Epoch Times - A New Experimental Active Immunotherapy for Treating Alzheimer’s

Jan. 23, 2026 - Epoch Times

02:30

A New Experimental Active Immunotherapy for Treating Alzheimer’s | Lou Reese

🔴 WATCH THE FULL EPISODE: https://ept.ms/4qDRpDoShow more A new experimental approach to Alzheimer's could potentially change the game for treating this devastating disease. The main culprit in Alzheimer's seems to be a sticky protein called amyloid beta that builds up in the brain, forming toxic clumps (like plaques and smaller tangles) that are believed to damage brain cells. Biotech entrepreneur Lou Reese has been working on a synthetic peptide-based active immunotherapy UB-311 to treat Alzheimer's. Show less
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Time	Text
Gently Activating the Immune System 00:02:30
	What if we can gently turn on the immune system to only generate these antibodies?
	No off-site reactions.
	The typical vaccine, as an example, generates over 95% towards the toxic carrier.
	That could be KLH, that could be any of the carriers, and less than 5% to the actual target.
	That's why immune systems get...
	And just to summarize, basically you're saying when you do a typical vaccine, most of the antibodies created are not...
	Yeah, virtually all are actively against the wrong thing.
	So in effect, think of it as riling up the immune system to get a minor response.
	What we do is actually, it's much more like CLTM6.
	We come in completely silently and the outcome is, so the immune system is completely silent, and then we take out the bad guys.
	So we pick up Maduro, there's no casualties, and we're out, right?
	And so that's what we designed.
	It was made for that.
	And that's exactly what we see in the clinic and in patients.
	And so in the future, and what I believe and what is true is that we can go where antibodies and monoclonals and biologics can't go, which is we can do multiple targets at the same time.
	We can go after multiple targets of the same protein or the same hormone that's causing autoimmune diseases.
	We can go after the thing that is causing Alzheimer's in this case, which is the toxic oligomeric and febrile forms of A-beta.
	That's the beginning of the decline.
	That's what people colloquially know as amyloid plaque, right?
	So actually, no.
	Plaque is a surrogate marker that can be measured easily by PET scan.
	It turns out that there are a huge number of Alzheimer's patients that do not have plaques.
	The reason that the side effects for going after the plaque are so horrendous in the existing drugs is that you have 17 to 34 percent rates of REE.
	That's a fancy formula.
	Brain swelling.
	Brain swelling.
	And all of the current approved therapies are monoclonal antibodies.
	The dilemma with those is that they're expensive, difficult to administer, and have these side effects.
	And so they're just not possible to use those in any way for prevention.
	So we basically generate only those specific antibodies, and they actually change, it's called antibody maturation, to match your personal version of those toxic oligomers and fibrils.
	So this is a personalized medicine approach.
	So it triggers your body to make those antibodies in quantity, and then it breaks up those fibrils and actually covers them with dendrites in the brain.
	And then that naturally alerts the immune system to clear them.

Time

Text

Gently Activating the Immune System 00:02:30

What if we can gently turn on the immune system to only generate these antibodies?

No off-site reactions.

The typical vaccine, as an example, generates over 95% towards the toxic carrier.

That could be KLH, that could be any of the carriers, and less than 5% to the actual target.

That's why immune systems get...

And just to summarize, basically you're saying when you do a typical vaccine, most of the antibodies created are not...

Yeah, virtually all are actively against the wrong thing.

So in effect, think of it as riling up the immune system to get a minor response.

What we do is actually, it's much more like CLTM6.

We come in completely silently and the outcome is, so the immune system is completely silent, and then we take out the bad guys.

So we pick up Maduro, there's no casualties, and we're out, right?

And so that's what we designed.

It was made for that.

And that's exactly what we see in the clinic and in patients.

And so in the future, and what I believe and what is true is that we can go where antibodies and monoclonals and biologics can't go, which is we can do multiple targets at the same time.

We can go after multiple targets of the same protein or the same hormone that's causing autoimmune diseases.

We can go after the thing that is causing Alzheimer's in this case, which is the toxic oligomeric and febrile forms of A-beta.

That's the beginning of the decline.

That's what people colloquially know as amyloid plaque, right?

So actually, no.

Plaque is a surrogate marker that can be measured easily by PET scan.

It turns out that there are a huge number of Alzheimer's patients that do not have plaques.

The reason that the side effects for going after the plaque are so horrendous in the existing drugs is that you have 17 to 34 percent rates of REE.

That's a fancy formula.

Brain swelling.

And all of the current approved therapies are monoclonal antibodies.

The dilemma with those is that they're expensive, difficult to administer, and have these side effects.

And so they're just not possible to use those in any way for prevention.

So we basically generate only those specific antibodies, and they actually change, it's called antibody maturation, to match your personal version of those toxic oligomers and fibrils.

So this is a personalized medicine approach.

So it triggers your body to make those antibodies in quantity, and then it breaks up those fibrils and actually covers them with dendrites in the brain.

And then that naturally alerts the immune system to clear them.