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James C. Vickers

Researcher at University of Tasmania

Publications -  237
Citations -  8384

James C. Vickers is an academic researcher from University of Tasmania. The author has contributed to research in topics: Neurofilament & Dementia. The author has an hindex of 49, co-authored 225 publications receiving 7469 citations. Previous affiliations of James C. Vickers include University of Geneva & Menzies Research Institute.

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The cause of neuronal degeneration in Alzheimer's disease.

TL;DR: Therapeutically, inhibition of the neuronal reaction to physical trauma may be a useful neuroprotective strategy in the earliest stages of Alzheimer's disease.
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The morphological phenotype of β-amyloid plaques and associated neuritic changes in Alzheimer’s disease

TL;DR: All morphologically defined beta-amyloid plaque variants were present in both early and late stages of Alzheimer's disease, and progression to clinical dementia was associated with both a shift to a higher proportion of fibrillar plaques that induced local neuritic alterations and a transformation of cytoskeletal proteins within associated abnormal neuronal processes.
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Distribution and synaptic localization of immunocytochemically identified NMDA receptor subunit proteins in sensory-motor and visual cortices of monkey and human

TL;DR: Data indicate that NMDAR1-immunoreactive cells in neocortex represent a morphologically, functionally, and neurochemically heterogeneous population.
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Focal demyelination in Alzheimer’s disease and transgenic mouse models

TL;DR: It is suggested that plaque-associated focal demyelination of the cortical grey matter might impair cortical processing, and may also be associated with aberrant axonal sprouting that underlies dystrophic neurite formation.
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Relationship between education and age-related cognitive decline: a review of recent research

TL;DR: The literature reveals little consistent evidence that normal age‐related cognitive decline is moderated by education attainment, which supports a passive theory of cognitive reserve: people with a higher level of education will continue to perform at a higherlevel of cognitive functioning than their lower educated peers, which may delay the onset of impairment in the future.