Zobrazeno 1 - 10
of 30
pro vyhledávání: '"John Xi Chen"'
Publikováno v:
PLoS ONE, Vol 8, Iss 1, p e54914 (2013)
Normal axonal mitochondrial transport and function is essential for the maintenance of synaptic function. Abnormal mitochondrial motility and mitochondrial dysfunction within axons are critical for amyloid β (Aβ)-induced synaptic stress and the los
Externí odkaz:
https://doaj.org/article/7365613d8e5f4b62ad4b8c60a0e19d04
Autor:
Heng Du, Du Fang, Molly Rabinowitz, Shiqiang Yan, John Xi Chen, Ottavio Arancio, Jhansi Rani Vangavaragu, Yongfu Wang, Zhihua Zhang, Shirley ShiDu Yan, Guy M. McKhann, Shijun Yan, Gang Hu, Elzbieta Glaser, Alexander A. Sosunov, Long Wu, Lan Guo, Qinru Sun, Changjia Zhong
Publikováno v:
Human Molecular Genetics. 24:5198-5210
Accumulation of amyloid-β (Aβ) in synaptic mitochondria is associated with mitochondrial and synaptic injury. The underlying mechanisms and strategies to eliminate Aβ and rescue mitochondrial and synaptic defects remain elusive. Presequence protea
Cyclophilin D deficiency rescues Aβ-impaired PKA/CREB signaling and alleviates synaptic degeneration
Autor:
Alexander A. Sosunov, Shirley ShiDu Yan, Xiaoping Wu, Guy M. McKhann, Lan Guo, Heng Du, John Xi Chen
Publikováno v:
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1842:2517-2527
The coexistence of neuronal mitochondrial pathology and synaptic dysfunction is an early pathological feature of Alzheimer's disease (AD). Cyclophilin D (CypD), an integral part of mitochondrial permeability transition pore (mPTP), is involved in amy
Publikováno v:
Journal of Alzheimer's Disease. 43:451-463
Diabetes is considered to be a risk factor in Alzheimer’s disease (AD) pathogenesis. Although recent evidence indicates that diabetes exaggerates pathologic features of AD, the underlying mechanisms are not well understood. To determine whether mit
Autor:
John Xi Chen, Xueqi Gan, Russell H. Swerdlow, Honglian Shi, Haiyang Yu, Long Wu, Shengbin Huang, Guangyue Li, Changjia Zhong, Shirley ShiDu Yan
Publikováno v:
Free Radical Biology and Medicine. 75:230-240
Mild cognitive impairment (MCI) occurs during the predementia stage of Alzheimer disease (AD) and is characterized by a decline in cognitive abilities that frequently represents a transition between normal cognition and AD dementia. Its pathogenesis
Autor:
Russell H. Swerdlow, Hongju Zhang, Yongfu Wang, John Xi Chen, Guangyue Li, Haiyang Yu, Long Wu, Shirley ShiDu Yan, Shengbin Huang, Xueqi Gan, Gang Hu
Publikováno v:
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease. 1842:220-231
Mitochondrial dysfunction is an early pathological feature of Alzheimer’s disease (AD). The underlying mechanisms and strategies to repair it remain unclear. Here, we demonstrate for the first time the direct consequences and potential mechanisms o
Autor:
John Xi Chen1, Shi Du Yan2 sdyl@columbia.edu
Publikováno v:
Journal of Alzheimer's Disease. 2007, Vol. 12 Issue 2, p177-184. 8p. 1 Diagram, 1 Graph.
Publikováno v:
Journal of Alzheimer's disease : JAD. 54(2)
Mitochondrial dysfunction and axonal degeneration are early pathological features of Alzheimer's disease (AD)-affected brains. The underlying mechanisms and strategies to rescue it have not been well elucidated. Here, we evaluated axonal mitochondria
Autor:
John Xi Chen, Catarina Moreira Pinho, Elzbieta Glaser, Lan Guo, Heng Du, Shirley ShiDu Yan, Shiqiang Yan, Nyosha Alikhani
Publikováno v:
Journal of Alzheimer's Disease. 27:75-87
Accumulation of amyloid-β peptide (Aβ), the neurotoxic peptide implicated in the pathogenesis of Alzheimer's disease (AD), has been shown in brain mitochondria of AD patients and of AD transgenic mouse models. The presence of Aβ in mitochondria le
Autor:
Ottavio Arancio, Doris Chen, Heng Du, Chaodong Wang, Jun Yao, Shirley ShiDu Yan, John Xi Chen, David M. Stern, Lan Guo, Frank J. Gunn Moore, Shiqiang Yan, Fang Fang, Lih-Fen Lue
Publikováno v:
The Journal of Neuroscience. 31:2313-2320
Amyloid- beta (A beta) peptide-binding alcohol dehydrogenase (ABAD), an enzyme present in neuronal mitochondria, exacerbates A beta-induced cell stress. The interaction of ABAD with A beta exacerbates A beta-induced mitochondrial and neuronal dysfunc