Zobrazeno 1 - 10
of 28
pro vyhledávání: '"Thomas E. Mahan"'
Publikováno v:
Molecular Neurodegeneration, Vol 17, Iss 1, Pp 1-20 (2022)
Abstract Background One of the key pathological hallmarks of Alzheimer disease (AD) is the accumulation of the amyloid-β (Aβ) peptide into amyloid plaques. The apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset AD and
Externí odkaz:
https://doaj.org/article/f3a88e4afff14cb6a4fc4d21da89f36f
Autor:
Tien-Phat V. Huynh, Chao Wang, Ainsley C. Tran, G. Travis Tabor, Thomas E. Mahan, Caroline M. Francis, Mary Beth Finn, Rebecca Spellman, Melissa Manis, Rudolph E. Tanzi, Jason D. Ulrich, David M. Holtzman
Publikováno v:
Molecular Neurodegeneration, Vol 14, Iss 1, Pp 1-23 (2019)
Abstract Background The apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer disease (AD). ApoE is produced by both astrocytes and microglia in the brain, whereas hepatocytes produce the majority of apoE found in
Externí odkaz:
https://doaj.org/article/f357dfcc10784835afff3f46b50a633c
Autor:
Stephen M. Day, Emily E. Caesar, Joseph P. Culver, Timothy E. Orr, Laura A. Cox, Celeste M. Karch, Colin G. Nichols, James A. Snipes, Adam Q. Bauer, Caitlin M. Carroll, Molly Stanley, Maria S. Remedi, John Grizzanti, Thomas E. Mahan, Debra I. Diz, Shannon L. Macauley, Annie R. Bice, Nildris Cruz-Diaz, David M. Holtzman, William Moritz
Hyperexcitability is a defining feature of Alzheimer’s disease (AD), where aberrant neuronal activity is both a cause and consequence of AD. Therefore, identifying novel targets that modulate cellular excitability is an important strategy for treat
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::9b8d595853b317568a849b574ca5313b
https://doi.org/10.1101/2021.08.11.455969
https://doi.org/10.1101/2021.08.11.455969
Autor:
Thomas E. Mahan, Deepti Lall, David M. Holtzman, Rita Sattler, A.K.M. Ghulam Muhammad, Michael Vazquez, Jesse Landeros, Daniel H. Geschwind, Hayk Davtyan, Ileana Lorenzini, Jacqueline G. O’Rourke, Jason D. Ulrich, Thomas A. Mota, Shaughn Bell, Junwon Kim, Jessica E. Rexach, Layla Ghaffari, Oksana Shelest, Mathew Blurton-Jones, Robert H. Baloh
Publikováno v:
Neuron, vol 109, iss 14
C9orf72 repeat expansions cause inherited amyotrophic lateral sclerosis (ALS)/frontotemporal dementia (FTD) and result in both loss of C9orf72 protein expression and production of potentially toxic RNA and dipeptide repeat proteins. In addition to AL
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a31b1ab4973804c5e9402cb574f064cf
https://escholarship.org/uc/item/9ws7v673
https://escholarship.org/uc/item/9ws7v673
Autor:
Rudolph E. Tanzi, Jason D. Ulrich, Thomas E. Mahan, Tien Phat V. Huynh, Chao Wang, Caroline M. Francis, Mary Beth Finn, Melissa Manis, G. Travis Tabor, David M. Holtzman, Ainsley C. Tran, Rebecca Spellman
Publikováno v:
Molecular Neurodegeneration, Vol 14, Iss 1, Pp 1-23 (2019)
Molecular Neurodegeneration
Molecular Neurodegeneration
BackgroundThe apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer disease (AD). ApoE is produced by both astrocytes and microglia in the brain, whereas hepatocytes produce the majority of apoE found in the perip
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::601de862373e444e096c5897236fc877
http://link.springer.com/article/10.1186/s13024-019-0337-1
http://link.springer.com/article/10.1186/s13024-019-0337-1
Autor:
Grace O. Robinson, David M. Holtzman, Jerrah K. Holth, Thomas E. Mahan, Andreia Silva da Rocha
Publikováno v:
Annals of Clinical and Translational Neurology
Objective Sleep disturbances are prevalent in human tauopathies yet despite the importance of sleep, little is known about its relationship with tau pathology. Here, we investigate this interaction by analyzing sleep and tau pathology throughout tauo
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f9a793bbac0eea62f6a68251e9590d38
https://doi.org/10.1002/acn3.390
https://doi.org/10.1002/acn3.390
Autor:
David M. Holtzman, Yaming Wang, Susan Gilfillan, Tyler K. Ulland, John A. Tzaferis, Thomas E. Mahan, Wilbur M. Song, Justin T. Hole, Jaime Grutzendler, Peng Yuan, Ronald B. DeMattos, Marco Colonna, Marina Cella, John R. Cirrito, Yang Shi, Jason D. Ulrich
Publikováno v:
The Journal of Experimental Medicine
Wang et al. report that TREM2 protects mice from Alzheimer's disease by enabling resident microglia to insulate and alter Aβ plaque structure, thereby limiting neuritic damage.
Triggering receptor expressed on myeloid cells 2 (TREM2) is a micro
Triggering receptor expressed on myeloid cells 2 (TREM2) is a micro
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::71e9c76abb1da46c864738f44834edbe
http://europepmc.org/articles/PMC4854736
http://europepmc.org/articles/PMC4854736
Autor:
David M. Holtzman, Christian B. Lessard, Jason D. Ulrich, Todd E. Golde, Samuel L. Malnik, Paramita Chakrabaty, Pedro E. Cruz, Marco Colonna, Thomas B. Ladd, Thomas E. Mahan, Yingyue Zhou, Yong Ran
Publikováno v:
EMBO Molecular Medicine, Vol 10, Iss 11, Pp n/a-n/a (2018)
EMBO Molecular Medicine
EMBO Molecular Medicine
Rare coding variants in the triggering receptor expressed on myeloid cells 2 (TREM2) are associated with increased risk for Alzheimer's disease (AD), but how they confer this risk remains uncertain. We assessed binding of TREM2, AD‐associated TREM2
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::50d6f4b7c3f969fd52b260db7f19db10
https://doaj.org/article/7dfbdafcfc1640e899512df47529113f
https://doaj.org/article/7dfbdafcfc1640e899512df47529113f
Autor:
Joel C. Geerling, David M. Holtzman, John R. Cirrito, Brendan P. Lucey, Chanung Wang, Thomas E. Mahan, Mary Beth Finn, Jerrah K. Holth, Nigel P. Pedersen, Patrick M. Fuller, Melissa Manis, Sarah K. Fritschi
Publikováno v:
Science (New York, N.Y.), vol 363, iss 6429
Sleep may protect the brain from AD Two main proteins accumulate in the brain in Alzheimer's disease (AD), β-amyloid (Aβ) and tau. Aβ appears to instigate AD, but tau appears to drive brain damage and cognitive decline. Sleep deprivation is known
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6e64fc850922af1a68a570165ff15221
https://pubmed.ncbi.nlm.nih.gov/30792288
https://pubmed.ncbi.nlm.nih.gov/30792288
Autor:
Todd E. Golde, Yong Ran, Jason D. Ulrich, Thomas E. Mahan, Pedro E. Cruz, David M. Holtzman, Christian B. Lessard, Yingyue Zhou, Samuel L. Malnik, Paramita Chakrabaty, Marco Colonna, Thomas B. Ladd
Rare coding variant in the Triggering receptor expressed on myeloid cells 2 (TREM2) are associated with increased risk for Alzheimer’s disease (AD), but how they confer this risk remains uncertain. We assessed binding of TREM2, AD associated TREM2
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::52a6621077f20f39dda4b65ff078847b
https://doi.org/10.1101/269787
https://doi.org/10.1101/269787