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Showing 1–3 of 3 results
Advanced filters: Author: Parinati Kharel Clear advanced filters

  • Release of α-synuclein aggregates by neurons instigates spread of pathology in synucleinopathies, but the mechanism remains unclear. Here the authors show that neuronally generated α-synuclein aggregates accumulate within neuronal lysosomes and are released via SNARE-dependent lysosomal exocytosis.

    • Ying Xue Xie
    • Nima N. Naseri
    • Manu Sharma
    ResearchOpen Access
    Nature Communications
    Volume: 13, P: 1-16

  • Mutations in cysteine string protein-α (CSPα) cause its aggregation and adult-onset neuronal ceroid lipofuscinosis. Abnormal binding of Fe–S clusters to CSPα mutants is now implicated in driving aggregation, which can be reversed in neurons by clinically approved iron chelators.

    • Nima N. Naseri
    • Burçe Ergel
    • Manu Sharma
    Research
    Nature Structural & Molecular Biology
    Volume: 27, P: 192-201

  • Munc18-1 is an evolutionary conserved gene whose mutations are linked to various neurological diseases in human. In order to better understand the exact nature of the mutations, the authors here utilize several model systems to show mutant Munc18-1 can aggregate and deplete functional pool of Wt protein, and that chemical chaperones can reverse the cellular deficits.

    • Noah Guy Lewis Guiberson
    • André Pineda
    • Jacqueline Burré
    ResearchOpen Access
    Nature Communications
    Volume: 9, P: 1-18