Results 81 to 90 of about 37,064 (267)

From regulatory mechanisms to cutting‐edge applications: Research progress of ultrasound, electrical, magnetic, and optical stimulation in neural modulation

open access: yesJournal of Intelligent Medicine, EarlyView.
Abstract In recent years, the clinical treatment and symptom management of neurological disorders have faced significant challenges due to the high complexity of the nervous system's structure and function. Against this backdrop, physical stimulation techniques have emerged as a vital complementary approach to traditional pharmacological treatments and
Wanying Li, Liqun Chen
wiley   +1 more source

Novel DNA Aptamers that Bind to Mutant Huntingtin and Modify Its Activity

open access: yesMolecular Therapy: Nucleic Acids, 2018
The CAG repeat expansion that elongates the polyglutamine tract in huntingtin is the root genetic cause of Huntington’s disease (HD), a debilitating neurodegenerative disorder.
Baehyun Shin   +12 more
doaj   +1 more source

In Vivo Mapping of Catecholaminergic Loss and Iron Deposition in Huntington's Disease

open access: yesMovement Disorders, EarlyView.
Abstract Background The pathophysiology of Huntington's disease (HD) remains obscure. Magnetic resonance imaging (MRI) can reveal in vivo molecular changes related to disease pathology. Objectives To investigate catecholaminergic neuronal integrity and subcortical brain iron accumulation in HD employing neuromelanin‐sensitive MRI, and quantitative ...
Edoardo R. de Natale   +11 more
wiley   +1 more source

The Cytotoxicity and Clearance of Mutant Huntingtin and Other Misfolded Proteins

open access: yesCells, 2021
Protein misfolding and aggregation are implicated in many neurodegenerative diseases. One of these diseases is Huntington’s, which is caused by increased glutamine-encoding trinucleotide repeats within the Huntingtin gene.
Austin Folger, Yanchang Wang
doaj   +1 more source

Oxidative stress parameters in plasma of Huntington's disease patients, asymptomatic Huntington's disease gene carriers and healthy subjects : a cross-sectional study [PDF]

open access: yes, 2007
BACKGROUND : Animal data and postmortem studies suggest a role of oxidative stress in the Huntington's disease (HD), but in vivo human studies have been scarce.
Babić, Tomislav   +5 more
core   +1 more source

An Open‐Label Phase 1b Study of the Safety, Pharmacokinetics, Pharmacodynamics, and Clinical Activity of ANX005 in Patients with Huntington's Disease

open access: yesMovement Disorders, EarlyView.
Complement activation is implicated in Huntington's disease; ANX005 is a potent inhibitor of component C1q. ANX005 exhibited a generally manageable safety profile with rapid reduction in C1q in the cerebrospinal fluid. Functional ability on composite Unified Huntington's Disease Rating Scale and total functional capacity was maintained, with potential ...
Rajeev Kumar   +15 more
wiley   +1 more source

The mTOR kinase inhibitor Everolimus decreases S6 kinase phosphorylation but fails to reduce mutant huntingtin levels in brain and is not neuroprotective in the R6/2 mouse model of Huntington's disease

open access: yesMolecular Neurodegeneration, 2010
Background Huntington's disease (HD) is a progressive neurodegenerative disorder caused by a CAG repeat expansion within the huntingtin gene. Mutant huntingtin protein misfolds and accumulates within neurons where it mediates its toxic effects. Promoting
Frentzel Stefan   +11 more
doaj   +1 more source

Mechanisms of copper ion mediated Huntington's disease progression. [PDF]

open access: yesPLoS ONE, 2007
Huntington's disease (HD) is caused by a dominant polyglutamine expansion within the N-terminus of huntingtin protein and results in oxidative stress, energetic insufficiency and striatal degeneration.
Jonathan H Fox   +9 more
doaj   +1 more source

Identification of hepta-histidine as a candidate drug for Huntington's disease by in silico-in vitro- in vivo-integrated screens of chemical libraries. [PDF]

open access: yes, 2016
We identified drug seeds for treating Huntington's disease (HD) by combining in vitro single molecule fluorescence spectroscopy, in silico molecular docking simulations, and in vivo fly and mouse HD models to screen for inhibitors of abnormal ...
Chen, Xigui   +17 more
core   +2 more sources

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