Strategies to Diminish the Ab Load in Alzheimers Disease

A.   C.   Cuello; K.   F.S.   Bell

doi:10.2174/1568015053202813

Abstract

Striking advances have been made in recent years toward potential therapies for Alzheimers disease. Alzheimers disease, which is the leading cause of dementia in the elderly, is pathologically defined by the presence of amyloid plaques, composed of the amyloid-beta protein, and neurofibrillary tangles. The amyloid pathology has been associated with decreased synaptic plasticity and neurodegeneration, thereby explaining the visibly decreased cognitive function and evident dementia. Subsequently, a large number of studies have been launched, which attempt to disrupt the progression from Ab aggregation to plaque formation. These studies have involved the use of beta-sheet breakers, secretase inhibition, immunotherapy and anti-inflammatories, the most notable findings of which are discussed in this review.

Keywords: alzheimers disease, amyloid-beta protein, amyloid precursor protein, amyloid plaques, secretase, inflammation, immunotherapy, beta-sheet breakers, transgenic