Zobrazeno 1 - 10
of 134
pro vyhledávání: '"Robert D. Moir"'
Autor:
Robert D. Moir, Rudolph E. Tanzi
Publikováno v:
Frontiers in Aging Neuroscience, Vol 11 (2019)
The argument is frequently made that the amyloid-β protein (Aβ) persists in the human genome because Alzheimer’s disease (AD) primarily afflicts individuals over reproductive age and, therefore, there is low selective pressure for the peptide’s
Externí odkaz:
https://doaj.org/article/e6123f5bf1124dc49d48c55ca9e33e7f
Autor:
Siddhita D. Mhatre, Vivek Satyasi, Mark Killen, Brie E. Paddock, Robert D. Moir, Aleister J. Saunders, Daniel R. Marenda
Publikováno v:
Disease Models & Mechanisms, Vol 7, Iss 3, Pp 373-385 (2014)
Alzheimer’s disease (AD) is an age-related neurodegenerative disease characterized by memory loss and decreased synaptic function. Advances in transgenic animal models of AD have facilitated our understanding of this disorder, and have aided in the
Externí odkaz:
https://doaj.org/article/c4ad97fcfa7e4458a465841d6ca134e5
Autor:
David G. Hunter, Frank Weng, Srikant Sarangi, Juliet A. Moncaster, Maria Ericsson, John I. Clark, Olga Minaeva, Yorghos Tripodis, Douglas S Parsons, Caitlin A Black, Kevin J. Washicosky, Robert D. Moir, Lee E. Goldstein, Rudolph E. Tanzi, Danielle M Ledoux
Publikováno v:
J Gerontol A Biol Sci Med Sci
The absence of clinical tools to evaluate individual variation in the pace of aging represents a major impediment to understanding aging and maximizing health throughout life. The human lens is an ideal tissue for quantitative assessment of molecular
Autor:
Juliet A. Moncaster, Robert D. Moir, Mark A. Burton, Oliver Chadwick, Olga Minaeva, Victor E. Alvarez, Maria Ericsson, John I. Clark, Ann C. McKee, Rudolph E. Tanzi, Lee E. Goldstein
Publikováno v:
Experimental Eye Research. 221:108974
Neuropathological hallmarks of Alzheimer's disease (AD) include pathogenic accumulation of amyloid-β (Aβ) peptides and age-dependent formation of amyloid plaques in the brain. AD-associated Aβ neuropathology begins decades before onset of cognitiv
Autor:
Kevin J. Washicosky, Teryn Mitchell, Robert D. Moir, Deepak Kumar, Rudolph E. Tanzi, Xandra O. Breakefield, Bence György, William A. Eimer, Nanda Kumar N. Shanmugam, Alex S. Rodriguez
Publikováno v:
Neuron. 100:1527-1532
Summary Amyloid-β peptide (Aβ) fibrilization and deposition as β-amyloid are hallmarks of Alzheimer's disease (AD) pathology. We recently reported Aβ is an innate immune protein that protects against fungal and bacterial infections. Fibrilization
Publikováno v:
Alzheimer's & Dementia. 14:1602-1614
Objective We explore here a novel model for amyloidogenesis in Alzheimer's disease (AD). This new perspective on AD amyloidosis seeks to provide a rational framework for incorporating recent and seemingly independent findings on the antimicrobial rol
Autor:
Juliet A Moncaster, Roberto Pineda, Robert D Moir, Suqian Lu, Mark A Burton, Joy G Ghosh, Maria Ericsson, Stephanie J Soscia, Anca Mocofanescu, Rebecca D Folkerth, Richard M Robb, Jer R Kuszak, John I Clark, Rudolph E Tanzi, David G Hunter, Lee E Goldstein
Publikováno v:
PLoS ONE, Vol 5, Iss 5, p e10659 (2010)
Down syndrome (DS, trisomy 21) is the most common chromosomal disorder and the leading genetic cause of intellectual disability in humans. In DS, triplication of chromosome 21 invariably includes the APP gene (21q21) encoding the Alzheimer's disease
Externí odkaz:
https://doaj.org/article/68140f0c02854f30afc460197196eda9
Autor:
Chantel Fitzsimmons, Katherine Conant, Coryse St. Hillaire, Daniel M. Johnstone, Monique F. Stins, Robert D. Moir, Carl H. Parsons, Elizabeth A. Milward
Publikováno v:
Analytical Methods. 9:110-116
The low-density lipoprotein receptor-related protein (LRP) is a large multifunctional cell surface membrane receptor capable of binding over 50 ligands. These include molecules important in Alzheimer's disease such as the amyloid β-protein precursor
Autor:
Rudolph E. Tanzi, Robert D. Moir
Publikováno v:
Frontiers in Aging Neuroscience
Frontiers in Aging Neuroscience, Vol 11 (2019)
Frontiers in Aging Neuroscience, Vol 11 (2019)
The argument is frequently made that the amyloid-β protein (Aβ) persists in the human genome because Alzheimer’s disease (AD) primarily afflicts individuals over reproductive age and, therefore, there is low selective pressure for the peptide’s