David Ghiyam

The ability of the mitochondria in these microglia to do their job and allow the microglia to nurture our brain cells, to nurture our synapses, to create chemicals that allow us to grow new brain cells and to shore up what is called the blood brain barrier is fully dependent upon their metabolism, their mitochondrial function. When mitochondrial function is threatened,

The ability of the mitochondria in these microglia to do their job and allow the microglia to nurture our brain cells, to nurture our synapses, to create chemicals that allow us to grow new brain cells and to shore up what is called the blood brain barrier is fully dependent upon their metabolism, their mitochondrial function. When mitochondrial function is threatened,

These wonderful, loving, nurturing cells shift to become the evil twin. The same cell now destroys our neurons, activates pathways in neurons to undergo apoptosis or pre-programmed cell death. It threatens and damages and destroys ultimately the synapses where communication takes place. It reduces the formation of this chemical to grow new brain cells.

These wonderful, loving, nurturing cells shift to become the evil twin. The same cell now destroys our neurons, activates pathways in neurons to undergo apoptosis or pre-programmed cell death. It threatens and damages and destroys ultimately the synapses where communication takes place. It reduces the formation of this chemical to grow new brain cells.

It increases the production of beta amyloid and ultimately threatens the integrity of the blood brain barrier. Same cell, two types, the nurturing M2 phenotype and the evil twin, the M1 phenotype.

It increases the production of beta amyloid and ultimately threatens the integrity of the blood brain barrier. Same cell, two types, the nurturing M2 phenotype and the evil twin, the M1 phenotype.

and the microglia can go back and forth and their ability to go back and forth and what motivates them to change from being the helpful twin to the evil twin are changes in their mitochondrial function and it is reversible. Really?

and the microglia can go back and forth and their ability to go back and forth and what motivates them to change from being the helpful twin to the evil twin are changes in their mitochondrial function and it is reversible. Really?

so we can go back to a wonderful nurturing brain that allows more synapses to to form that allows new brain cells to generate in the brain who wouldn't want that especially in the brain's memory center and really creates an environment that's nurturing for you on brain but is it possible if dementia has gone too far into alzheimer's and

so we can go back to a wonderful nurturing brain that allows more synapses to to form that allows new brain cells to generate in the brain who wouldn't want that especially in the brain's memory center and really creates an environment that's nurturing for you on brain but is it possible if dementia has gone too far into alzheimer's and

Well, the duration of the issue is less important as how aggressive it is. So, as one would expect, as one would see with other degenerative conditions or even cancer, some people get attacked more aggressively and decline more quickly based upon their metabolic health and others don't. Can it be reversed? Yes.

Well, the duration of the issue is less important as how aggressive it is. So, as one would expect, as one would see with other degenerative conditions or even cancer, some people get attacked more aggressively and decline more quickly based upon their metabolic health and others don't. Can it be reversed? Yes.

Are there new studies demonstrating that targeting metabolism has a dramatic effect on the brain in an existing Alzheimer's patient? Yes. And this gets back to our GLP-1 agonist story.

Are there new studies demonstrating that targeting metabolism has a dramatic effect on the brain in an existing Alzheimer's patient? Yes. And this gets back to our GLP-1 agonist story.

So let me run through the dots, because this will be on the quiz. Why we want to target metabolism, why the GLP-1 drugs have such an opportunity to be game changers. And again, my focus has never been medication, but my commitment has been to never take anything off the table. under the doctrine of above all do no harm and looking at things like risk-benefit ratio.

So let me run through the dots, because this will be on the quiz. Why we want to target metabolism, why the GLP-1 drugs have such an opportunity to be game changers. And again, my focus has never been medication, but my commitment has been to never take anything off the table. under the doctrine of above all do no harm and looking at things like risk-benefit ratio.

What I'm saying is that metabolism is the central focus. This is one avenue that seems to target metabolism and does so aggressively. Long term, how might that play out? We don't know yet.

What I'm saying is that metabolism is the central focus. This is one avenue that seems to target metabolism and does so aggressively. Long term, how might that play out? We don't know yet.

But a poster presentation that was at the American, rather the Alzheimer's Association International Conference about two and a half months ago revealed a one-year study in which the actual Alzheimer's patients over a one-year period compared to control, their rate of brain shrinkage receiving a GLP-1 agonist drug was reduced by 50%, the rate of shrinkage of their brain.

But a poster presentation that was at the American, rather the Alzheimer's Association International Conference about two and a half months ago revealed a one-year study in which the actual Alzheimer's patients over a one-year period compared to control, their rate of brain shrinkage receiving a GLP-1 agonist drug was reduced by 50%, the rate of shrinkage of their brain.