Caffeine as Treatment for Alzheimer's Disease: A Review

Abstract

In current research, amyloid peptide (bA) remains characteristic in the histopathology of Alzheimer’s disease (AD). As a major component in the amyloid precursor protein (APP), the entire bA sequence is thought to be involved in the processing of APP through two major pathways where APP-related membrane- bound fragments are generated from an endosomal/lysosomal pathway. Although it is generally believed APP/bA has a consequence in AD, the mechanism through which bA influences the biology and vulnerability of neural cells remains tenuous. In addition, it has been postulated that caffeine may have an attenuating effect on both accumulation of bA plaques, as well as symptomatic presentation. This review focuses on the hypothesized correlation between the biochemistry and pathology of APP and bA deposition in the context of AD. In addition, this review aims to identify the hypothesized role of caffeine in reducing bA levels and its link with AD.