The Role of Astrocytes in the Relationship Between Amyloid-ß Accumulation and Synaptic Dysfunction in Alzheimer’s Disease

Abstract

Alzheimer’s disease is a progressive neurodegenerative disorder and is the most common cause of dementia worldwide. The disease is characterized by the accumulation of Amyloid-ß plaques, aggregation of tau protein resulting in neurofibrillary tangles, and the dysfunction of neuronal synapses, all of which lead to cognitive impairment and memory loss. Although previous research has focused more on the neuronal aspect of Alzheimer’s disease, recent research has implicated the role of glial cells, most notably astrocytes, to have a significant impact on the disease’s pathogenesis. Astrocytes are the most abundant type of glial cell in the central nervous system and are important in maintaining neuron homeostasis through their various functions in gliotransmission, phagocytosis, and synaptic regulation. The main objective of this review is to examine the role of astrocytes in Alzheimer's disease, specifically in the relationship between Amyloid-ß accumulation and synaptic dysfunction. After reviewing the literature, it can be concluded that Amyloid-ß accumulation induces several changes in astrocytic functions that promote the malfunction of synaptic transmission, thus resulting in synaptic dysfunction in Alzheimer’s Disease. As there has been no cure or highly efficient treatment for Alzheimer’s disease thus far, further research into the role of astrocytes in the relationship between Amyloid-ß accumulation and synaptic dysfunction in the disease could provide alternative pathways and targets for therapeutic treatment.