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The uniform failure of recent drug trials in Alzheimers disease has highlighted the critical need for a more accurate understanding of the fundamental nature of Alzheimers disease. Dr. Bredesens research has led to new insight that explains the erosion of memory seen in Alzheimers disease, and has opened the door to a new therapeutic approach. He has found evidence that Alzheimers disease stems from an imbalance in nerve cell signaling: in the normal brain, specific signals foster nerve connections and memory making, while balancing signals support memory breaking, allowing irrelevant information to be forgotten. But in Alzheimers disease, the balance of these opposing signals is disturbed, nerve connections are suppressed, and memories are lost. This model is contrary to popular dogma that Alzheimers is a disease of toxicity, caused by the accumulation of sticky plaques in the brain. Bredesen believes the amyloid beta peptide, the source of the plaques, has a normal function in the brain -- promoting signals that allow some of the nerve connections to lapse. Thus the increase in the peptide that occurs in Alzheimers disease shifts the memory-making vs. memory-breaking balance in favor of memory loss. This work has led to the identification of several new therapeutic candidates that are currently in pre-clinical trials. Dr. Bredesens novel insights into the fundamental nature of Alzheimers disease recently attracted an investment of $3.5 million toward a $10 million goal for initial clinical trials of these new therapeutics. This generous support came from the private venture capitalist Douglas Rosenberg, who is helping to fund the Alzheimers Drug Discovery Network, centered at the Buck Institute. The unit is screening drug candidates to find those that can preserve a healthy balance in the signaling pathways that support memory. Dr. Bredesens work on nerve cell signaling is also the focus of a collaboration between the Buck Institute and BioMarin Pharmaceuticals, Inc., which is seeking treatments for a rare form of Alzheimers disease, early onset Familial Alzheimers Disease (eFAD), which may develop in people as young as 30 years of age.
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论文共 348 篇作者统计合作学者相似作者
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Biomedicinesno. 8 (2024)
Journal of Alzheimer's diseaseno. 2 (2023): 429-437
Rammohan V. Rao, Kaavya G. Subramaniam,Julie Gregory, Aida L. Bredesen,Christine Coward,Sho Okada,Lance Kelly,Dale E. Bredesen
biorxiv(2023)
Journal of Alzheimer's disease : JADno. 3 (2023): 1051-1058
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#Papers: 349
#Citation: 41092
H-Index: 95
G-Index: 199
Sociability: 7
Diversity: 0
Activity: 1
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