Zobrazeno 1 - 10
of 39
pro vyhledávání: '"Ching Pang Chang"'
Publikováno v:
Neurobiology of Disease, Vol 201, Iss , Pp 106672- (2024)
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder caused by a mutant huntingtin protein with an abnormal CAG/polyQ expansion in the N-terminus of HTT exon 1. HD is characterized by progressive neurodegeneration and metabol
Externí odkaz:
https://doaj.org/article/aea99a4fd40047b0b5414155e0f1db5f
Publikováno v:
Journal of Biomedical Science, Vol 28, Iss 1, Pp 1-25 (2021)
Abstract In modern societies, with an increase in the older population, age-related neurodegenerative diseases have progressively become greater socioeconomic burdens. To date, despite the tremendous effort devoted to understanding neurodegenerative
Externí odkaz:
https://doaj.org/article/7a4488a5dd2743c1a2546ca3cdf7573b
Autor:
Ching-Pang Chang, Ya-Gin Chang, Pei-Yun Chuang, Thi Ngoc Anh Nguyen, Kuo-Chen Wu, Fang-Yi Chou, Sin-Jhong Cheng, Hui-Mei Chen, Lee-Way Jin, Kevin Carvalho, Vincent Huin, Luc Buée, Yung-Feng Liao, Chun-Jung Lin, David Blum, Yijuang Chern
Publikováno v:
Acta Neuropathologica Communications, Vol 9, Iss 1, Pp 1-18 (2021)
Abstract Tau pathology is instrumental in the gradual loss of neuronal functions and cognitive decline in tauopathies, including Alzheimer’s disease (AD). Earlier reports showed that adenosine metabolism is abnormal in the brain of AD patients whil
Externí odkaz:
https://doaj.org/article/8e4c10b7573a4385835d8307e2cb35af
Autor:
Jian Jing Siew, Hui-Mei Chen, Huan-Yuan Chen, Hung-Lin Chen, Chiung-Mei Chen, Bing-Wen Soong, Yih-Ru Wu, Ching-Pang Chang, Yi-Chen Chan, Chun-Hung Lin, Fu-Tong Liu, Yijuang Chern
Publikováno v:
Nature Communications, Vol 10, Iss 1, Pp 1-18 (2019)
The authors show that Galectin-3 is up–regulated in brain tissues from patients and a mouse model of Huntington’s disease (HD) and correlates with disease severity. Galectin-3 accumulates at damaged lysosomes in HD microglia, prevents the clearan
Externí odkaz:
https://doaj.org/article/a6e1aa100a154ae9b970e162e6e98c2c
Autor:
Xavier Guitart, Jordi Bonaventura, William Rea, Marco Orrú, Lucrezia Cellai, Ilaria Dettori, Felicita Pedata, Marc Brugarolas, Antonio Cortés, Vicent Casadó, Ching-Pang Chang, Manikandan Narayanan, Yijuang Chern, Sergi Ferré
Publikováno v:
Neurobiology of Disease, Vol 96, Iss , Pp 47-53 (2016)
The initial goal of this study was to investigate alterations in adenosine A2A receptor (A2AR) density or function in a rat model of Huntington disease (HD) with reported insensitivity to an A2AR antagonist. Unsuspected negative results led to the hy
Externí odkaz:
https://doaj.org/article/5f0fc91ff1fc465fa5369d2dd9737a1f
Publikováno v:
Journal of Biomedical Science, Vol 28, Iss 1, Pp 1-25 (2021)
Journal of Biomedical Science
Journal of Biomedical Science
In modern societies, with an increase in the older population, age-related neurodegenerative diseases have progressively become greater socioeconomic burdens. To date, despite the tremendous effort devoted to understanding neurodegenerative diseases
Autor:
Ya Gin Chang, Luc Buée, Kuo Chen Wu, Ching Pang Chang, Fang Yi Chou, Vincent Huin, Lee-Way Jin, Sin-Jhong Cheng, David Blum, Yung-Feng Liao, Pei Yun Chuang, Thi Ngoc Anh Nguyen, Hui Mei Chen, Chun-Jung Lin, Yijuang Chern, Kevin Carvalho
Publikováno v:
Acta Neuropathologica Communications
Acta Neuropathologica Communications, 2021, 9 (1), pp.112. ⟨10.1186/s40478-021-01213-7⟩
Acta Neuropathologica Communications, Vol 9, Iss 1, Pp 1-18 (2021)
Acta Neuropathologica Communications, BioMed Central part of Springer Science, 2021, 9 (1), pp.112. ⟨10.1186/s40478-021-01213-7⟩
Acta neuropathologica communications, vol 9, iss 1
Acta Neuropathologica Communications, 2021, 9 (1), pp.112. ⟨10.1186/s40478-021-01213-7⟩
Acta Neuropathologica Communications, Vol 9, Iss 1, Pp 1-18 (2021)
Acta Neuropathologica Communications, BioMed Central part of Springer Science, 2021, 9 (1), pp.112. ⟨10.1186/s40478-021-01213-7⟩
Acta neuropathologica communications, vol 9, iss 1
Tau pathology is instrumental in the gradual loss of neuronal functions and cognitive decline in tauopathies, including Alzheimer’s disease (AD). Earlier reports showed that adenosine metabolism is abnormal in the brain of AD patients while consequ
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a6f0ba8cb343743295eb8124c0c2fa3c
https://www.hal.inserm.fr/inserm-03366697/file/s40478-021-01213-7.pdf
https://www.hal.inserm.fr/inserm-03366697/file/s40478-021-01213-7.pdf
Autor:
Luc Buée, Lee-Way Jin, Fang-Yi Chou, Sin-Jhong Cheng, David Blum, Kevin Carvalho, Hui-Mei Chen, Ya-Gin Chang, Pei-Yun Chuang, Thi Ngoc Anh Nguyen, Vincent Huin, Yung-Feng Liao, Ching-Pang Chang, Chun-Jung Lin, Yijuang Chern
Tau hyperphosphorylation favors the formation of neurofibrillary tangles and triggers the gradual loss of neuronal functions in tauopathies, including Alzheimer’s disease. Herein, we demonstrated that chronic treatment with an inhibitor (J4) of equ
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::bc6e466674c609fe8aabcda03b5d180b
https://doi.org/10.1101/2020.10.25.334201
https://doi.org/10.1101/2020.10.25.334201
Autor:
Ming-Jen Lee, Ching-Pang Chang, Yi-Hsin Lee, Yi-Chih Wu, Hsu-Wen Tseng, Yu-Ying Tung, Min-Tzu Wu, Yen-Hui Chen, Lu-Ting Kuo, Dennis Stephenson, Shuen-Iu Hung, Jer-Yuarn Wu, Chen Chang, Yuan-Tsong Chen, Yijuang Chern
Publikováno v:
PLoS ONE, Vol 4, Iss 11, p e7868 (2009)
BACKGROUND:Normal-pressure hydrocephalus (NPH) is a neurodegenerative disorder that usually occurs late in adult life. Clinically, the cardinal features include gait disturbances, urinary incontinence, and cognitive decline. METHODOLOGY/PRINCIPAL FIN
Externí odkaz:
https://doaj.org/article/0ffa8da6c72d4d118d450ac150f08ff3
Autor:
Ya-Gin Chang, Chon-Haw Tsai, Jian-Jing Siew, Yijuang Chern, Hui-Mei Chen, Ching-Pang Chang, Yi Ting Hsu
Publikováno v:
Movement Disorders. 32:1600-1609
Background: Disruptions in gamma-aminobutyric (GABA) acid signaling are believed to be involved in Huntington's disease pathogenesis, but the regulation of GABAergic signaling remains elusive. Here we evaluated GABAergic signaling by examining the fu