Although the exact biochemical basis of Alzheimers disease hasnt been completely

understood yet, AD has been associated with accumulation of abnormally folded

amyloid beta protein in the brain.
Amyloid beta monomers, when at sufficiently high concentrations, undergo a
dramatic change forming beta sheet-rich tertiary structure that aggregates to form
amyloid fibrils. These fibrils deposit outside neurons in dense formations which can
be described as senile plaques or neuritic plaques or sometimes in the walls of
small blood vessels in the brain. (amyoild angiopathy)
Another protein that is considered to aggregate in Alzheimers disease is the tau
protein, a microtubule-associated protein expressed in neurons that normally acts to
stabilize microtubules in the cell cytoskeleton. This leads to formation of
neurofibrillary tangles and dystrophic neuritis associated with amyloid plaques.
This then causes transneuronal degeneration especially in the cerebral cortex and
certain subcortical regions leading to gross atrophy. As a result, this will
consequently result to loss of mental function (dementia).
Source: http://www.dementiatoday.com/biochemistry-of-alzheimers-disease/

Two theories on the cause of Alzheimers Disease has been formulated and these
are based on what is examined on the brain of a patient who suffered from
Alzheimers Disease as follows:
1. Plaque formation beta-amyloid caggregation.
2. Tangles tau, a protein necessary for the normal functioning of the brain cells
become twisted into abnormal tagles leading to failure of transport system.
NEW STUDY: TAU
http://www.medicaldaily.com/new-theory-alzheimers-it-tau-proteins-not-plaquetriggers-brain-cell-death-308792