Mechanistically, it was found that phosphorylated STAT6 (pSTAT6) enhanced autophagy, which reduced the burden of senescent microglia and thereby ameliorated CSVD-induced VCI, providing insights into the potential of targeting the STAT6 pathway in VCI associated with CSVD.
Growing evidence suggests that impaired phagocytosis/autophagy and histone deacetylase 3 (HDAC3)‐mediated microglial activation contribute significantly to Alzheimer's disease (AD) pathogenesis by promoting pathological protein aggregation. The ketogenic diet (KD) has demonstrated neuroprotective effects in AD, poten...
Mingxiao Zheng, Gabriele Loers, Sheng-Nan Lin et al.· Food Frontiers· 0 citations
White matter injury after chronic cerebral ischemia is characterized by demyelination and impaired remyelination, representing a major contributor to neurological deficits and cognitive impairment. With the accelerating global aging population, the burden of cerebral small vessel disease and vascular cognitive impairme...
A “double-hit” model in which hypoxia-associated stress may amplify α-Syn-induced microglial dysfunction through HIF1A-linked metabolic remodeling and impaired autophagy-related protein handling is supported, which supports a “double-hit” model for advanced PD.
Alzheimer's disease (AD) frequently co-occurs with vascular pathology, and this overlap is increasingly recognized as a major driver of cognitive decline in mixed dementia and vascular cognitive impairment and dementia (VCID). Disruption of the neurovascular unit (NVU) creates a perivascular microenvironment rich in in...
M. Olazabal-Chias, M. Kratochvil, A. I. Rojo· Neurochemistry International· 0 citations
Objective Alzheimer's disease (AD) progression involves cerebral microvascular endothelial cell senescence induced by brain hypoperfusion, which contributes to blood-brain barrier (BBB) dysfunction. While Notch1 signaling is known to exacerbate endothelial senescence and neuroinflammation via vascular cell adhesion mol...
De-Hui Huang, Rong-Jing Zhou, J. Ling· Frontiers in Aging Neuroscie...· 0 citations
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