Lysosomal dysfunction causes microglia-specific epigenetic and transcriptional changes linked to neurodegenerative diseases, with a significant impact observed in Sgsh-deficient mice.
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Moving in bioRxiv, Cellular & molecular immunology, eLife, Immunity, Nature Genetics, Neuron.
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Lysosomal dysfunction causes microglia-specific epigenetic and transcriptional changes linked to neurodegenerative diseases, with a significant impact observed in Sgsh-deficient mice.
Deletion of SPI1 in microglia worsens amyloid pathology by reducing microglial response and phagocytosis in Alzheimer's disease models.
Microglia exhibit diverse activation states and cellular subpopulations, enabling dual neuroprotective or neurotoxic roles in neuroinflammatory conditions.
A disease-associated microglial subtype with elevated GPNMB expands with Alzheimer's pathology and depends on TREM2 for neuroprotection.
Sibling-derived microglia comprise up to 52% of microglial cells in marmoset brains, highlighting extensive hematopoietic chimerism within neural tissue.
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A human iPSC-derived spheroid model reveals that remyelinated axons have thinner myelin sheaths after injury, advancing understanding of human myelin repair mechanisms.
Oligodendrocytes actively support CNS function and contribute to disease, with their heterogeneity influencing roles across development, aging, and pathology.
AI-based analysis of over 6 million nuclei reveals specific cell subpopulations linked to diverse Alzheimer's disease phenotypes.
TRAM enables receptor-free myddosome formation, sustaining hours-long NF-κB activation and inflammatory gene expression in TLR signaling.
Coenzyme A activates TLR4 and boosts IL-4-driven macrophage activation via MyD88, revealing a new metabolic pathway influencing immune responses.
PLA2G2D in tumour-draining lymph nodes acts as a novel immune checkpoint that suppresses anti-tumour T cell responses, with inhibition reducing tumour growth in melanoma models.
Gastrointestinal infections induce long-lasting, antigen-specific memory CD4(+) T cells in the brain and meninges, with up to 80% of dural T cells being gut-derived.
Impaired bone marrow myelopoiesis driven by IFN-I response limits monocyte brain homing and accelerates Alzheimer's disease progression in mouse models and patients.
Trogocytosis-related CLDN18.2 impairs CD8(+) T cell cytotoxicity and promotes pancreatic cancer progression by degrading β-catenin and inducing immune senescence.
Single-cell resolution spatial isoform sequencing reveals cell-type-specific isoform variability in multiple brain cell types, with over 450 million barcodes analyzed.
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Moving areas, week to 3 Oct 2026