Neurological Disease Mechanisms and Treatments

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In mouse cortex after stroke, divergent-to-convergent capillary subtypes show the highest capillary stall risk, with stalls and flow changes occurring within the same vascular networks.

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Hypertension markedly elevates cerebral endothelial Piezo1 activity in two mouse models, and endothelial Piezo1 deletion protects against impaired vasomotion and functional hyperemia.

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Greater arteriolosclerosis severity in an autopsy-confirmed cohort of 1,269 decedents is linked to worse memory, executive function, and language z-scores.

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A pericyte-specific knockout of laminin-γ1 shows several cerebral small vessel disease–typical features at 11 months of age in the mouse model.

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GSK2256294, an inhibitor of sEH, produced an odds ratio for benefit of 1.28 (95% CI 0.99–1.65; P <0.05) in a multilaboratory ischemic stroke rodent trial.

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TIA1 microglial conditional knockout in PS19 P301S tauopathy mice suppresses microglial activation, linked to reduced cytokines and sensome markers and decreased tau pathology.

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Microglia in a modular human forebrain organoid reconstituting Alzheimer’s disease pathology mediate amyloid-β clearance and neuronal maturation while also recruiting CD8(+) T cells via CCL4/5–CCR1/5 and CXCR3 signaling.

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In a p.R47H TREM2 carrier treated with aducanumab, brain regions with very low residual amyloid showed less tau pathology and slower cortical atrophy (β = -0.50; P < .001).