Chemical Underpinnings of Alzheimer’s Disease Symptoms and Causative Factors: A Systematic Review

Abstract

The brain depends on a complex network of chemical interactions to maintain its homeostasis and functionality. Accordingly, the pathology of neurodegenerative diseases, such as Alzheimer’s disease (AD), has been shown to disrupt the chemical mechanisms that support the brain to carry out its degenerative effect. However, the nature of these disruptions remain elusive. AD is biologically defined by the deposition of Amyloid-Beta (Aβ) plaques and tau neurofibrillary tangles, and has been shown to be strongly correlated with the expression of the Apolipoprotein E4 (ApoE4) allele. Recent findings in the field of neurochemistry indicate the chemical underpinnings of hallmark signs of AD. This review will discuss the process of pathogenesis of AD, from the formation to the causal effects of AD markers, through a chemical lens. The fibrillization of Aβ isoforms as well as the fluent molecular mixing of tau isoforms and hyperphosphorylation of tau observed in mouse lines are discussed as precursor processes to Aβ plaques and tau neurofibrillary tangles. Furthermore, the pathology of Aβ plaques through redox chemistry in the brain, tau neurofibrillary tangles through microtubule disassembly, and ApoE4 through reactive oxygen species (ROS) formation are also presented. Current therapeutic approaches targeted towards specific facets of AD, such as Aducanumab, have found moderate success in treatment, and this progress indicates neurochemical pathways as a potential target for future therapeutic procedures to counteract the degenerative effects of AD.