BrainStorm Live Episode 15: How Amprion Enables Effective Drug Development
Amprion’s CEO Dr. Russ Lebovitz explains the bad actors that drive the progression of Alzheimer’s and Parkinson’s—three types of Prions named Abeta, Tau and Synuclein in their soluble aggregate forms. By detecting these elusive rogue proteins early, Amprion’s breakthrough Prion Early Detection Science℠ can accelerate the development of drugs for Alzheimer’s and Parkinson’s.
Developing Drugs for Alzheimer’s & Parkinson’s
Amprion’s role includes helping patients and their doctors understand who has which molecular defect. Also, Amprion helps the development of drugs for Alzheimer’s and Parkinson’s. So just to recap, Alzheimer’s appears to be caused by misfolding of two predominant brain proteins. One is ABETA amyloid, one is TAU. And ABETA and TAU, both can misfold in several different ways. So we have the normal protein, we have a misfolded form that leads to very large insoluble aggregates, and we have a second misfolded form that leads to soluble, small aggregates that appear to be able to spread, and this is probably the carrier of the disease in the brain.
So in general, the normal forms of these proteins can be detected by very standard methodologies. However, the normal form doesn’t reflect the disease. The misfolded form in this form of large, soluble aggregates can be detected initially under the microscope but since we would like to avoid doing biopsies for brain they can also be detected more and more by imaging. However, these large, insoluble aggregates do not appear to be linked so tightly with the disease.
There are many patients with Alzheimer’s that don’t seem to have plaques or tangles and there are many patients who are normal aging who have plague and tangle and don’t appear to have the disease. So, Amprion focuses on the small, soluble misfolded aggregates that many people believe are the actual carrier of the disease. Amprion can uniquely detect the small, soluble aggregates. We can detect them in the cerebral spinal fluid. We are working to be able to detect them in the blood and we believe that this is the hallmark of the disease, this is the carrier of the disease. This is what spreads it between cells without knowing about how much and what these structures are of these small, soluble aggregates.
It’s very difficult to have a handle on the disease and I think it’s fair to say that if you only look at the normal and the large clumps, that doesn’t give a sufficient picture to be able to understand what’s going on in a patient. However, looking at the small, soluble aggregates appears to be necessary and maybe necessary and sufficient to diagnose and treat that disease.
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