A Systematic Review of Amyloid-β and Tau’s contribution to Neuroinflammation in Alzheimer's Disease Progression

Abstract

Alzheimer’s Disease (AD) is classified as the most common neurodegenerative disease that triggers and furthers the onset of neuronal cell death as a consequence of hallmark pathological changes. Since there is yet no cure for dementias such as Alzheimer’s Disease, there is perpetual cognitive function and developmental decline in diseased patients. The hallmarks of AD include abnormal amyloid-β plaques, neurofibrillary tangles, and neuroinflammation. While these neuronal processes are interlinked, it is not entirely understood how they are related or regulate each other. This review will focus on the association of neuronal processes and Alzheimer’s Disease pathology - more specifically the influence of amyloid-β peptide aggregation on tau tangles, and microglial inflammation. In this paper, the interaction between amyloid-β and tau tangles including how this interaction leads to proinflammatory patterns, which results in neuroinflammation observed in Alzheimer’s Disease, was analyzed. In context, evidence for induction and progression of tau hyperphosphorylation and neuroinflammation were observed through analysis of iPSC neurons. In examining the pathological hallmarks for Alzheimer’s Disease, neuronal abnormalities and dysfunctions have been analyzed with the intent of uncovering new potential therapeutic approaches for rescuing degenerative cell function and structure.