Results 81 to 90 of about 9,184,817 (390)
Lecithin Alleviates Memory Deficits and Muscle Attenuation in Chinese Older Adults and SAMP8 Mice
This study opens a new avenue for safeguarding cognition and muscle health, averting disability in older age, and treating age‐related pathologies through lecithin supplementation. It serves as a promising nonpharmacological intervention for the crosstalk of muscle and cognition.
Xianyun Wang+16 more
wiley +1 more source
Yixuan Zeng,1,2,* Wenyuan Guo,1,* Guangqing Xu,3 Qinmei Wang,4 Luyang Feng,1,2 Simei Long,1 Fengyin Liang,1 Yi Huang,1 Xilin Lu,1 Shichang Li,5 Jiebin Zhou,5 Jean-Marc Burgunder,6 Jiyan Pang,5 Zhong Pei1,2 1Department of Neurology, National Key Clinical
Zeng YX+13 more
doaj
Listerin Alleviates Alzheimer's Disease through IRE1‐mediated Decay of TLR4 mRNA
Alzheimer's disease (AD) progression is influenced by microglia‐mediated neuroinflammation. Here, it is demonstrated that Listerin suppresses neuroinflammatory signaling and cognitive impairment in AD models by triggering IRE1α‐mediated TLR4 mRNA decay. Adenoviral Listerin delivery reduces amyloid‐β pathology, positioning it as a new therapeutic target.
Fei Qin+9 more
wiley +1 more source
Clinical and Epidemiological Aspects of Huntington Disease in the Republic of Tatarstan
his study aimed to evaluate the epidemiological features ofHuntington disease (HD), based on data from the Centre for Extrapyramidal Pathology and Botulinum Toxin Therapy of theRepublic ofTatarstan. Materials and methods.
Sabina E. Munasipova+1 more
doaj +1 more source
Astrocyte molecular signatures in Huntington’s disease
Astrocyte gene expression is altered in mouse models of Huntington’s disease and in postmortem brain samples from patients with HD. A shared signature Huntington’s disease is a neurodegenerative disorder caused by a dominant mutation in the HTT gene ...
Blanca Díaz-Castro+4 more
semanticscholar +1 more source
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
Huntington's disease: An immune perspective [PDF]
Copyright © 2011 Annapurna Nayaketal. This article has been made available through the Brunel Open Access Publishing Fund.Huntington's disease (HD) is a progressive neurodegenerative disorder that is caused by abnormal expansion of CAG trinucleotide ...
Ansar, R+4 more
core +3 more sources
Huntington’s disease (HD) is a neurodegenerative disorder that manifests with movement dysfunction. The expression of mutant Huntingtin (mHTT) disrupts the functions of brain cells.
Jian-Jing Siew+11 more
semanticscholar +1 more source
The Neuropsychology of Huntington's Disease [PDF]
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
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