:

Yeah.

638

:

Osama: if we go to the,

website clinical trials.gov,

639

:

we do find a lot of,

clinical trials using tACS.

640

:

I'm not, pessimistic, but, because

we were still discovering how tACS is

641

:

working and how to optimize the parameter.

642

:

I think this is a very important

aspect in tACS as we didn't reach,

643

:

the optimal conditions, or let's

say we didn't set the stage.

644

:

To further, apply it with

prominent hope, to treat patients.

645

:

But hopefully, the other colleagues

will really find some important,

646

:

results in clinical populations.

647

:

but we do still have to apply, very basic

research to optimize the tACS parameters

648

:

and to, further discover how it's really

working and how to maximize its effects.

649

:

so I would say, in the coming

five years, I personally might

650

:

exclude, that it would be approved,

unfortunately, because we do have, a

651

:

huge myriad of parameters to consider.

652

:

there would be a lot of positive

results in the literature.

653

:

but again, it's about reproducibility and,

convince legalization, to get it approved.

654

:

I think it might not be convincing

for that stage in 10 years for sure.

655

:

we do have hope that we will do it.

656

:

especially that it's quite

practical, practical to apply it.

657

:

it's really practical to, compare it

to TMS, for example, TMS, should be

658

:

applied with a specific, device is

quite huge and, it has its own call.

659

:

And this technical, her, let's

say, tACS on the other side.

660

:

Could be the device and the technical

equipment could be minimized.

661

:

And, I think there is a hope or

there is kind of hope for, even

662

:

home applicable stimulation.

663

:

I think there is, for example,

some, companies, in Europe at

664

:

least, which I have seen, they do

provide, home applicable electrical

665

:

stimulatory devices, for tDCS.

666

:

And they are quite convenient.

667

:

I have tried them on my own head, and I

think this would be really comfortable

668

:

for, for the patients, to have something,

at home and we could even, connect it

669

:

with the internet and we have control

over it as a researcher, as, clinicians.

670

:

something this would be

Pushing us, in this direction.

671

:

But again, five years would be really

hard in 10 years I would assume.

672

:

So, hopefully.

673

:

Mike: Mm-hmm.

674

:

Yeah, no, it's, it's important

to be hopeful about it.

675

:

And I guess that's, it's, it's an

exciting time, especially to be launching,

676

:

a research career and to be also

combining that with a clinical career.

677

:

and to be in a field that's in its

infancy as well must be very exciting

678

:

because there's so many different

potential opportunities and directions

679

:

for exploring the science and, and this

particular technology in terms of all of

680

:

the possible therapeutic applications.

681

:

Osama: Yeah, indeed.

682

:

And, again, I would say, because

it's a really practical to, to apply

683

:

it, I think, this would, encourage

a lot of researchers, a lot of

684

:

clinicians, to apply it in the future.

685

:

Mike: Yeah.

686

:

And then I guess maybe on a closing note,

I'm just curious, is there any particular

687

:

guidance or advice that you might give

to students or, early stage researchers,

688

:

people who are working towards their PhDs?

689

:

in terms of Yeah, the, their direction

or what you might encourage, them

690

:

in terms of, your own experience

and, and where you see the field

691

:

of neuromodulation in general.

692

:

Heading.

693

:

Any words of wisdom for them.

694

:

Osama: That's a, that's a very hard

question, but I, I would say I'm still

695

:

as well, post, so I'm, I'm still as

well in this stage, on this stage.

696

:

I would say, we, we, we, research on its

own, it's really, competitive for sure.

697

:

It's really kind of hard to, to,

to, to, especially if you combine

698

:

it with your clinical field.

699

:

I mean, for me, for example, I'm

a psychiatrist, I think the most

700

:

important thing that, to keep

passionate, to keep motivation, that

701

:

you do something that you really like.

702

:

I mean, don't jump in in a PhD program

or kind of, I don't know, a field of

703

:

research that you don't really like.

704

:

I remember that, I worked sometimes,

day and night you order to

705

:

discover or trying to discover a

very specific, piece of results.

706

:

Whatsoever.

707

:

if I didn't have the passion to

do so, them motivation to do so, I

708

:

would not expect, spend that time.

709

:

And, for sure.

710

:

The, the second thing would be

we have to ask also, because

711

:

neurosciences are really, really

branching and there is a lot of

712

:

multidisciplinary, multidisciplinary

approaches and so on and so forth.

713

:

we have to ask ourselves.

714

:

I, I do categorize it in this way.

715

:

which field you like to work in?

716

:

Because I work a lot of sub

years in neuroscience, which

717

:

method you like to use?

718

:

and which organism that

you'd like to work on?

719

:

Because if you'd like to have some

invasives of more, let's say, access.

720

:

To the brain, you could consider

something like rodents or monkeys where

721

:

you could invasively, for sure, some

limitations according to the ethical

722

:

regulations you could, approach, the

brain, the methods you are using.

723

:

for example, in humans, we,

we do have some that again,

724

:

we have already discussed.

725

:

There are limitations like, MRI or EEG.

726

:

and the fourth factor would be the topic.

727

:

what you, what you'd like to, to discover.

728

:

you'd like to work on something, in my,

in my case, like oral hallucinations,

729

:

schizophrenia patients or depression

treatment or just, the discovering the

730

:

pathophysiology and so on and so forth.

731

:

So in a nutshell, you have to, you

have to really, really spend a lot of

732

:

time to choose the field that, grasp

your, would grasp your motivation.

733

:

And it would be, depending on these

four factors, the field you would like

734

:

to work on and methodology, organism.

735

:

And, for sure the very specific

topic, of your research.

736

:

Mike: Hmm.

737

:

Thanks so much.

738

:

it's so clear that, that you're passionate

about that and, and I really appreciate

739

:

you taking the time to share your story

and your passion, your insights, and

740

:

really helping us to navigate this

exciting frontier in neurostimulation,

741

:

helping us to understand tACS and

all of these fascinating potential

742

:

applications, all the way from the

diagnostic biomarker side through to

743

:

the personalized therapeutic side.

744

:

it's clear to me from this conversation

that tACS holds great promise for

745

:

psychiatry, but it also raises important

questions that will need ongoing, careful,

746

:

rigorous investigation in the years ahead.

747

:

As you say, it's in its infancy relative

to some other treatments, but bringing all

748

:

of these treatment and diagnostic options

together to personalize the approach

749

:

for patients is really, I think, going

to be the key in the upcoming years.

750

:

And so thank you again, Dr.

751

:

Elyamani, for joining us.

752

:

for viewers and listeners,

I'm going to link Dr.

753

:

Elyamani's.

754

:

team lab's, key papers in the show notes.

755

:

So I do encourage you to check those out

and, please add comments or questions in

756

:

the show note in comment section below.

757

:

And I'd be happy to get

back to you with that.

758

:

And yeah, thanks again Dr.

759

:

Elyamani.

760

:

really appreciate the conversation

and just wish you and your lab all

761

:

the best in your research endeavors

and in your clinical work also.

762

:

Thanks so much.

763

:

Osama: Thank you very

much for the invitation.

764

:

I do thank you as well for your words.

765

:

And maybe a last message from my side.

766

:

feel free to drop us some messages.

767

:

we don't buy it.

768

:

if you'd like to consider

the young researchers.

769

:

Mike: Fantastic.

770

:

Yeah, that's great.

771

:

It'll be wonderful to keep in touch

and hopefully we'll be able to meet

772

:

at a future conference, something like

that in the next months and years.

773

:

So thanks again.

774

:

Thank you.

775

:

And so for viewers and listeners,

thanks again for tuning in.

776

:

until next time, be well, stay curious

and join us next time as we discuss and

777

:

explore new frontiers in the boundaries

of neurostimulation and neuroscience.

778

:

Thanks very much.

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About the Podcast

The Neurostimulation Podcast
Exploring the frontier of interventional mental health.
Welcome to The Neurostimulation Podcast — a deep dive into the expanding frontier of interventional mental health.

Hosted by Dr. Michael Passmore, a psychiatrist specializing in neurostimulation and geriatric mental health, this show explores how cutting-edge interventions — from non-invasive brain stimulation (TMS, tDCS, and beyond) to ketamine-assisted psychotherapy — are reshaping the landscape of modern psychiatry and neuroscience.

Each episode bridges science, clinical experience, and human insight, featuring thought leaders and innovators who are redefining how we understand and treat the mind.

Whether you’re a clinician, researcher, student, or simply fascinated by the brain, you’ll discover practical knowledge, fresh ideas, and inspiring conversations that illuminate the evolving art and science of mental health care.

Subscribe for episodes that stimulate your mind, deepen your understanding, and connect you to the future of brain-based healing.

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About your host

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Michael Passmore

Dr. Michael Passmore is a psychiatrist based in Vancouver, BC, with expertise in non-invasive neurostimulation therapies, geriatric mental health and ketamine-assisted psychotherapy. 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. At Sea to Sky NeuroClinic (seatoskyneuro.clinic), Dr. Passmore offers interventional mental health treatments tailored to clients across Canada.​