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Article type: Research Article
Authors: Anderson, Mariaa | Xu, Fengb | Ou-Yang, Ming-Hsuanb | Davis, Judianneb | Van Nostrand, William E.b | Robinson, John K.a; *
Affiliations: [a] Department of Psychology, Stony Brook University Stony Brook, NY, USA | [b] Departments of Neurosurgery & Medicine, Stony Brook University Stony Brook, NY, USA
Correspondence: [*] Correspondence to: Dr. John K. Robinson, Department ofPsychology, Integrative Neuroscience Area, Stony Brook University, Stony Brook, NY 11794-2500, USA. Tel.: +1 631 632 7832; Fax: +1 631 632 7876; E-mail: John.Robinson@stonybrook.edu.
Abstract: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that is the leading cause of dementia in the elderly. Amyloid-β protein (Aβ) depositions in both the brain parenchyma and the cerebral vasculature are recognized as important pathological components that contribute to the cognitive impairments found in individuals with AD. Because pharmacological options have been minimally effective in treating cognitive impairment to date, interest in the development of preventative lifestyle intervention strategies has increased in the field. One controversial strategy, cognitive-specific stimulation, has been studied previously in human participants and has been widely commercialized in the form of ‘brain-training games.’ In the present study, we developed a highly controlled, isolated cognitive training intervention program for mice. Two transgenic mouse lines, one that develops Aβ deposition largely in brain parenchyma, and another in the cerebral microvasculature, progressed through a series of domain-specific tasks for an average of 4 months. Despite the high intensity and duration of the intervention, we found little evidence of positive benefits for AD amyloid pathologies and post-training cognitive testing in these two models. Taken together, these results support the current evidence in human studies that cognitive-specific stimulation does not lead to a measurable reduction in AD pathology or an improvement in general brain health.
Keywords: Alzheimer’s disease, amyloid-beta, Barnes maze, cerebral amyloid angiopathy, cognitive training, transgenic mouse
DOI: 10.3233/JAD-160674
Journal: Journal of Alzheimer's Disease, vol. 55, no. 3, pp. 1109-1121, 2017
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