The Role of Inflammatory Mediators in the Pathogenesis of Alzheimer's Disease

Abstract

Alzheimer's disease (AD), a neurodegenerative disorder associated with advanced age, is the most common cause of dementia globally. AD is characterised by cognitive dysfunction, deposition of amyloid plaques, neurofibrillary tangles and neuro-inflammation. Inflammation of the brain is a key pathological hallmark of AD. Thus, clinical and immunopathological evidence of AD could be potentially supported by inflammatory mediators, including cytokines, chemokines, the complement system, acute phase proteins and oxidative mediators. In particular, oxidative mediators may actively contribute to the progression of AD and on-going inflammation in the brain. This review provides an overview of the functions and activities of inflammatory mediators in AD. An improved understanding of inflammatory processes and their role in AD is needed to improve therapeutic research aims in the field of AD and similar diseases.

Keywords: Acute Phase Proteins; Alzheimer’s Disease; Chemokines; Complement System Proteins; Cytokines; Inflammation Mediators.

Figure 1:

The immunological function of microglia in Alzheimer’s disease. Aβ = amyloid β; TLR = Toll-like receptors; CD = cluster of differentiation; RAGE = receptor for advanced glycation end-products; FcγR = fragment crystallisable gamma receptor; MHC II = major histocompatibility complex class II; CR = complement receptor.