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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
National Tsing Hua University, Hsinchu, Taiwan.
Background: Abnormal brain inflammation is an important feature of Alzheimer's disease (AD). Central nervous system (CNS) inflammation is highly related to immune cell activation. Homeostasis of immune cell activity regulation is crucial for CNS autoimmune response.
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Alzheimers Dement
December 2024
Institut de recherches cliniques de Montréal (IRCM), Montréal, QC, Canada.
Background: Soluble Aβ oligomers (AβOs) induce synapse dysfunction, leading to cognitive impairment and memory deficits in Alzheimer's disease (AD). Our laboratory and several research groups characterized neurexin family members' physiological roles, pivotal synaptic adhesion molecules for development, plasticity, and maintenance. Beyond their normal functions, we found neurexins binding to AβOs causes AβO-induced neurexin dysregulation.
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Alzheimers Dement
December 2024
Department of Neurology and Neurological Sciences, Stanford University, Stanford, CA, USA.
Background: Vascular dysfunction, blood-brain barrier (BBB) dysregulation, and neuroinflammation are thought to participate in Alzheimer`s disease (AD) pathogenesis, though the mechanism is poorly understood. Among pathways of interest, AD pathology appears to affect vascular endothelial growth factor-A (VEGFA) signaling in a bidirectional manner. Higher VEGF levels are thought to have a protective role and slow cognitive decline.
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Alzheimers Dement
December 2024
UK Dementia Research Institute, University of Edinburgh, Edinburgh, United Kingdom.
Background: Small vessel disease (SVD) is a disorder of the brain's microvessels and a common cause of dementia and stroke. Evidence links normal ageing features to SVD progression, involving endothelial activation, pericyte dysfunction, BBB failure, and microglia response. Here, we aim to examine this relationship through a series of translational investigations.
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Alzheimers Dement
December 2024
University of Southern California, Los Angeles, CA, USA.
Background: APOE4 carriers exhibit cerebrovascular dysfunction which may contribute to the development of cognitive decline and dementia; however, the mechanisms underlying this pathophysiology remain unknown. Impaired cerebrovascular reactivity (CVR) may be associated with vascular injury, inflammation, and endothelial dysfunction. To examine whether these processes may be involved in CVR deficits in APOE4 carriers, we explored whether plasma levels of vascular injury markers indicative of inflammation and endothelial dysfunction are associated with impaired CVR to hypercapnia and hypocapnia in older APOE4 carriers.
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