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Jiong Shi, MD PhD

Affiliations: 
Neurology Barrow Neurological Institute, Phoenix, AZ, United States 
Area:
Director, Cognitive and Behavioral Neurology Program
Website:
http://www.thebarrow.org/Neurological_Services/Hydrocephalus_Clinic/204560
Google:
"Jiong Shi"
Bio:

http://www.azalz.org/Scientists/Directory-of-Scientists/Jiong-Shi.aspx

Mean distance: 16.91 (cluster 28)
 
SNBCP
Cross-listing: Neuropathology Tree - Alzheimer's Tree

BETA: Related publications

Publications

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Decourt B, Noorda K, Noorda K, et al. (2022) Review of Advanced Drug Trials Focusing on the Reduction of Brain Beta-Amyloid to Prevent and Treat Dementia. Journal of Experimental Pharmacology. 14: 331-352
Chaudhari K, Wang L, Kruse J, et al. (2021) Early loss of cerebellar Purkinje cells in human and a transgenic mouse model of Alzheimer's disease. Neurological Research. 1-12
Sabbagh MN, Pope E, Cordes L, et al. (2021) Therapeutic considerations for APOE and TOMM40 in Alzheimers disease: A tribute to Allen Roses MD. Expert Opinion On Investigational Drugs. 30: 39-44
Yin J, Li S, Nielsen M, et al. (2018) Sirtuin 3 attenuates amyloid-β induced neuronal hypometabolism. Aging
Sabbagh MN, Shi J, Arnold L, et al. (2017) [P2-255]: SALIVARY AMYLOID-BETA PROTEIN LEVELS CAN DIAGNOSE ALZHEIMER DISEASE AND PREDICT ITS FUTURE ONSET Alzheimer's & Dementia. 13: P710-P711
Yin JX, Maalouf M, Han P, et al. (2016) Ketones block amyloid entry and improve cognition in an Alzheimer's model. Neurobiology of Aging. 39: 25-37
Han P, Tang Z, Yin J, et al. (2014) Pituitary adenylate cyclase-activating polypeptide protects against β-amyloid toxicity. Neurobiology of Aging. 35: 2064-71
Yin J, Turner GH, Coons SW, et al. (2014) Association of amyloid burden, brain atrophy and memory deficits in aged apolipoprotein ε4 mice. Current Alzheimer Research. 11: 283-90
Friedland RP, Shi J, Smith MA, et al. (2004) P2-003 Cholesterol feeding enhances cerebral amyloid beta pathology in beagles Neurobiology of Aging. 25: S224
Aliev G, Seyidova D, Neal ML, et al. (2002) Atherosclerotic lesions and mitochondria DNA deletions in brain microvessels as a central target for the development of human AD and AD-like pathology in aged transgenic mice. Annals of the New York Academy of Sciences. 977: 45-64
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