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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Michigan, Ann Arbor, MI, USA.
Background: Inhibitory interneurons normally regulate neural networks underlying memory and cognition, but are disrupted in Alzheimer's disease. Proper interneuron activity reduces amyloid-beta, whereas hyperexcitability elevates amyloid levels. Still, the underlying pathologic processes mediating interneuron dysfunction remain unknown.
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Alzheimers Dement
December 2024
NYU Grossman School of Medicine, New York, NY, USA.
Background: How tauopathy disrupts direct entorhinal cortex (EC) inputs to CA1 and their plasticity is understudied, despite its critical role in memory. Moreover, dysfunction of lateral EC (LEC) input is less clear, despite its relevance to early Alzheimer's disease pathogenesis. Here we examined how tau impacts long-term potentiation (LTP) of LEC→CA1 input in a transgenic model of tauopathy.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
the University of Texas at Austin, Austin, TX, USA.
Background: Imbalanced Fe levels can lead to oxidative stress and initiate ferroptosis, an Fe-dependent cell death that involves lipid peroxidation and can lead to neuron cell loss in neurodegenerative diseases including Alzheimer's disease (AD). While the Fe/Fe ratio has been identified as the primary determining factor for lipid peroxidation, the role of Fe redox equilibrium and dynamic in AD is not well understood, due to limited tools for visualizing Fe and Fe simultaneously. To overcome this limitation, we recently reported DNAzyme-based sensors for simultaneous imaging of Fe and Fe.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Stevens Neuroimaging and Informatics Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Background: Alzheimer's disease (AD) is a neurological disorder marked by progressive cognitive decline, memory deficits, and neuronal cell loss (Knopman, 2021). A brain region significantly impacted by the progression of AD is the subiculum, a structure responsible for spatial navigation, cognitive processes, and the modulation of emotional and affective behaviors within the hippocampus (Fanselow and Dong, 2010). Although subiculum cell loss has been well-established as an early indicator of AD (Carlesimo et al.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Cornell University, Ithaca, NY, USA.
Background: Alzheimer's disease (AD) is characterized by progressive, irreversible neurodegeneration, leading to memory loss and cognitive decline. In mouse models of AD, global decreases in cerebral blood flow (CBF) are brought on by the plugging of capillaries by arrested neutrophils, and the administration of the neutrophil-specific antibody against Ly6G (anti-Ly6G) reduces these capillary stalls in minutes and improves cognitive function within hours. This suggests that at least some aspects of neural activity impairment are reversible, but the mechanism of this recovery - and what specific neural activity is normalized - is not yet known.
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