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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE, DISTALZ, Lille, France.
Background: BIN1 is a major susceptibility gene for AD and BIN1 protein interacts with Tau. However, the contribution of BIN1 and its isoforms to AD pathogenesis remains unclear. We recently described that human BIN1 isoform1 (BIN1iso1) induces an accumulation of early endosome vesicles leading to neurodegeneration in Drosophila retina and that the early endosome size regulation was conserved in human induced neurons.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
CEDOC - Nova Medical School - Universidade NOVA de Lisboa, Lisboa, Portugal.
Background: Alzheimer's disease (AD), an untreatable synaptic disorder, is the most frequent cause of dementia. It is still unclear which mechanisms drive the early synapse dysfunction in the most common late-onset AD (LOAD). The second most important LOAD risk gene identified, BIN1, is an endocytic regulator.
View Article and Find Full Text PDFDefective glycosylation and ELFN1 binding of mGluR6 congenital stationary night blindness mutants.
Life Sci Alliance
March 2025
Retina and Optic Nerve Research Laboratory, Dalhousie University, Halifax, Canada
Synaptic transmission from photoreceptors to ON-bipolar cells (BCs) requires the postsynaptic metabotropic glutamate receptor mGluR6, located at BC dendritic tips. Binding of the neurotransmitter glutamate initiates G protein signaling that regulates the TRPM1 transduction channel. mGluR6 also interacts with presynaptic ELFN adhesion proteins, and these interactions are important for mGluR6 synaptic localization.
View Article and Find Full Text PDFThe VGCC auxiliary subunit α2δ1 is an extracellular GluA1 interactor and regulates LTP, spatial memory, and seizure susceptibility.
bioRxiv
December 2024
Department of Anatomy & Neurobiology, University of California at Irvine, CA, 92617, USA.
Activity-dependent synaptic accumulation of AMPA receptors (AMPARs) and subsequent long-term synaptic strengthening underlie different forms of learning and memory. The AMPAR subunit GluA1 amino-terminal domain is essential for synaptic docking of AMPAR during LTP, but the precise mechanisms involved are not fully understood. Using unbiased proteomics, we identified the epilepsy and intellectual disability-associated VGCC auxiliary subunit α2δ1 as a candidate extracellular AMPAR slot.
View Article and Find Full Text PDFAltered expression of Presenilin2 impacts endolysosomal homeostasis and synapse function in Alzheimer's disease-relevant brain circuits.
Nat Commun
November 2024
Laboratory for Membrane Trafficking, VIB Center for Brain and Disease Research, Leuven, Belgium.
Rare mutations in the gene encoding presenilin2 (PSEN2) are known to cause familial Alzheimer's disease (FAD). Here, we explored how altered PSEN2 expression impacts on the amyloidosis, endolysosomal abnormalities, and synaptic dysfunction observed in female APP knock-in mice. We demonstrate that PSEN2 knockout (KO) as well as the FAD-associated N141IKI mutant accelerate AD-related pathologies in female mice.
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