Neuroinflammation and Alzheimer’s Disease

Abstract

At neuropathological level Alzheimer’s disease (AD) is characterized by the deposition of abnormal fibrils in two characteristic fibrous lesions, the senile plaque and the neurofibrillary tangle. A neurofibrillary tangle consists of bundles of paired helical filaments which are formed from the aberrantly hyperfosforylated protein tau that belongs to the microtubuli associated proteins. The clinical manifestation of AD appears closely related to the degree of neuritic tau pathology, e.g. neurofibrillary tangles and neuropil threads. The main constituent of senile plaque is the β-amyloid (Aβ) protein, a 39–43 amino-acid peptide, derived from the β-amyloid precursor protein (β-APP). The mismetabolism of the β-APP with the concominant production and enhanced deposition of Aβ is considered as a crucial event in the pathogenesis of AD(1). However, it is becoming clear that AD results from a complex range of events that goes beyond the production and deposition of Aβ alone(2). Here we review evidence to suggest that inflammatory processes are intimately involved in several crucial events in the pathological cascade and that anti-inflammatory drugs are interesting therapeutic tools to prevent or to retard the progression of AD.