Zobrazeno 1 - 10
of 215
pro vyhledávání: '"G William Rebeck"'
Publikováno v:
PLoS ONE, Vol 16, Iss 6, p e0252958 (2021)
Spatial inhibition of return (IOR) refers to the phenomenon by which individuals are slower to respond to stimuli appearing at a previously cued location compared to un-cued locations. Here with a group of older adults (n = 56, 58-80 (67.9±5.2) year
Externí odkaz:
https://doaj.org/article/742a30dabad84377ad5ab5e2b59ce884
Autor:
Mitsuru Shinohara, Takahisa Kanekiyo, Masaya Tachibana, Aishe Kurti, Motoko Shinohara, Yuan Fu, Jing Zhao, Xianlin Han, Patrick M Sullivan, G William Rebeck, John D Fryer, Michael G Heckman, Guojun Bu
Publikováno v:
eLife, Vol 9 (2020)
Although the ε2 allele of apolipoprotein E (APOE2) benefits longevity, its mechanism is not understood. The protective effects of the APOE2 on Alzheimer’s disease (AD) risk, particularly through their effects on amyloid or tau accumulation, may co
Externí odkaz:
https://doaj.org/article/546486e15f5a428a8f12cebb5e03daec
Publikováno v:
Frontiers in Cellular Neuroscience, Vol 10 (2016)
Reelin is a neurodevelopmental protein important in adult synaptic plasticity and learning and memory. Recent evidence points to the importance for Reelin proteolysis in normal signaling and in cognitive function. Support for the dysfunction of Reeli
Externí odkaz:
https://doaj.org/article/7d2f646122484d3684952c78d419ca3c
Publikováno v:
Molecular Neurodegeneration, Vol 19, Iss 1, Pp 1-17 (2024)
Abstract Microglia are highly dynamic cells that play a critical role in tissue homeostasis through the surveillance of brain parenchyma and response to cues associated with damage. Aging and APOE4 genotype are the strongest risk factors for Alzheime
Externí odkaz:
https://doaj.org/article/7936248805824daca77f40ec975cc4d4
Publikováno v:
Frontiers in Human Neuroscience, Vol 8 (2014)
Alzheimer’s disease (AD) risk genes alter brain structure and function decades before disease onset. Apolipoprotein E (APOE) is the strongest known genetic risk factor for Alzheimer’s disease, and a related gene, apolipoprotein J (APOJ), also aff
Externí odkaz:
https://doaj.org/article/fa60a84d14e144e7889d7121c4ccfe72
Publikováno v:
Frontiers in Aging Neuroscience, Vol 6 (2014)
We used a lentiviral system for expressing secreted human Aβ in the brains of young and old APOE knock-in mice. This system allowed us to examine Aβ metabolism in vivo, and test the effects of both aging and APOE genotype, two of the strongest risk
Externí odkaz:
https://doaj.org/article/70d48df9425b4db187ff0dbc01118143
Publikováno v:
PLoS ONE, Vol 9, Iss 3, p e93120 (2014)
Under normal conditions, brain apolipoprotein E (apoE) is secreted and lipidated by astrocytes, then taken up by neurons via receptor mediated endocytosis. Free apoE is either degraded in intraneuronal lysosomal compartments or released. Here we iden
Externí odkaz:
https://doaj.org/article/56c708e509254d20b45ef0deb3e52294
Publikováno v:
PLoS ONE, Vol 9, Iss 10, p e110845 (2014)
Apolipoprotein E Receptor 2 (ApoER2) and the tyrosine kinase Fyn are both members of the Reelin pathway, a signaling pathway essential for the laminar formation of the cortex during development and proper dendritic spine density and long-term potenti
Externí odkaz:
https://doaj.org/article/c77746498cab476a97718d67319719d1
Autor:
Sonya B Dumanis, Hyun-Jung Cha, Jung Min Song, Justin H Trotter, Matthew Spitzer, Ji-Yun Lee, Edwin J Weeber, R Scott Turner, Daniel T S Pak, G William Rebeck, Hyang-Sook Hoe
Publikováno v:
PLoS ONE, Vol 6, Iss 2, p e17203 (2011)
Apolipoprotein E receptor 2 (ApoEr2) is a postsynaptic protein involved in long-term potentiation (LTP), learning, and memory through unknown mechanisms. We examined the biological effects of ApoEr2 on synapse and dendritic spine formation-processes
Externí odkaz:
https://doaj.org/article/746b792ebb2b4594be3396e2f48cfa3a
Autor:
Griffin A. Greco, Mitchell Rock, Matthew Amontree, Maria Fe Lanfranco, Holly Korthas, Sung Hyeok Hong, R. Scott Turner, G. William Rebeck, Katherine Conant
Publikováno v:
Neurobiology of Disease, Vol 179, Iss , Pp 106057- (2023)
The APOE4 allele increases the risk for Alzheimer's disease (AD) in a dose-dependent manner and is also associated with cognitive decline in non-demented elderly controls. In mice with targeted gene replacement (TR) of murine APOE with human APOE3 or
Externí odkaz:
https://doaj.org/article/fd4b70330d404358b61b5d8721a3fd22