Results 51 to 60 of about 32,987 (207)

Astrocytes and Huntington’s Disease

open access: yesACS Chemical Neuroscience, 2014
In this Viewpoint, we summarize and discuss the recent serendipitous discovery of an astrocyte Kir4.1 potassium channel dysfunction in two mouse models of Huntington's disease (HD). Restoration of Kir4.1 channels within astrocytes in vivo attenuated neuronal dysfunction, some aspects of motor dysfunction and increased survival time in a HD mouse model.
Khakh, Baljit S, Sofroniew, Michael V
openaire   +5 more sources

A short review on toxin-induced animal models of Huntington’s disease

open access: yesChronic Diseases Journal
BACKGROUND: Huntington's disease (HD) is a hereditary neurodegenerative motor and cognitive disorder. Different animal models of HD have been provided to study the different aspects of the disease, such as pathophysiology and treatment, and also the cure.
Ahmad Fotoohi
doaj   +1 more source

Clustering of multiallele DNA markers near the Huntington's disease gene. [PDF]

open access: bronze, 1989
Marcy E. MacDonald   +9 more
openalex   +1 more source

Huntington Disease in Asia

open access: yesChinese Medical Journal, 2015
The objective was to review the major differences of Huntington disease (HD) in Asian population from those in the Caucasian population.Data cited in this review were obtained from PubMed database and China National Knowledge Infrastructure (CNKI) from 1994 to 2014.
Zhi-Ying Wu, Miao Xu
openaire   +4 more sources

Homozygotes for Huntington's disease [PDF]

open access: green, 1987
Nancy S. Wexler   +18 more
openalex   +1 more source

Moderate Hyperhomocysteinemia in Patients with Huntington's Disease

open access: yesPteridines, 2002
Hyperhomocysteinemia is considered to be an independent risk factor for cardiovascular diseases and atherosclerosis. Also patients with dementia, either of Alzheimer's or of vascular type, may present with elevated homocysteine levels.
Laich Andreas   +5 more
doaj   +1 more source

Expression of expanded polyglutamine targets profilin for degradation and alters actin dynamics

open access: yesNeurobiology of Disease, 2008
Huntington's disease is caused by polyglutamine expansion in the huntingtin protein. Huntingtin directly interacts with profilin, a major actin monomer sequestering protein and a key integrator of signals leading to actin polymerization.
Barrington G. Burnett   +4 more
doaj  

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