The most common cause of dementia in the USA is Alzheimer's disease (AD). In 2000 there were 4.5 million persons with Alzheimer's disease in USA.
Histopathologic markers of Alzheimer's disease include senile plaques (aggregations of abnormal amyloid protein), neurofibrillary tangles (hyperphosphorylation of tau protein), and brain cell death. Neurofibillary tangles are preferentially distributed in the medial temporal lobe, hippocampus, and amygdala, whereas senile plaques are widely scattered throughout the cerebral cortex.
Overall, the researches for effective disease-modifying therapies for AD bring us frustration and disappointment. A strong etiopathogenic/pathophysiologic concept is that amyloid-β peptide (Aβ) struggles the neuropathology of AD, and so anti-amyloid therapies are expected to slow AD progression efficiently.
Tarenflurbil is a selective Aβ42-lowering drug which modulates ɣ-secretase activity and reduces production of Aβ42 without effect on production of Aβ40. Tarenflurbil was the first gamma-secretase modulator to be tested in a phase 3 trial.

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