This study reports that chronic exposure to microplastic and nanoplastic particles differentially affects Kupffer cells, which impairs their function and has consequences on both liver and systemic me...

A spatial lipidomic atlas of the mouse brain reveals more than 500 biochemical territories that mirror cell types and connectivity, capture oligodendrocyte heterogeneity and ventricular zonation, and ...

Alzheimer’s disease (AD) exhibits a pronounced sex bias, with women facing disproportionately higher risk and more severe pathology. Postmenopausal estrogen decline is implicated in this vulnerability...

Semaglutide treatment for 3 months in female mice improved physiological function, attenuated hallmarks of ageing and modulated nutrient sensors and conserved genetic regulators of ageing.

The authors identify peripheral dendritic cell priming of T cells as a key driver of brain inflammation and neurodegeneration in a mouse model of tauopathy, providing new insights into immune mechanis...

CFH is a key mediator of neuronal resilience across the central nervous system in mice and humans.

Inherited variations in the Apolipoprotein E (APOE) gene are the largest genetic determinant for late-onset Alzheimer’s disease, with the APOEε4 allele conferring the highest risk. While APOE was show...

Here, using a mouse model of tauopathy, the authors reveal that disruption of the gut microbiome drives tau pathology and cognitive decline, and identify five microbial metabolites that directly promo...

Adaptive immune responses may influence vulnerability and resilience in Alzheimer′s disease (AD), but relevant T-cell states remain unclear. We profiled peripheral immune cells by mass cytometry in 20...

Axons require intracellular transport of cargoes between the soma and the terminus. The authors show a related logistical challenge exists at smaller scale with respect to the interaction of process-b...

Researchers identify mitochondrial plaques, a previously unrecognized and highly acidic mitochondria-based pathological structure in Alzheimer’s disease, and demonstrate that they result from the dual...

BACKGROUND Genetic variants affecting microglial function can influence Alzheimer's disease (AD) risk, yet the underlying mechanisms remain unclear. The AD-associated ABI3S209F (Abi3S212F in mouse) ...

Myelin is a hallmark of vertebrate nervous systems, yet its roles in central axons remain elusive. Using optical and electrical recordings from thi...

Alzheimer’s disease (AD) features amyloid-β plaques and tau pathology, yet the mechanism underlying early and clinically significant myelin loss remains unresolved. Here, we report human iPSC-derived ...

Compagnion et al. show that TDP-43 loss in microglia causes myelin defects, oligodendrocyte precursor cell imbalance and motor deficits in mice. They identify TDP-43 as a regulator of the TREM2-DAP12 ...

Complement component 1q (C1q), the initiator of the classical complement cascade, mediates synaptic elimination in development and disease, yet the triggers for its deposition on synapses remain uncle...

The ARP2/3 complex works together with actomyosin in an oscillatory program at the soma to govern neuronal polarization.

Alzheimer’s disease (AD) is increasingly recognized as a systemic disorder, with skeletal muscle dysfunction contributing substantially to frailty and…

INTRODUCTION Early Alzheimer's disease (AD) involves subtle cortical changes that may precede atrophy. Magnetic resonance imaging (MRI) microstructural markers may detect earlier pathology than clas...

Molecular Psychiatry - Early oligodendrocyte dysfunction signature in Alzheimer’s disease: Insights from DNA methylomics and transcriptomics

Nuclear and cytoplasmic proteomics uncover a nuclear pool of cytoskeletal proteins, including MAP1B, whose shuttling to the nucleus increases BRG1/BAF chromatin association and regulates brain development.

This Perspective discusses female biology and resilience regarding Alzheimer disease despite pathologic risk.

Microglial CD31 is increased in Alzheimer’s disease and limits amyloid clearance. Reducing CD31 enhances Aβ degradation, alleviates pathology, and improves cognitive function in mouse models.

In PS19 mice, microglia-derived glycoprotein nonmetastatic melanoma protein B promotes mitochondrial extracellular vesicle secretion, enabling mitochondrial transfer to astrocytes. This improves astro...

Early compact myelin is essential for the establishment but not the maintenance of consistent paw preference in mice. Congenital myelin absence reduces lateralization and creates a leftward bias, und...

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder traditionally defined by the accumulation of amyloid‑β plaques and neurofibrillary tangles. Increasing evidence suggests that white...

Foamy microglia are associated with multiple sclerosis progression, linking phagocytosis, altered lipid metabolism (oxylipins) and lysosomal stress to nonclassical neuroinflammation and disease severi...

Adult hippocampal neurogenesis is a major process of neuronal plasticity involved in mood regulation and memory and is tightly regulated by the neurog…

Myeloid cells show marked heterogeneity in Alzheimer’s disease. This study introduces CODEX-CNS, a single-cell spatial proteomics pipeline, and identifies a human microglial subpopulation enriched in ...

Macrophages can sample antigens from living cells through a trogocytosis-like mechanism that routes ingested material away from degradation, a finding that delineates a previously unknown pathway...

A transient grey matter microgliosis is required for remyelination, the failure of which results in a chronic neuroinflammatory state seen in neurodegenerative disorders.

Communication between distant brain regions is mediated by plastic networks of gap junction-coupled astrocytes.

Gut microbial metabolites abnormity links to Alzheimer’s disease (AD) progression, yet the mechanism remains unknown. Here, we observed a markedly dec…

The EMF-inducible gene switch (Ei) platform provides precise spatiotemporal control of gene expression through Cyb5b-mediated calcium oscillations. This system enables Ei-OSK-driven in vivo rejuvenation reprogramming, Ei-mutant APP expression in the context of Alzheimer’s disease, and behavioral rescue in depression through Ei-Tph2-mediated neuromodulation.

Young, cognitively normal APOE4 mice display hippocampal network hyperactivity that predicts later memory decline. This phenotype is driven by neuronal APOE4 expression, which causes hyperexcitability...