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Basic Science and Pathogenesis.
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.
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Alzheimers Dement
December 2024
University of Florida, Gainesville, FL, USA.
Background: Severe systemic infections can trigger cognitive decline, but the underlying mechanisms and their impact on the manifestation and progression of Alzheimer's disease and other neurodegenerative diseases are poorly understood. The current COVID-19 pandemic has brought a surge of severe viral illness and highlights the importance of understanding the impact of acute infections on cognition and the manifestation of neurodegenerative disease in survivors. A wealth of observational and clinical data suggests major short- and long-term effects of severe infections on cognition, but detailed and systematic analyses of neuropathological changes after acute infections are scarce.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Kentucky, Lexington, KY, USA.
Background: Compared with the E3 allele of Apolipoprotein E (APOE), E4 increases late-onset Alzheimer's Disease (AD) risk up to 15-fold, while the E2 allele substantially decreases risk. In the CNS, ApoE is predominantly synthesized by astrocytes and microglia, making these two cell types promising targets for ApoE-directed therapeutic approaches. Our lab has generated an inducible "switch" mouse model (APOE4s2) in which we can conditionally replace E4 with the protective E2 in a cell-specific manner.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Interdisciplinary Institute for Neuroscience (UMR 5297), University of Bordeaux, Bordeaux, Gironde, France.
Background: PhospholipaseC γ2 (PLCG2) is known to have direct link with genetic risk factors for Alzheimer's like dementia (AD). PLCG2 has been previously demonstrated to have association with Aß uptake through microglia. And mostly expressed in dentate gyrus (DG) network of hippocampus.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
San Francisco VA Medical Center, University of California San Francisco, San Francisco, CA, USA.
Background: Effective disease-modifying regimens for Alzheimer's Disease (AD) remain lacking due to insufficient understanding of its pathogenic drivers. It was shown previously that upregulation of the calcium-sensing receptor (CaSR), an excitatory family C GPCR, induces neurodegeneration by interfering with the inhibitory γ-aminobutyric acid (GABA) signaling following acute brain injuries (Ann_Clin_Transl_Neurol, 1:851-66). Herein, we determined whether CaSR overexpression is causally associated with the AD.
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