Presenilin 1 increases association with synaptotagmin 1 during normal aging
نویسندگان
چکیده
منابع مشابه
Presenilin-1 regulates neuronal differentiation during neurogenesis.
Mutations in Presenilin-1 (PS1) are a major cause of familial Alzheimer's disease. Our previous studies showed that PS1 is required for murine neural development. Here we report that lack of PS1 leads to premature differentiation of neural progenitor cells, indicating a role for PS1 in a cell fate decision between postmitotic neurons and neural progenitor cells. Neural proliferation and apoptot...
متن کاملNo association between a presenilin 1 polymorphism and Alzheimer disease.
BACKGROUND Homozygosity of allele 1 of a presenilin 1 intron 8 polymorphism (PS1-1) has been associated with doubling of the risk of sporadic late-onset Alzheimer disease (LOAD), in some, but not all studies. OBJECTIVE To genotype the PS1 intron 8 polymorphism in predominantly Hispanic families with LOAD to test for association and for linkage between this polymorphism and LOAD. DESIGN A fa...
متن کاملVersatility of presenilin 1.
Mutations in PSEN1 and PSEN2 genes, encoding presenilin 1 (PS1) and presenilin 2 (PS2), respectively, cause autosomal-dominant Alzheimer’s disease (ADAD) (1, 2). The precise mechanism by which PS1 mutations lead to AD is under active investigation. Multiple theories have been suggested to explain the role of PS1 and PS2 mutations on AD pathogenesis, including the effects on γ-secretase activity...
متن کاملPresenilin 1 Glu318Gly polymorphism: interpret with caution.
BACKGROUND The significance of the presenilin 1 (PSEN1) Glu318Gly polymorphism has been described as either a causal mutation with reduced penetrance or a benign polymorphism. When this polymorphism is found in a symptomatic person with a family history of dementia, counseling on recurrence risk becomes very problematic. OBJECTIVE To demonstrate that the PSEN1 Glu318Gly polymorphism should be...
متن کاملProtein Topology of Presenilin 1
Mutations in a gene encoding a multitransmembrane protein, termed presenilin 1 (PS1), are causative in the majority of early-onset cases of AD. To determine the topology of PS1, we utilized two strategies: first, we tested whether putative transmembranes are sufficient to export a protease-sensitive substrate across a lipid bilayer; and second, we examined the binding of antibodies to specific ...
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ژورنال
عنوان ژورنال: Neurobiology of Aging
سال: 2020
ISSN: 0197-4580
DOI: 10.1016/j.neurobiolaging.2019.10.006