Zobrazeno 1 - 8
of 8
pro vyhledávání: '"Christopher Shenton"'
Autor:
Kanae Iijima-Ando, Stephen A Hearn, Christopher Shenton, Anthony Gatt, Lijuan Zhao, Koichi Iijima
Publikováno v:
PLoS ONE, Vol 4, Iss 12, p e8310 (2009)
The amyloid-beta 42 (Abeta42) is thought to play a central role in the pathogenesis of Alzheimer's disease (AD). However, the molecular mechanisms by which Abeta42 induces neuronal dysfunction and degeneration remain elusive. Mitochondrial dysfunctio
Externí odkaz:
https://doaj.org/article/10608321c8e74fb383c4cf827e9a3782
Publikováno v:
PLoS ONE, Vol 4, Iss 12, p e8498 (2009)
The cAMP-responsive transcription factor CREB functions in adipose tissue and liver to regulate glycogen and lipid metabolism in mammals. While Drosophila has a homolog of mammalian CREB, dCREB2, its role in energy metabolism is not fully understood.
Externí odkaz:
https://doaj.org/article/3bbb22b2ee274821b2e150e8c1e0cee7
Autor:
Koichi Iijima, Hsueh-Cheng Chiang, Stephen A Hearn, Inessa Hakker, Anthony Gatt, Christopher Shenton, Linda Granger, Amy Leung, Kanae Iijima-Ando, Yi Zhong
Publikováno v:
PLoS ONE, Vol 3, Iss 2, p e1703 (2008)
Aggregation of the amyloid-beta-42 (Abeta42) peptide in the brain parenchyma is a pathological hallmark of Alzheimer's disease (AD), and the prevention of Abeta aggregation has been proposed as a therapeutic intervention in AD. However, recent report
Externí odkaz:
https://doaj.org/article/6ac9f0014d1c45a1a2a3f517597fc1ea
Publikováno v:
KN - Journal of Cartography and Geographic Information. 50:151-162
Publikováno v:
Human molecular genetics. 19(10)
Hyperphosphorylation of the microtubule associated protein tau is detected in the brains of individuals with a range of neurodegenerative diseases including Alzheimer's disease (AD). An imbalance in phosphorylation and/or dephosphorylation of tau at
Autor:
Koichi M. Iijima, Christopher Shenton, Anthony Gatt, Kanae Iijima-Ando, Stephen Hearn, Lijuan Zhao
Publikováno v:
PLoS ONE
PLoS ONE, Vol 4, Iss 12, p e8310 (2009)
PLoS ONE, Vol 4, Iss 12, p e8310 (2009)
The amyloid-beta 42 (Abeta42) is thought to play a central role in the pathogenesis of Alzheimer's disease (AD). However, the molecular mechanisms by which Abeta42 induces neuronal dysfunction and degeneration remain elusive. Mitochondrial dysfunctio
Autor:
Anthony Gatt, Inessa Hakker, Kanae Iijima-Ando, Hsueh Cheng Chiang, Koichi M. Iijima, Christopher Shenton, Yi Zhong, Linda Granger, Stephen Hearn
The amyloid-beta42 (Abeta42) peptide has been suggested to play a causative role in Alzheimer disease (AD). Neprilysin (NEP) is one of the rate-limiting Abeta-degrading enzymes, and its enhancement ameliorates extracellular amyloid pathology, synapti
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::84f622a995e77fe2f8cfcf307c896918
https://europepmc.org/articles/PMC2441542/
https://europepmc.org/articles/PMC2441542/
Autor:
Linda Granger, Anthony Gatt, Koichi M. Iijima, Yi Zhong, Stephen Hearn, Amy Leung, Hsueh Cheng Chiang, Kanae Iijima-Ando, Christopher Shenton, Inessa Hakker
Publikováno v:
PLoS ONE, Vol 3, Iss 2, p e1703 (2008)
PLoS ONE
PLoS ONE
Aggregation of the amyloid-beta-42 (Abeta42) peptide in the brain parenchyma is a pathological hallmark of Alzheimer's disease (AD), and the prevention of Abeta aggregation has been proposed as a therapeutic intervention in AD. However, recent report