Synaptic dysfunction is an early feature of Alzheimer's disease (AD) and proper localization of proteins involved in pre‐ and post‐synaptic composition is dependent on endosomal recycling and trafficking, cellular processes involving the AD risk gene sortilin‐related receptor 1 (SORL1).
Co‐pathologies – including Lewy body, vascular, and TDP‐43 lesions – are common in Alzheimer's disease (AD), contributing to its clinical and pathological heterogeneity. Genetic risk factors may drive mixed pathology presentation, but their influence on the development of specific co‐pathologies remains unclear.
Madison M. Reeves, Anna Calliari, Tiffany W. Todd et al.· Alzheimer's & Dementia· 0 citations
The consequences of oligodendrocyte involvement in Alzheimer’s disease are poorly understood. Could a key role of gray-matter oligodendrocytes—activity-dependent adaptive myelination to sustain changes in activity—be perturbed, leading to cognitive loss?
Charles ffrench-Constant· PLoS Biology· 0 citations
Apolipoprotein E (APOE) ε4 is the strongest genetic risk factor for late‐onset Alzheimer's disease (AD), but its contribution to disease pathogenesis remains incompletely understood.
A. Shvetcov, Shannon Thomson, Mark E. Graham et al.· Alzheimer's & Dementia· 1 citation
The impact of CKD transcriptional risk on AD endophenotypes is assessed by assessing the impact of CKD transcriptional risk on AD endophenotypes in individuals with chronic kidney disease.
Jung-Min Pyun, Young Ho Park, Jiyun Hwang et al.· Alzheimer's & Dementia· 0 citations
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