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Home › Research › Topic

Inflammation, microglia and astrocytes

730 studies in this group. A computer grouped them by what their titles and summaries are about, not by a hand-made list. The name describes most of the group, not every study in it.

Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.

Highest usefulness score first. Studies without a score come last.

  1. Electroacupuncture alleviate cognitive impairment via activation of TREM2-positive microglia in APP/PS1 mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-16 TREM2 and immune genetics

    EA ameliorated cognitive impairment in APP/PS1 mice by enhancing TREM2⁺ microglia-mediated Aβ clearance and suppressing neuroinflammation. scRNA-seq further revealed that EA reshaped microglial transcriptional states and intercellular communication networks in a TREM2-dependent manner.

  2. Endothelial CD36 links arteriolar remodeling to metabolic and immune alterations in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-14 Risk genes beyond APOE

    Alzheimer’s disease (AD) is accompanied by profound cerebrovascular dysfunction, yet it remains unclear whether endothelial abnormalities reflect only vascular injury or altered regulatory states connecting vascular remodeling with metabolic and immune function.

  3. Progranulin deficiency promotes neuroinflammation through cathepsin B-mediated activation of the NLRP3 inflammasome

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-13 Drug development

    Haploinsufficiency of progranulin (resulting from mutations in the GRN gene) is a major genetic cause of frontotemporal dementia (FTD), which is characterized by profound changes in personality and behavior, progressive impairments in executive function, speech, language and/or movement, TDP-43 pathology, lysosomal dysfunction, and neuroinflammation.

  4. Oligodendrocyte stress response as a driver of vascular dementia

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-13 Risk factors

    Vascular dementia (VaD) is a prevalent and devastating neurocognitive disorder characterized by profound white matter damage, yet the precise cellular mechanisms linking cerebrovascular stress to demyelination remain poorly understood.

  5. Mechanistic study of PHLDA1 in cognitive dysfunction of Alzheimer’s disease model mice via FoxO1‑mediated neuroinflammation

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-12 Biomarkers

    Neuroinflammation is a core driver of Alzheimer’s disease (AD) progression.

  6. A rapid, genetically-tractable human iPSC-derived model for studying tissue-resident macrophage biology in Alzheimer’s and other diseases

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-12 Genetics

    Large-scale genetic and preclinical studies strongly implicate myeloid cells, particularly brain-resident macrophages, in the pathogenesis of Alzheimer’s disease (AD).

  7. DAP12-deficient microglia adopt a TREM2-independent antigen-presenting state with a glial-to-neuronal cascade in Nasu-Hakola disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-11 TREM2 and immune genetics

    Nasu-Hakola disease (NHD), a dementia with about 200 cases worldwide, is caused by loss-of-function mutation of TYROBP , encoding DAP12, or its receptor TREM2 .

  8. ASC specks and α-synuclein amplify microglial NLRP3 inflammasome activation and co-localize with Lewy body pathology

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-10 Brain tissue and pathology

    Neuroinflammation is a hallmark of several chronic neurodegenerative disorders, including Parkinson’s disease (PD) and other synucleinopathies, and is closely associated with microglial activation.

  9. Disease stage-sensitive MFSD2A-caveolae axis insigates hippocampal blood–brain barrier disruption in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-08 Vascular contributions

    Blood-brain barrier (BBB) malfunction contributes to pathophysiology of Alzheimer’s disease (AD), yet the mechanisms that confer hippocampal endotheliocytes vulnerability remain unclear.

  10. Cross-Tissue Inflammatory Convergence Supports a Putative Muscle–Brain Axis in Alzheimer’s Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-08 Mild cognitive impairment

    Aging muscle showed increased inflammatory, extracellular-matrix, and stromal communication programs.

  11. Human multiscale transcriptomics identifies the NLRP3 inflammasome as a convergent druggable target in Alzheimer’s disease: validation with dimethyl itaconate in 5xFAD mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-07 Brain tissue and pathology

    Neuroinflammation is a hallmark of Alzheimer’s disease (AD); however, which neuroinflammatory effectors are consistently altered across independent human cohorts, brain regions, and microglial states—and can be engaged by available compounds—remains incompletely defined.

  12. TLR7-mediated autoimmunity targets Robo3 to drive astrogliosis in frontotemporal dementia

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-07 Disease mechanisms

    Mutations in GRN and C9orf72 are common causes of frontotemporal dementia (FTD).

  13. Cross-Dataset Reanalysis of Mouse Alzheimer Disease Single-Cell RNA-Sequencing Data Reveals a Reproducible Innate Immune Activation Signature

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-06 TREM2 and immune genetics

    Single-cell RNA sequencing (scRNA-seq) studies of Alzheimer’s disease (AD) mouse models have proliferated across independent laboratories, brain regions, and platforms, yet the cross-study reproducibility of transcriptional signatures derived from such data remains underexplored.

  14. Brain-wide Cerebrospinal Fluid Recirculation Collapse in Alzheimer’s Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-04 Tau biomarkers

    Cerebrospinal fluid (CSF) flow and the glymphatic system are essential for maintaining brain homeostasis, yet the precise mechanisms driving their profound failure in Alzheimer’s disease (AD) remain largely elusive.

  15. APOE4 reduction in vascular-associated fibroblasts decreases cerebral amyloid angiopathy and associated vascular dysfunction

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-04 Vascular contributions

    Cerebral amyloid angiopathy (CAA), characterized by cerebrovascular amyloid deposition, is strongly associated with Alzheimer’s disease, ischemic injury, and lobar hemorrhages.

  16. The Alzheimer’s Disease-associated gene CD2AP regulates permeability of endothelial cells and transendothelial migration of immune cells

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-02 Vascular contributions

    Variants at the CD2AP locus, which encodes a branched-actin regulator, are associated with late-onset Alzheimer’s disease (AD), and CD2AP-deficient mice show increased blood-brain barrier (BBB) permeability.

  17. PDE2A Modulation Attenuates Aβ-Induced Neuronal Injury and Associated Oxidative, Inflammatory, and Apoptotic Responses

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-01 Disease mechanisms

    Across cellular and animal Aβ injury models, BML-288 attenuated oxidative and inflammatory disturbances, modulated apoptosis-related protein expression, and improved cognitive outcomes.

  18. Plasma immune signatures associate with neurodegeneration in frontotemporal lobar degeneration

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-09-29 Biomarkers

    In exploratory full-cohort models, the multivariate CNS signature achieved an area under the curve of 0.93, compared with 0.82 for the multivariate inflammation signature.

  19. Neurodegeneration-inducing macromolecules exit the brain via nanovascular conduits formed by reticular fibroblasts

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-27 Vascular contributions

    Accumulation of proteins such as amyloid β (Aβ), hyperphosphorylated tau and α-synuclein within the brain alters neural information processing and causes neurodegeneration 1–3 , but how toxic solutes are cleared from the brain remains highly controversial 4,5 .

  20. Extracellular CIRP induces neurotoxic astrocytes via TREM-1 in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-24 Biomarkers

    Extracellular cold-inducible RNA-binding protein (eCIRP) is a crucial neuroinflammatory mediator in ischemic stroke and alcohol-induced memory impairment.

  21. Reducing Neutrophil Sialic Acid Residues Alleviates Cerebral Hypoperfusion in Alzheimer’s Models

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-24 Vascular contributions

    Elevated terminal sialylation of neutrophil glycoproteins contributes to capillary stalling and cerebral hypoperfusion in AD.

  22. A self-limiting, TREM2-dependent anabolic program confers microglial resilience in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-20 TREM2 and immune genetics

    Microglia are key drivers of Alzheimer’s disease (AD), and TREM2, one of the strongest genetic risk factors, enables the disease-associated microglia (DAM) state required for plaque engagement.

  23. The protein and lipid compositions of brain apolipoprotein E particles are cell type-specific

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-14 Tau biomarkers

    Genetic variation in APOE , which encodes a lipid transporter apolipoprotein E (apoE), is the strongest risk factor for late-onset Alzheimer’s disease (AD).

  24. A sphingomyelin-cholesterol complex regulates TLR4 activation in microglia

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-14 TREM2 and immune genetics

    Microglial activation in response to lipopolysaccharide (LPS) requires Toll-like receptor 4 (TLR4) redistribution into cholesterol- and sphingolipid-rich membrane domains, yet the lipid determinants of this process remain unclear.

  25. Cell type-specific histone acetylation landscape in Alzheimer’s disease reveals a putative role of MITF in microglia

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-14 Disease mechanisms

    Alzheimer’s disease (AD) is characterised by aberrant amyloid beta and tau aggregation, neuroinflammation, demyelination and neurodegeneration, which have been linked to changes in cell-specific gene expression signatures.

From across this topic

10 of the 730 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.

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