J
J. Wesson Ashford
Researcher at VA Palo Alto Healthcare System
Publications - 99
Citations - 4258
J. Wesson Ashford is an academic researcher from VA Palo Alto Healthcare System. The author has contributed to research in topics: Dementia & Alzheimer's disease. The author has an hindex of 30, co-authored 89 publications receiving 3710 citations. Previous affiliations of J. Wesson Ashford include University of Kentucky & United States Department of Veterans Affairs.
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Journal ArticleDOI
ApoE genotype accounts for the vast majority of AD risk and AD pathology.
TL;DR: Evidence is provided that apolipoprotein E (apoE) genotype accounts for the majority of Alzheimer's disease (AD) risk and pathology.
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Improving dementia care: The role of screening and detection of cognitive impairment
Soo Borson,Lori Frank,Peter J. Bayley,Malaz Boustani,Marge Dean,Pei-Jung Lin,J. Riley McCarten,John C. Morris,David P. Salmon,Frederick A. Schmitt,Richard G. Stefanacci,Marta S. Mendiondo,Susan Peschin,Eric J. Hall,Howard Fillit,J. Wesson Ashford,J. Wesson Ashford +16 more
TL;DR: The value of screening for cognitive impairment, including dementia and Alzheimer's disease, has been debated for decades as discussed by the authors, and recent research on causes of and treatments for cognitive impairments has converged to challenge previous thinking about screening.
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APOE genotype effects on Alzheimer's disease onset and epidemiology.
TL;DR: The authors reviewed the onset, diagnosis, and epidemiology of AD, specifically with regard to the apolipoprotein E (APOE) genotype and the interaction of the genotype with age.
Journal ArticleDOI
Leptin reduces pathology and improves memory in a transgenic mouse model of Alzheimer's disease.
Steven J. Greco,Kathryn J. Bryan,Sraboni Sarkar,Xiongwei Zhu,Mark A. Smith,J. Wesson Ashford,Jane M. Johnston,Nikolaos Tezapsidis,Gemma Casadesus +8 more
TL;DR: The efficacy of leptin in ameliorating the Alzheimer's disease (AD)-like pathology in 6-month old CRND8 transgenic mice (TgCRND8) following 8 weeks of treatment is examined, solidly demonstrating the potential for leptin as a disease modifying therapeutic in transgenic animals of AD, driving optimism for its safety and efficacy in humans.
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Ascending monoaminergic systems alterations in Alzheimer's disease. Translating basic science into clinical care
Ludwig Trillo,Devsmita Das,Wayne Hsieh,Brian Medina,Sarah Moghadam,Bill Lin,Van Dang,Martha Millan Sanchez,Zurine De Miguel,J. Wesson Ashford,J. Wesson Ashford,Ahmad Salehi,Ahmad Salehi +12 more
TL;DR: This review aims to explore the link between abnormalities in the MA-ergic systems and AD symptomatology as well as the therapeutic strategies targeting these systems, and to examine possible mechanisms behind basic vulnerability ofMA-ergic neurons in AD.