Autopsies show that there are two abnormal structures in the brain with AD called plaques and tangles. Plaques are made from a protein known as Beta-amyloid and tangles are made of Tau protein. These proteins also exist in a healthy brain. What make them to lose their normal function and cause the cell death?
When tau is hyperphosphorylated it is saturated and this disrupt the microtubules structure and function leading to failure in neuronal cell connection to other neurons this saturated tau that differs from normal tau is the reason.
As for amyloid it is delivered from amyloid protein precursor and it is cleaved by beta and gamma secretases .. when cleavage is at point 42 this will lead to insoluble amyloid beta42 that accumulates in the form of plaques and also has role in Alz disease development.
The question is it tau that begins the pathology or amyloid is the initiator.
While a very debated topic, one would be just as correct in looking at the abnormal "deposits" as the result of damage from a different etiology. Disrupting function or the result of disrupted function (?) both would be a good debate. As for amyloid - very challenging to even know what specifically the reference will be as "amyloid" is not one structure - but rather proteins that are found in nature and when dealing with a specific (42) many other labels are left out in the collection of those samples. I consider amyloid to be part of a system that we do not have good understanding of and when evaluated under the watchful research eye - the snapshots in time may not reflect all of the footprints that lead up to the finding of amyloid. Folding and other well studied mechanisms could be a normal response and ends up being rather efficient for the brain to use because these "scars" are very durable!
The latest opinion that Herpes Virus is a causative agent for Beta-amyloid
Adib Valibeygi
more: to me, the question is "what makes some brain more resilient than others, bearing the same amount of toxic [misfolded] proteins ?"
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