Zobrazeno 1 - 9
of 9
pro vyhledávání: '"Caodu Buren"'
Autor:
Mandi E. Schmidt, Caodu Buren, James P. Mackay, Daphne Cheung, Louisa Dal Cengio, Lynn A. Raymond, Michael R. Hayden
Publikováno v:
BMC Biology, Vol 16, Iss 1, Pp 1-12 (2018)
Abstract Background Huntington disease (HD) is a fatal neurodegenerative disorder caused by a CAG expansion in the huntingtin (HTT) gene, leading to selective and progressive neuronal death predominantly in the striatum. Mutant HTT expression causes
Externí odkaz:
https://doaj.org/article/a375911085d048ab94d74e1ba76b8a3c
Publikováno v:
Neurobiology of Disease, Vol 87, Iss , Pp 80-90 (2016)
Huntington's disease (HD) is a genetically inherited neurodegenerative disease caused by a mutation in the gene encoding the huntingtin protein. This mutation results in progressive cell death that is particularly striking in the striatum. Recent evi
Externí odkaz:
https://doaj.org/article/69503d38398843d8b380997d19fb92c7
Autor:
James P. Mackay, Amy I. Smith-Dijak, Ellen T. Koch, Peng Zhang, Evan Fung, Wissam B. Nassrallah, Caodu Buren, Mandi Schmidt, Michael R. Hayden, Lynn A. Raymond
Publikováno v:
The Journal of Neuroscience. :JN-RM
Action potential-independent (miniature) neurotransmission occurs at all chemical synapses, but remains poorly understood, particularly in pathological contexts. Axonal endoplasmic reticulum (ER) Ca2+stores are thought to influence miniature neurotra
Publikováno v:
Journal of Huntington's disease. 9(2)
Background Huntington's disease (HD) is an inherited neurodegenerative disorder caused by expansion of CAG repeats in the Huntingtin gene (HTT). Studies suggest cortical to striatal (C-S) projections, which regulate movement and provide cell survival
Autor:
Caodu Buren, James P. Mackay, Mandi E. Schmidt, Louisa Dal Cengio, Michael R. Hayden, Daphne Cheung, Lynn A. Raymond
Publikováno v:
BMC Biology
BMC Biology, Vol 16, Iss 1, Pp 1-12 (2018)
BMC Biology, Vol 16, Iss 1, Pp 1-12 (2018)
Background: Huntington disease (HD) is a fatal neurodegenerative disorder caused by a CAG expansion in the huntingtin (HTT) gene, leading to selective and progressive neuronal death predominantly in the striatum. Mutant HTT expression causes dysfunct
Autor:
Anne N. Murphy, Martina Wallace, Brenda L. Bloodgood, Kelly M Martyniuk, Edward H. Y. Li, Christian M. Metallo, Thekla Cordes, Ajit S. Divakaruni, Caodu Buren, Ian J. Reynolds, Jerel Adam Fields, Alexander Y. Andreyev, Lynn A. Raymond
Publikováno v:
The Journal of cell biology, vol 216, iss 4
The Journal of Cell Biology
The Journal of Cell Biology
In cortical neurons and hippocampal slice cultures, blocking mitochondrial pyruvate uptake rewires metabolism to increase reliance on glutamate to fuel the TCA cycle. This diminishes the readily releasable pool of neuronal glutamate and minimizes the
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::0209143bf4a0beb1e2c1985641ccccc9
https://escholarship.org/uc/item/0j26r8kv
https://escholarship.org/uc/item/0j26r8kv
Corticostriatal cocultures are utilized to recapitulate the cortex-striatum connection in vitro as a convenient model to investigate the development, function, and regulation of synapses formed between cortical and striatal neurons. However, optimiza
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::fdedd0e5e5a5bc702087302d41912118
https://europepmc.org/articles/PMC4969384/
https://europepmc.org/articles/PMC4969384/
Publikováno v:
Journal of Huntington's disease. 3(4)
Background: Huntington’s disease (HD), caused by polyglutamine expansion in huntingtin (Htt), results in severe neurodegeneration in the striatum, and to a lesser extent, cortex and hippocampus. In contrast, non-expanded huntingtin (wildtype, wtHtt
Autor:
Caodu Buren, Matthew P. Parsons, Shaun S. Sanders, Michael R. Hayden, Lynn A. Raymond, Alejandro Dau, Rujun Kang, Crystal N. Doty, Amber L. Southwell
Publikováno v:
The Journal of biological chemistry. 289(6)
Huntington disease is associated with early alterations in corticostriatal synaptic function that precede cell death, and it is postulated that ameliorating such changes may delay clinical onset and/or prevent neurodegeneration. Although many of thes