Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Miranda L. Bader Lange"'
Autor:
Miranda L. Bader Lange, Daret St. Clair, William R. Markesbery, Christa M. Studzinski, M. Paul Murphy, D. Allan Butterfield
Publikováno v:
Neurobiology of Disease, Vol 38, Iss 1, Pp 104-115 (2010)
Using APPNLh/APPNLh x PS-1P246L/PS-1P246L human double knock-in (APP/PS-1) mice, we examined whether phosphatidylserine (PtdSer) asymmetry is significantly altered in brain of this familial Alzheimer disease mouse model in an age-dependent manner as
Externí odkaz:
https://doaj.org/article/98b19aae5a2c40e69b84eb51b22f708a
Autor:
Miranda L. Bader Lange, Giovanna Cenini, Marta Piroddi, Hafiz Mohmmad Abdul, Rukhsana Sultana, Francesco Galli, Maurizio Memo, D. Allan Butterfield
Publikováno v:
Neurobiology of Disease, Vol 29, Iss 3, Pp 456-464 (2008)
Oxidative stress, a hallmark of Alzheimer disease (AD), has been shown to induce lipid peroxidation and apoptosis disrupting cellular homeostasis. Normally, the aminophospholipid phosphatidylserine (PtdSer) is asymmetrically distributed on the cytoso
Externí odkaz:
https://doaj.org/article/b61adca706b54e4d985f46e5379189f4
Autor:
Daret K. St. Clair, M. Paul Murphy, D. Allan Butterfield, Christa M. Studzinski, Miranda L. Bader Lange, William R. Markesbery
Publikováno v:
Neurobiology of Disease. 38:104-115
Using APPNLh/APPNLh x PS-1P246L/PS-1P246L human double knock-in (APP/PS-1) mice, we examined whether phosphatidylserine (PtdSer) asymmetry is significantly altered in brain of this familial Alzheimer disease mouse model in an age-dependent manner as
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::80ed0fc1635d927f86d2b9bb217e106c
https://doi.org/10.1016/j.nbd.2010.01.004
https://doi.org/10.1016/j.nbd.2010.01.004
Publikováno v:
Journal of Alzheimer's Disease. 20:369-393
Recently, the oxidoreductase, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), has become a subject of interest as more and more studies reveal a surfeit of diverse GAPDH functions, extending beyond traditional aerobic metabolism of glucose. As a re
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::e2e1bed5e4fb626589a4bca4f6503521
https://doi.org/10.3233/jad-2010-1375
https://doi.org/10.3233/jad-2010-1375
Autor:
Veronica Galvan, Joanna Fombonne, Rukhsana Sultana, Dale E. Bredesen, Junli Zhang, D. Allan Butterfield, Huidong Tang, Patricia Spilman, Olivia Gorostiza, Miranda L. Bader Lange, Renã A. Sowell
Publikováno v:
Free Radical Biology and Medicine. 48:136-144
Numerous studies have demonstrated oxidative damage in the central nervous system in subjects with Alzheimer disease and in animal models of this dementing disorder. In this study, we show that transgenic mice modeling Alzheimer disease-PDAPP mice wi
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f1d8c79f131164097d9680aac712d31e
https://doi.org/10.1016/j.freeradbiomed.2009.10.035
https://doi.org/10.1016/j.freeradbiomed.2009.10.035
Publikováno v:
Journal of Neurochemistry. 111:915-933
Enolase enzymes are abundantly expressed, cytosolic carbon-oxygen lyases known for their role in glucose metabolism. Recently, enolase has been shown to possess a variety of different regulatory functions, beyond glycolysis and gluconeogenesis, assoc
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1e02f8c64af024489d26b501a6e2e3df
https://doi.org/10.1111/j.1471-4159.2009.06397.x
https://doi.org/10.1111/j.1471-4159.2009.06397.x
Autor:
Hafiz Mohmmad Abdul, Giovanna Cenini, Francesco Galli, D. Allan Butterfield, Miranda L. Bader Lange, Marta Piroddi, Maurizio Memo, Rukhsana Sultana
Publikováno v:
Neurobiology of Disease, Vol 29, Iss 3, Pp 456-464 (2008)
Oxidative stress, a hallmark of Alzheimer disease (AD), has been shown to induce lipid peroxidation and apoptosis disrupting cellular homeostasis. Normally, the aminophospholipid phosphatidylserine (PtdSer) is asymmetrically distributed on the cytoso
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::08f706cdc4491dfd979ca8df59600a3b
https://doi.org/10.1016/j.nbd.2007.11.004
https://doi.org/10.1016/j.nbd.2007.11.004
Autor:
Austin S. Baker, Renã A. S. Robinson, Rukhsana Sultana, Ada Fiorini, Miranda L. Bader Lange, Veronica Galvan, Joanna Fombonne, Jian Cai, William M. Pierce, Dale E. Bredesen, D. Allan Butterfield, Junli Zhang, Olivia Gorostiza
Publikováno v:
Antioxidantsredox signaling. 17(11)
The single methionine (Met/M) residue of amyloid-beta (Aβ) peptide, at position 35 of the 42-mer, has important relevance for Aβ-induced oxidative stress and neurotoxicity. Recent in vivo brain studies in a transgenic (Tg) Alzheimer disease (AD) mo
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::18617f6b3975612e08b08584f24b195a
https://pubmed.ncbi.nlm.nih.gov/22500616
https://pubmed.ncbi.nlm.nih.gov/22500616
Autor:
William M. Pierce, Govind Warrier, Dale E. Bredesen, Junli Zhang, Renã A. S. Robinson, Olivia Gorostiza, Rukhsana Sultana, David Allan Butterfield, J. Cai, Veronica Galvan, Joanna Fombonne, Miranda L. Bader Lange
Publikováno v:
Neuroscience. 177
Among the pathological factors known to be associated with Alzheimer disease (AD), oxidative stress induced by the amyloid-β peptide (Aβ) has been demonstrated to play a key role in human brain and animal models of AD. Recently, we reported elevate
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8c10c617ec84a9c77c36a0cbcec4b760
https://pubmed.ncbi.nlm.nih.gov/21223993
https://pubmed.ncbi.nlm.nih.gov/21223993
Publikováno v:
Biochimica et biophysica acta. 1801(8)
Alzheimer's disease (AD) is an age-related neurodegenerative disorder. A number of hypotheses have been proposed to explain AD pathogenesis. One such hypothesis proposed to explain AD pathogenesis is the oxidative stress hypothesis. Increased levels
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a475742a185642e7a1fe273a7e9f1a9f
https://pubmed.ncbi.nlm.nih.gov/20176130
https://pubmed.ncbi.nlm.nih.gov/20176130