Synaptogenix Inc (SNPX)

[InTheTrenches]

More proof that many Alzheimer's researchers still believe Amyloid-Beta (ultimately leading to neuronal death) is the cause of Alzheimer's Disease.

"The accumulation of amyloid beta is thought to trigger a neurotoxic cascade, leading to plaque formation, phosphorylation of tau protein, formation of neurofibrillary tangles, inflammation, synaptic loss and eventually neuronal death."

https://www.cell.com/current-biology/fulltext/S0960-9822(18)30552-9

While the focus is still on Amyloid-Beta, it is now believed that anti-Amyloid drugs must be given much earlier in the disease process, BEFORE neurons die.

The excerpt below reveals many researchers flawed logic in the cause of AD: research shows a strong correlation between mutation of AD genes and amyloid deposition. Therefore, amyloid deposition must be the cause of AD. Note that lack of synaptic density is also mentioned as a sequelae of amyloid deposition--not the cause of AD, as hypothesized by Dr. Alkon.

"There has been a substantial amount of skepticism towards the amyloid hypothesis ever since its first description in the 1980s. Critics often claim amyloid precursor protein (APP) has neurotropic effects, sharing similar structural features with the precursor of epidermal growth factor, suggesting that increased expression of APP and subsequent increases in amyloid deposition are a response to neuronal injury rather than a pathological driver of the disease. The large amount of failed therapeutic trials targeting amyloid deposition is often used as confirmation of this theory. However, the strong correlation between mutations in the PSEN1, PSEN2 and APP genes and trisomy 21, which all lead to increased accumulation of amyloid plaques and the development of early-onset familial Alzheimer’s disease, strongly supports the amyloid hypothesis. PSEN1 and PSEN2 are important components of the ?-secretase complexes responsible for the cleavage and release of Aß. The APP gene is located in chromosome 21 and mutations in the gene itself or trisomy 21 result in increased levels of amyloid beta. Also Aß42 peptides isolated from late-onset Alzheimer’s disease human brains cause memory deficits, long-term synaptic depression and decreased synapse density when injected to rodent brains, thereby providing further support for the amyloid hypothesis."