Zobrazeno 1 - 5
of 5
pro vyhledávání: '"Nay Saw"'
Autor:
Mehrdad Faizi, Patrick L. Bader, Christine Tun, Angelo Encarnacion, Alexander Kleschevnikov, Pavel Belichenko, Nay Saw, Matthew Priestley, Richard W. Tsien, William C. Mobley, Mehrdad Shamloo
Publikováno v:
Neurobiology of Disease, Vol 43, Iss 2, Pp 397-413 (2011)
Down syndrome (DS) is the most prevalent form of mental retardation caused by genetic abnormalities in humans. This has been successfully modeled in mice to generate the Ts65Dn mouse, a genetic model of DS. This transgenic mouse model shares a number
Externí odkaz:
https://doaj.org/article/f188a5db605b48878574da22609cc487
Akademický článek
Tento výsledek nelze pro nepřihlášené uživatele zobrazit.
K zobrazení výsledku je třeba se přihlásit.
K zobrazení výsledku je třeba se přihlásit.
Autor:
Tao Yang, Frank M. Longo, Tony Wyss-Coray, Stephen M. Massa, Lisa N. Quach, Lin Shen, Nay Saw, Lilith Vander Griend, Mehrdad Shamloo, Thuy-Vi V. Nguyen, Nadia P. Belichenko
Publikováno v:
Journal of Alzheimer's Disease. 42:459-483
The p75 neurotrophin receptor (p75NTR ) is involved in degenerative mechanisms related to Alzheimer’s disease (AD). In addition, p75NTR levels are increased in AD and the receptor is expressed by neurons that are particularly vulnerable in the dise
Autor:
Mehrdad Faizi, Simret Beraki, Tony Wyss-Coray, Nay Saw, Mehrdad Shamloo, Thuy-Vi V. Nguyen, Patrick Bader, Frank M. Longo
Publikováno v:
Brain and Behavior
Alzheimer's disease (AD), the most common form of dementia, is an age-dependent progressive neurodegenerative disorder. β-amyloid, a metabolic product of the amyloid precursor protein (APP), plays an important role in the pathogenesis of AD. The Thy
Autor:
Nay Saw, William C. Mobley, Matthew Priestley, Christine Tun, Patrick Bader, Mehrdad Faizi, Pavel V. Belichenko, Richard W. Tsien, Mehrdad Shamloo, Alexander M. Kleschevnikov, Angelo Encarnacion
Publikováno v:
Neurobiology of Disease, Vol 43, Iss 2, Pp 397-413 (2011)
Down syndrome (DS) is the most prevalent form of mental retardation caused by genetic abnormalities in humans. This has been successfully modeled in mice to generate the Ts65Dn mouse, a genetic model of DS. This transgenic mouse model shares a number