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Michael Valenzuela

Researcher at University of Sydney

Publications -  140
Citations -  10321

Michael Valenzuela is an academic researcher from University of Sydney. The author has contributed to research in topics: Cognition & Dementia. The author has an hindex of 46, co-authored 133 publications receiving 8429 citations. Previous affiliations of Michael Valenzuela include University of New South Wales & University of Helsinki.

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Brain reserve and dementia: a systematic review.

TL;DR: In this article, the authors quantitatively reviewed evidence for the effect of brain reserve on incident dementia and found that higher brain reserve was associated with a lowered risk for incident dementia (summary odds ratio, 0.54; 95% confidence interval, 0·49-0·59).
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Whitepaper: Defining and investigating cognitive reserve, brain reserve, and brain maintenance

TL;DR: The reserve, resilience, and protective factors professional interest area established a whitepaper workgroup to develop consensus definitions for cognitive reserve, brain reserve, and brain maintenance and evaluated measures that have been used to implement these concepts in research settings and developed guidelines for research that explores or utilizes these concepts.
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Computerized cognitive training in cognitively healthy older adults: a systematic review and meta-analysis of effect modifiers.

TL;DR: The evidence that computerized cognitive training improves cognitive skills in older adults with normal cognition is systematically reviewed and meta-analyzed.
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Computerized Cognitive Training in Older Adults With Mild Cognitive Impairment or Dementia: A Systematic Review and Meta-Analysis

TL;DR: This intervention warrants longer-term and larger-scale trials to examine effects on conversion to dementia, as evidence for efficacy in people with dementia is weak and limited to trials of immersive technologies.
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The neuropsychological profile of vascular cognitive impairment in stroke and TIA patients.

TL;DR: The cognitive deficits in VaD and VCI are characterized by disturbance of frontal functions, with less verbal memory impairment, and the brain lesions that best account for these deficits are noninfarct subcortical white matter and gray matter changes due to ischemia.