This review synthesizes recent findings across four key domains: proteostasis, gliotransmission/synapse regulation, blood-brain barrier integrity and metabolism, and microglial crosstalk, and examines signaling pathways that govern astrocyte reactivity and the potential of astrocyte-derived biomarkers.
Abstract
In Alzheimer's disease, pathological stimuli reshape astrocyte functions, which in turn act on neurons, making astrocytes critical modulators of disease progression. A comprehensive understanding of how astrocytes dynamically shift from physiology to pathology across multiple functional domains remains to be established. This review synthesizes recent findings across four key domains: proteostasis, gliotransmission/synapse regulation, blood-brain barrier integrity and metabolism, and microglial crosstalk. For each domain, we compare homeostatic and pathological functions, analyze how supportive roles turn detrimental, and discuss effects on neuronal fate. We also examine signaling pathways that govern astrocyte reactivity and the potential of astrocyte-derived biomarkers. By tracing these dynamic transitions, we aim to refine Alzheimer's disease mechanisms and identify state-targeted therapeutic opportunities.
Sleep is a fundamental regulator of brain homeostasis, yet how distinct brain cell types contribute to this process remains poorly understood. Microglia, the resident immune cells of the central nervous system, actively regulate neuroinflammatory tone, metabolic waste clearance, and synaptic remodeling, thereby contrib...
Sara Calafate, R. Mancuso· Trends in Neurosciences· 0 citations
Alzheimer’s disease (AD) and related dementias are closely associated with alterations in microglial states. These microglial changes occur in response to amyloid-β (Aβ) accumulation and aberrant tau phosphorylation and can either protect against or exacerbate AD progression, depending on factors such as disease stage,...
Julia Cai, Yellamandayya Vadlamudi, Praveen Agrawal· Geromedicine· 0 citations
This review systematically outlines the fundamental characteristics of microglial glucose metabolism and focuses on how the dynamic metabolic reprogramming it undergoes during AD progression regulates microglial immune behavior and inflammatory responses.
Qing-Yu Cao, Meng-Meng Shen, Yan Liu et al.· Journal of Alzheimer's Disea...· 0 citations
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by β-amyloid (Aβ) deposition, tau pathology and cognitive decline. Increasing evidence from genetic, transcriptomic, experimental and clinical studies has identified microglia as key regulators of AD pathogenesis. Under physiological con...
Maria-Raluca Gogu, Ivona Mazarianu, G. Stanciu et al.· Pharmaceuticals· 0 citations
Current evidence supports a dynamically reconfigured system rather than a uniformly escalating inflammatory response, which should move beyond broad anti-inflammatory approaches to preserve effective pathological clearance within appropriate disease windows, limit maladaptive synaptic injury, and restore glial and neur...
Tong Wang, Lu Wang, Jia-Ning Cao et al.· Frontiers in Immunology· 0 citations
Alzheimer’s disease (AD) is characterized by progressive neuroinflammation involving microglia whose functional responses extend far beyond the classical M1/M2 framework and form a dynamically heterogeneous continuum. Here, we review recurrent disease-associated microglia (DAM) states and transcriptional programs, incl...
Si-Min Han, Shan-Shan Wang, Jing-Jing Liu et al.· Frontiers in Cell and Develo...· 0 citations
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