Two proteins in the brain are heavily involved in the development of Alzheimer’s, agree most scientists. Beta-amyloid (A) reaches abnormal levels in the brain of people with Alzheimer’s and forms plaques that collect between neurons and disrupt cell function. The amyloid cascade hypothesis considers that the deposition of the amyloid- peptide in the brain parenchyma is a central event in Alzheimer’s disease pathology.
Tau proteins forms neurofibrillary tangles inside neurons which block the neuron’s transport system.
However, it is not clearly known exactly how these proteins relate to each other.
Impairments in cholesterol and glucose metabolism, inflammation, oxidative stress and dysfunctional ‘garbage collection system of the brain’ are all supposed to help push the amyloid accumulation, which then probably causes damage to the synapses leading to tau aggregation.
New findings show both A and tau oligomers bind to amyloid- protein precursor (APP). And the presence of this protein is required for both A
and tau to enter neurons and induce abnormal synaptic function and memory. It is also proposed that extracellular oligomers of A and tau act in parallel and upstream of APP in Alzheimer’s pathogenesis.
However, therapeutic approaches aimed at decreasing A levels and tau-based clinical trials are yet to produce positive findings.