PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
February 20, 2026SHILAP Revista de lepidopterología2 citationsOpen Access

Glioinflammation: disease-associated microglia and astrocytes in psychiatric disorders, neurodegeneration, and senescence

KUKumiko UemuraSHShunya HiroSASuthinee Attachaipanich

Key Points

  • The review aims to synthesize advances in understanding the roles of reactive microglia and astrocytes in various neurological conditions.
  • Reviewed recent studies on disease-associated microglia and astrocytes.
  • Compared glial heterogeneity across mouse models and human neuropathology.
  • Discussed molecular determinants like inflammation and metabolic changes.
  • Identified distinct disease-associated glial phenotypes relevant to psychiatric disorders and neurodegeneration.
  • Highlighted the complexity and heterogeneity of stress-induced glial states.
  • Proposed an integrative framework for understanding glial stress responses and their implications for therapy.

Abstract

In this review, we synthesize recent conceptual and experimental advances in neuroscience, highlighting selected studies that delineate the roles of reactive microglia and astrocytes in the contexts of developmental inflammatory stress, neurodegenerative diseases, and cellular senescence. Since the characterization of disease-associated glial phenotypes in 2017, building on earlier pioneering discoveries, we focus here on disease-associated microglia (DAM) and disease-associated astrocyte (DAA) to reassess their contributions to glio-inflammation. It is now recognized that the stress-induced glial states are far from uniform; however, the ontogeny, molecular determinants, and functional consequences of this heterogeneity remain incompletely understood, particularly in psychiatric disorders, Alzheimer's disease, and amyotrophic lateral sclerosis. Accordingly, we compare the glial heterogeneity and its underlying mechanisms across translational mouse models and human neuropathology, considering their evolutionary and physiological contexts. While this review does not aim to be exhaustive, we propose an integrative framework that redefines glial stress responses through the combined lenses of inflammation, transcriptomics, mitochondrial dynamics, lipid metabolism, epigenomic regulation, and cellular senescence. Finally, we outline emerging frontiers for AI-enabled multi-omic physiological and pathological approaches, emphasizing their potential to illuminate glial state transitions and accelerate therapeutic discovery in the near future.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Uemura et al. (2026) studied this question.

synapsesocial.com/papers/6997f941ad1d9b11b345231ahttps://doi.org/10.3389/fncel.2025.1669272
Ask AI
Helpful
Bookmark
Share
View Full Paper

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Harnessing Artificial Intelligence in Multimodal Omics Data Integration: Paving the Path for the Next Frontier in Precision Medicine2024 · 129 citations
  2. 2Gene expression profiling of 12633 genes in Alzheimer hippocampal CA1: Transcription and neurotrophic factor down‐regulation and up‐regulation of apoptotic and pro‐inflammatory signaling2002 · 521 citations
  3. 3Autoimmune response to C9orf72 protein in amyotrophic lateral sclerosis2025 · 17 citations
  4. 4An inverse-Warburg effect and the origin of Alzheimer’s disease2012 · 94 citations
  5. 5Maternal immune activation followed by peripubertal stress combinedly produce reactive microglia and confine cerebellar cognition2025 · 9 citations