title: Intensive 'Brain Training' Intervention Fails to Reduce Amyloid Pathologies or Cognitive Deficits in Transgenic Mouse Models of Alzheimer's Disease.
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.
authors: Department of Psychology, Stony Brook University Stony Brook, NY, USA.
authors: Maria
authors: M
authors: Anderson
authors: Departments of Neurosurgery & Medicine, Stony Brook University Stony Brook, NY, USA.
authors: Feng
authors: F
authors: Xu
authors: Departments of Neurosurgery & Medicine, Stony Brook University Stony Brook, NY, USA.
authors: Ming-Hsuan
authors: MH
authors: Ou-Yang
authors: Departments of Neurosurgery & Medicine, Stony Brook University Stony Brook, NY, USA.
authors: Judianne
authors: J
authors: Davis
authors: Departments of Neurosurgery & Medicine, Stony Brook University Stony Brook, NY, USA.
authors: William E
authors: WE
authors: Van Nostrand
authors: Department of Psychology, Stony Brook University Stony Brook, NY, USA.
authors: John K
authors: JK
authors: Robinson
mesh_terms: D000544:Alzheimer Disease / Q000150:complications* / Q000235:genetics; D000682:Amyloid / Q000235:genetics / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000235:genetics / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000473:pathology; D003072:Cognition Disorders / Q000209:etiology / Q000473:pathology / Q000534:rehabilitation; D015928:Cognitive Behavioral Therapy / Q000379:methods*; D004195:Disease Models, Animal; D005260:Female; D008297:Male; D018782:Maze Learning / Q000502:physiology; D008570:Memory, Short-Term / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D055806:Microvessels / Q000473:pathology; D009043:Motor Activity / Q000235:genetics / Q000502:physiology; D009154:Mutation / Q000235:genetics; D053764:Presenilin-1 / Q000235:genetics; D011930:Reaction Time / Q000235:genetics / Q000502:physiology; D012054:Reinforcement, Psychology; D016875:tau Proteins / Q000235:genetics / Q000378:metabolism
chemical_list: D000682:Amyloid; D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D053764:Presenilin-1; D016875:tau Proteins
keywords: Alzheimer’s disease; Barnes maze; amyloid-beta; cerebral amyloid angiopathy; cognitive training; transgenic mouse