Abstract
Even though Alzheimer’s disease (AD) is of significant interest to the scientific community, its pathogenesis is very complicated and not well-understood. A great deal of progress has been made in AD research recently and with the advent of these new insights more therapeutic benefits may be identified that could help patients around the world. Much of the research in AD thus far has been very neuron-oriented; however, recent studies suggest that glial cells, i.e., microglia, astrocytes, oligodendrocytes, and oligodendrocyte progenitor cells (NG2 glia), are linked to the pathogenesis of AD and may offer several potential therapeutic targets against AD. In addition to a number of other functions, glial cells are responsible for maintaining homeostasis (i.e., concentration of ions, neurotransmitters, etc.) within the central nervous system (CNS) and are crucial to the structural integrity of neurons. This review explores the: (i) role of glial cells in AD pathogenesis; (ii) complex functionalities of the components involved; and (iii) potential therapeutic targets that could eventually lead to a better quality of life for AD patients.
Highlights
A debilitating neurological disorder, Alzheimer’s disease (AD) is characterized by β-amyloid (Aβ) induced senile plaques and hyper-phosphorylated tau protein aggregation in the brain leading to a loss in cognitive ability in patients and eventually dementia [1]
Regardless of the challenges, murine models have been a useful tool in identifying the roles of various glial cells in the pathogenesis of AD and this review focuses on these individual cell types and their potential therapeutic applications separately
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Summary
A debilitating neurological disorder, Alzheimer’s disease (AD) is characterized by β-amyloid (Aβ) induced senile plaques and hyper-phosphorylated tau protein aggregation in the brain leading to a loss in cognitive ability in patients and eventually dementia [1]. Familial AD symptoms appear in patients between the age of 30 and 50; and this specific disorder is characterized by mutations in amyloid precursor protein or presenilin 1 and 2 genes as well as tau protein hyperphosphorylation. SAD accounts for the majority of AD cases and the usual age of onset is observed to be 65 onwards. There is significant evidence to support that a major mechanism by which ApoE influences AD is through ApoE induced Aβ peptide deposition. There are several methods of assessment available for AD patients, including tests of episodic memory and attention span, but a more definite diagnosis of AD can only be made by post-mortem histological analysis These histological analyses reveal cerebral cortical atrophy, amyloid plaques, neurofibrillary tangles (NFTs) and vascular amyloidosis that collectively represent Aβ peptide deposits in the brain [8,9]. Much of the research on AD far has been very neuron-oriented but, recently, the interest in glial cells in this particular topic is markedly increasing
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