Results 61 to 70 of about 9,105,589 (353)
Neurobiology of Disease, 2023 Huntington's disease is an autosomal, dominantly inherited neurodegenerative disease caused by an expansion of the CAG repeats in exon 1 of the huntingtin gene. Neuronal degeneration and dysfunction that precedes regional atrophy result in the impairment
Tamara Vasilkovska +10 more
doaj
Neural Regeneration Research, 2018 γ-Aminobutyric acid (GABA), plays a key role in all stages of life, also is considered the main inhibitory neurotransmitter. GABA activates two kind of membrane receptors known as GABAA and GABAB, the first one is responsible to render tonic inhibition ...
Abraham Rosas-Arellano +4 more
doaj +1 more source
Oxidative Medicine and Cellular Longevity, 2016 Neurodegenerative diseases affect not only the life quality of aging populations, but also their life spans. All forms of neurodegenerative diseases have a massive impact on the elderly.
S. Manoharan +5 more
semanticscholar +1 more source
Advanced Science, EarlyView.We demonstrate that Foxp1± mice, modeling FOXP1 haploinsufficiency, exhibit behavioral deficits, striatal neuroinflammatory changes including altered microglial complexity and synaptic pruning, and markedly reduced Pde10a expression. Pde10a inhibition starting immediately after birth restores Foxp1± behavior, microglial morphology, and pruning ...
Henning Fröhlich +8 more
wiley +1 more source
Journal of Neuroscience, 1999 Transgenic mice expressing exon 1 of the human Huntington’s disease (HD) gene carrying a 141–157 CAG repeat (line R6/2) develop a progressive neurological phenotype with motor symptoms resembling those seen in HD. We have characterized the motor deficits
R. Carter +8 more
semanticscholar +1 more source
The Neuropsychology of Huntington's Disease [PDF]
Archives of Clinical Neuropsychology, 2017 Huntington's disease is an inherited, degenerative brain disease, characterized by involuntary movements, cognitive disorder and neuropsychiatric change. Men and women are affected equally. Symptoms emerge at around 40 years, although there is wide variation. A rare juvenile form has onset in childhood or adolescence.
Julie S. Snowden, Julie S. Snowden
openaire +3 more sources
Advanced Science, EarlyView.SeNSs provide a biocompatible, anti‐inflammatory UC therapy. SeNSs form protein coronas enriched with AKT/PI3K/NF‐κB pathway proteins, suppress GP130 via hydrophobic interactions, and inhibit pro‐inflammatory cytokines. In DSS‐induced UC mice, SeNSs reduce inflammation, tissue damage, and disease activity by modulating cytokine, chemokine, and ...
Dingyi Shen +5 more
wiley +1 more source
Nuclear and Neuropil Aggregates in Huntington’s Disease: Relationship to Neuropathology
Journal of Neuroscience, 1999 The data we report in this study concern the types, location, numbers, forms, and composition of microscopic huntingtin aggregates in brain tissues from humans with different grades of Huntington’s disease (HD).
C. Gutekunst +9 more
semanticscholar +1 more source
Activation of Kir4.1 Channels by 2‐D08 Promotes Myelin Repair in Multiple Sclerosis
Advanced Science, EarlyView.Multiple sclerosis causes myelin loss and neurological dysfunction. This study shows that 2‐D08, a small molecule targeting Kir4.1 channels, promotes OPCs differentiation via FYN tyrosine kinase phosphorylation and the FYN/MYRF pathway. It significantly improves myelin repair and motor deficits in EAE mice and marmosets, highlighting its potential as a
Mingdong Liu +17 more
wiley +1 more source
Advanced Science, EarlyView.SUMOylation regulates mitochondrial processes, but its impact on protein import remains unclear. TOM40 is identified, a mitochondrial outer membrane channel protein, as a substrate of deSUMOylase SENP6. TOM40 SUMOylation disrupts outer membrane complex assembly, inhibits protein import, and compromises mitochondrial homeostasis.
Liubing Hu +13 more
wiley +1 more source