Utilize este identificador para referenciar este registo: https://hdl.handle.net/1822/57896

TítuloExcess synaptojanin 1 contributes to place cell dysfunction and memory deficits in the aging hippocampus in three types of Alzheimer's disease
Autor(es)Miranda, André Miguel Lopes
Herman, Mathieu
Cheng, Rong
Nahmani, Eden
Barrett, Geoffrey
Micevska, Elizabeta
Fontaine, Gaelle
Potier, Marie-Claude
Head, Elizabeth
Schmitt, Frederick A.
Lott, Ira T.
Jiménez-Velázquez, Ivonne Z.
Antonarakis, Stylianos E.
Di Paolo, Gilbert
Lee, Joseph H.
Hussaini, S. Abid
Marquer, Catherine
Palavras-chavehyperexcitability
in vivo electrophysiology
Long-term memory
neurodegenerative disorders
single nucleotide polymorphisms
synaptic dysfunction
SYNJ1
Data5-Jun-2018
EditoraElsevier 1
RevistaCell Reports
Citação130. Miranda, A. M., Herman, M., Cheng, R., Nahmani, E., Barrett, G., Micevska, E., . . . Marquer, C. (2018). Excess Synaptojanin 1 Contributes to Place Cell Dysfunction and Memory Deficits in the Aging Hippocampus in Three Types of Alzheimer's Disease. [Article]. Cell Reports, 23(10), 2967-2975. doi: 10.1016/j.celrep.2018.05.011
Resumo(s)The phosphoinositide phosphatase synaptojanin 1 (SYNJ1) is a key regulator of synaptic function. We first tested whether SYNJ1 contributes to phenotypic variations in familial Alzheimer's disease (FAD) and show that SYNJ1 polymorphisms are associated with age of onset in both early- and late-onset human FAD cohorts. We then interrogated whether SYNJ1 levels could directly affect memory. We show that increased SYNJ1 levels in autopsy brains from adults with Down syndrome (DS/AD) are inversely correlated with synaptophysin levels, a direct readout of synaptic integrity. We further report age-dependent cognitive decline in a mouse model overexpressing murine Synj1 to the levels observed in human sporadic AD, triggered through hippocampal hyperexcitability and defects in the spatial reproducibility of place fields. Taken together, our findings suggest that SYNJ1 contributes to memory deficits in the aging hippocampus in all forms of AD.
TipoArtigo
URIhttps://hdl.handle.net/1822/57896
DOI10.1016/j.celrep.2018.05.011
ISSN2211-1247
e-ISSN2211-1247
Versão da editorahttps://www.cell.com/cell-reports/fulltext/S2211-1247(18)30744-7
Arbitragem científicayes
AcessoAcesso aberto
Aparece nas coleções:ICVS - Artigos em revistas internacionais / Papers in international journals

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