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Showing 1–10 of 10 results
Advanced filters: Author: Lary C. Walker Clear advanced filters
  • The prion paradigm – the hypothesis that the seeded aggregation of certain proteins is key to understanding age-related neurodegenerative disorders – is evaluated in relation to recent studies and disease models; the paradigm suggests a unifying pathogenic principle with broad relevance to a large class of currently intractable diseases.

    • Mathias Jucker
    • Lary C. Walker
    Reviews
    Nature
    Volume: 501, P: 45-51
  • People who died of the neurodegenerative condition Creutzfeldt-Jakob disease after treatment with cadaver-derived human growth hormone also developed some of the pathological traits of Alzheimer's disease. See Letter p.247

    • Mathias Jucker
    • Lary C. Walker
    News & Views
    Nature
    Volume: 525, P: 193-194
  • Several neurodegenerative disorders are linked to the build-up of abnormal α-synuclein protein in distinct cell types. It emerges that differing intracellular factors dictate the properties of this protein in each cell type.

    • Lary C. Walker
    News & Views
    Nature
    Volume: 557, P: 499-500
  • The sustained metabolic activation of the brain's default-mode network is thought to render the system vulnerable to Alzheimer's disease. Recent results with transgenic mice support this view by linking neuronal activity to interstitial fluid amyloid-β levels and the development of amyloid-β plaques.

    • Lary C Walker
    • Mathias Jucker
    News & Views
    Nature Neuroscience
    Volume: 14, P: 669-670
  • Medin promotes the formation of vascular aggregates with amyloid-β in mouse models and in human patients with Alzheimer’s disease, and is associated with vascular defects and cognitive decline.

    • Jessica Wagner
    • Karoline Degenhardt
    • Jonas J. Neher
    ResearchOpen Access
    Nature
    Volume: 612, P: 123-131
  • Credible evidence suggests that, under extraordinary circumstances, Alzheimer’s disease may be transmitted by a prion-like mechanism — yielding insights into both the basic biology of this neurodegenerative disorder and strategies for early prevention.

    • Mathias Jucker
    • Lary C. Walker
    News & Views
    Nature Medicine
    Volume: 30, P: 344-345
  • Misfolded Aβ proteins can form proteopathic seeds that drive initiation, progression, and spreading of amyloidosis in the brain. Jucker and colleagues report that Aβ seeds can persist in mouse brain for months in the absence of host-derived Aβ and can then regain propagative and pathogenic activity in the presence of host Aβ.

    • Lan Ye
    • Sarah K Fritschi
    • Mathias Jucker
    Research
    Nature Neuroscience
    Volume: 18, P: 1559-1561