Shocking Study Finds Decreased Proteins – Not Amyloid Plaques – Cause Alzheimer’s Disease (new study 2022)
The prevailing theory is that Alzheimer’s disease is caused by the buildup of amyloid plaques in the brain. However, new research finds that it is actually caused by a decline in levels of a specific protein. Contrary to a prevailing theory that has been recently called into question, new research from the University of Cincinnati (UC) bolsters a hypothesis that Alzheimer’s disease is caused by a decline in levels of a specific protein.
The research found that people can remain cognitively normal regardless of the amount of amyloid plaques in their brains as long as they maintain a baseline level of soluble amyloid-beta in the brain above 270 picograms per milliliter.
Study Proposes Increasing Soluble Beta-Amyloid to Treat Alzheimer’s Disease
Amyloid beta – Wikipedia https://en.wikipedia.org/wiki/Amyloid_beta
Amyloid beta (Aβ or Abeta) denotes peptides of 36–43 amino acids that are the main component of the amyloid plaques found in the brains of people with Alzheimer’s disease.[2] The peptides derive from the amyloid precursor protein (APP), which is cleaved by beta secretase and gamma secretase to yield Aβ in a cholesterol-dependent process and substrate presentation.[3] Aβ molecules can aggregate to form flexible soluble oligomers which may exist in several forms. It is now believed that certain misfolded oligomers (known as “seeds”) can induce other Aβ molecules to also take the misfolded oligomeric form, leading to a chain reaction akin to a prion infection. The oligomers are toxic to nerve cells.[4] The other protein implicated in Alzheimer’s disease, tau protein, also forms such prion-like misfolded oligomers, and there is some evidence that misfolded Aβ can induce tau to misfold.[5][6]
A study has suggested that APP and its amyloid potential is of ancient origins, dating as far back as early deuterostomes.[7]
