Astrocyte dysfunction is central to Alzheimer's disease (AD), yet expression patterns of astrocytic markers remain poorly defined. We measured Aquaporin‐4 (AQP4) and glial fibrillary acidic protein (GFAP) in post‐mortem frontal cortex of AD patients and controls across BrainNet Europe (BNE) stages.
Metabolic dysfunction is a defining but poorly understood feature of Alzheimer's disease. Du et al. show that a brain-penetrant GLP-1 receptor agonist rewires astrocyte-neuron metabolic coupling through lactate-driven histone lactylation, linking astrocytic glycolysis to neuronal lipid homeostasis and positioning metabolite signaling as a therapeutic axis in neurodegeneration.
Jessica Furtado, M. Schneeberger· Cell Metabolism· 0 citations
Alzheimer's disease (AD) features amyloid beta (Aβ) plaques and tau tangles, yet how their coexistence reshapes brain transcriptomic programs remains unclear.
Jung Hyun Park, Byungwook Kim, M. Al-Amin et al.· Alzheimer's & Dementia· 0 citations
Based on the “vascular-inflammation axis” analytical framework, this study evaluates the pathophysiological significance of plasma glial fibrillary acidic protein (GFAP) in Alzheimer’s disease (AD). We systematically analyze its expression heterogeneity and clinical interpretive boundaries, specifically comparing late-onset AD (LOAD) and early-onset AD (EOAD).
Yi-Chen Chao, Yong-Chang Diwu· Journal of Artificial Intell...· 0 citations
Cerebral amyloid angiopathy (CAA) frequently co‐occurs with Alzheimer's disease (AD), generating mixed vascular–neurodegenerative phenotypes. Plasma phosphorylated tau (p‐tau)217 is a robust biomarker of AD, but its performance in CAA remains unclear.
A. Fernández-Lebrero, J. Jiménez-Balado, G. García‐Escobar et al.· Alzheimer's & Dementia· 0 citations
Neuroinflammatory processes may play a central role in promoting mixed pathologies and cognitive impairment in the oldest‐old. We hypothesize that elevated neuroinflammation, indicated by reactive astrocytosis, acts on cerebrovascular disease and separately, on amyloid beta (Aβ) pathology, to promote downstream medial temporal lobe atrophy and memory impairment.
Batool M. Rizvi, P. Maillard, A. Posis et al.· Alzheimer's & Dementia· 0 citations
Alzheimer's disease neuropathologic change (ADNC) and limbic‐predominant age‐related transactive response DNA‐binding protein 43 kDa (TDP‐43) encephalopathy neuropathologic change (LATENC) are common in older adults, yet differences in brain morphometry patterns when one or both pathologies are present remain unclear.
Khalid Saifullah, A. Ridwan, Arnold M. Evia et al.· Alzheimer's & Dementia· 0 citations
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