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4 results for “Sporadic disease”

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  1. Prions induce an early Arc response and a subsequent reduction in mGluR5 in the hippocampus.

    Neurobiology of disease · 2022 · 172: 105834

    Synapse dysfunction and loss are central features of neurodegenerative diseases, caused in part by the accumulation of protein oligomers. Amyloid-β, tau, prion, and α-synuclein oligomers bind to the cellular prion protein (PrP<sup>C),</sup> resulting in the activation of macromolecular complexes and …

    PMID 35905927 DOI ↗

  2. Aberrant NOVA1 function disrupts alternative splicing in early stages of amyotrophic lateral sclerosis.

    Acta neuropathologica · 2022 · 144(3): 413-435

    Amyotrophic lateral sclerosis (ALS) is a fatal disease characterized by aberrant alternative splicing (AS). Nuclear loss and cytoplasmic accumulation of the splicing factor TDP-43 in motor neurons (MN) are hallmarks of ALS at late stages of the disease. However, it …

    PMID 35778567 DOI ↗

  3. Th17 Lymphocytes Induce Neuronal Cell Death in a Human iPSC-Based Model of Parkinson's Disease.

    Cell stem cell · 2018 · 23(1): 123-131.e6

    Parkinson's disease (PD) is a neurodegenerative disorder characterized by the progressive degeneration of midbrain neurons (MBNs). Recent evidence suggests contribution of the adaptive immune system in PD. Here, we show a role for human T lymphocytes as cell death inducers …

    PMID 29979986 DOI ↗

  4. Targeted degradation of sense and antisense C9orf72 RNA foci as therapy for ALS and frontotemporal degeneration.

    Proceedings of the National Academy of Sciences of the United States of America · 2013 · 110(47): E4530-9

    Expanded hexanucleotide repeats in the chromosome 9 open reading frame 72 (C9orf72) gene are the most common genetic cause of ALS and frontotemporal degeneration (FTD). Here, we identify nuclear RNA foci containing the hexanucleotide expansion (GGGGCC) in patient cells, including …

    PMID 24170860 DOI ↗

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