Abstract
Background: There is a dearth of precise information for molecular and cellular mechanisms responsible for the development of Alzheimer’s disease (AD). However, convincing data from clinical research and basic molecular biology have shown that inflammation of the brain is an integral part of AD. In this review, the role of inflammation in AD will be highlighted.
 Methods: Articles from credible scientific databases, such as ScienceDirect, Scopus, PubMed, Google Scholar and Mendeley, were searched and retrieved using keywords ‘inflammation’, ‘Alzheimer’s disease’, ‘tau’, and ‘beta amyloid’.
 Results: At present, there is no local inflammatory-inciting factor that is closely associated with AD, although it has been proposed that inflammation could be induced by pathologic hallmarks of AD, such as beta amyloid (Aβ) peptide plagues and neurofibrillary tangles (NFTs), or fragments of degenerated neurons. However, it is still unclear whether inflammation leads to the development of AD or if the pathological hallmarks of AD induce inflammation.
 Conclusion: Inflammation is, indeed, an integral part of AD. Further studies on inflammatory-targeted therapies for AD are highly recommended.
Highlights
There is a dearth of precise information for molecular and cellular mechanisms responsible for the development of Alzheimer’s disease (AD)
The amyloid beta hypothesis of AD is a highly favored one and the most commonly applied hypothesis in the field of AD research. It has provided the rationale for the development of various treatment modalities. The principle behind this hypothesis is that Aβ peptides produced by the amyloid precursor protein (APP) are the main culprits in AD pathogenesis [5,6]
This revolutionary study disclosed that secretion of IL-1β by microglial stimulation leads to elevation of tau phosphorylation through activation of p38-mitogen-activated protein kinases (MAPK)
Summary
Alzheimer’s disease (AD), the commonest cause of dementia among the elderly people, is an irreversible and progressive neurodegenerative disorder that slowly destroys memory, thinking skills, cognitive functions, and subsequently, the ability to carry out day-to-day activities [1]. The amyloid beta hypothesis of AD is a highly favored one and the most commonly applied hypothesis in the field of AD research It has provided the rationale for the development of various treatment modalities. The principle behind this hypothesis is that Aβ peptides produced by the amyloid precursor protein (APP) are the main culprits in AD pathogenesis [5,6] Based on this hypothesis, several mechanisms for Aβ generation and deposition in the brain have been suggested. Genome-wide association studies (GWAS) have revealed a robust relationship between immunological function-regulating genes and AD [14,15,16] Substantiating these observations, both tau and amyloid pathologies have been shown to be induced by pro-inflammatory stimuli [17,18]. We attempt to highlight the role of inflammation in AD
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