Abstract
Recent studies implicate astrocytes in Alzheimer’s disease (AD); however, their role in pathogenesis is poorly understood. Astrocytes have well-established functions in supportive functions such as extracellular ionic homeostasis, structural support, and neurovascular coupling. However, emerging research on astrocytic function in the healthy brain also indicates their role in regulating synaptic plasticity and neuronal excitability via the release of neuroactive substances named gliotransmitters. Here, we review how this “active” role of astrocytes at synapses could contribute to synaptic and neuronal network dysfunction and cognitive impairment in AD.
Highlights
The main independent variable linked to the risk of suffering Alzheimer’s disease (AD) is aging [1,2,3]
Aβ plaques leads toactivity sustained to the dysregulated function of neuronal networks in calcium oscillations in the reactive astrocytes [103], which may trigger the release of intra- It has this calciumexcitability hyperactivity of astrocytes networks may contribute cellular glutamate,been thushypothesized enhancing that the neuronal leading to excitotoxicity
Tau accumulation in astrocytes led to impairments in spatial memory tests. These results compellingly indicate that the accumulation of tau in astrocytes contributes to the pathogenesis of AD disease
Summary
The main independent variable linked to the risk of suffering Alzheimer’s disease (AD) is aging [1,2,3]. The central role of the Aβ peptide in AD pathogenesis has been supported by the fact that familial forms of the disease are caused by its overproduction. The contribution of microtubule-associated protein tau in AD pathology has been proposed [12,13]. In this hypothesis, the presence of abnormally high levels of tau protein in the hyperphosphorylated state promotes the production of toxic oligomeric tau and paired helical filaments, which further assemble into toxic neurofibrillary tangles. Astrocytes in the human brain play key roles in numerous functions within the central nervous system such as structural support, ionic balance of the extracellular space, neurotransmitter clearance at synapses, and modulation of synaptic signaling. The present review focuses instead on the role of dysregulated bidirectional communication of neurons and astrocytes in AD pathology
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