Cognitive Training for Early-Stage Alzheimer’s Disease and Dementia By: Fang Yu, Karen M. Rose, Sandra C. Burgener, Cindy Cunningham, Linda L. Buettner, Elizabeth Beattie, Ann L. Bossen, Kathleen C. Buckwalter, Donna M. Fick, Suzanne Fitzsimmons, Ann Kolanowski, Janet K. Pringle Specht, Nancy E. Richeson, Ingelin Testad, and Sharon E. McKenzie Yu, F, Rose, K, Burgener, S, Cunningham, C, Buettner, L , Beattie, E, Bossen, A, Buckwalter, K, Fick, D, Fitzsimmons, S, Kolanowski, A, Specht, J, Richeson, N, Testad, I, & McKenzie, S 2009, 'Cognitive training for early-stage Alzheimer's disease and dementia', Journal of Gerontological Nursing, 35, 3, pp. 23-29. Made available courtesy of Slack, Inc.: http://www.slackjournals.com/jgn ***Reprinted with permission. No further reproduction is authorized without written permission from Slack, Inc.. This version of the document is not the version of record. Figures and/or pictures may be missing from this format of the document.*** Abstract: The purpose of this article is to critically review and synthesize the literature on the effects of nonpharmacological cognitive training on dementia symptoms in early-stage Alzheimer’s disease (AD) and related dementia. Electronic databases MEDLINE (PubMed), CINAHL, PsycInfo, and the Cochrane Library were searched using the keywords cognition, reality orientation, Alzheimer’s disease, psychosocial factors, cognitive therapy, brain plasticity, enriched environments, and memory training. The findings support that cognitive training improves cognition, activities of daily living, and decision making. Interventions are more effective if they are structured and focus on specific known losses related to the AD pathological process and a person’s residual ability, or are combined with cognitive- enhancing medications. Nursing implications are also discussed. Article: Individuals differ considerably in their cognitive capability and their susceptibility to aging and neurodegenerative diseases. The concept of cognitive reserve is used to explain these differences, supporting that there is no simple threshold model for the pathology that leads to impaired cognitive function (Whalley, Deary, Appleton, & Starr, 2004). Cognitive impairment is likely a product of multiple factors, including individual differences in intelligence, methods for processing tasks, occupation, education, work environment, coping skills for stressful experiences, choice of cognitively stimulating leisure pursuits, and use of health services (Stern, 2006; Whalley et al., 2004). Recent scientific advances suggest that after damage the human brain can reorganize and experience functional improvements, even in cases of neurodegenerative diseases such as Alzheimer’s disease (AD) (Bach-yRita, 2003). Neurons affected by AD exhibit atrophic changes and metabolic impairments, which may contribute to neuronal dysfunction (Swaab, Dubelaar, Scherder, van Someren, & Verwer, 2003). Neuronal damage used to be considered irrecoverable, but neurons are now understood to be plastic and regenerative (Bach-y-Rita, 2003). It is postulated that neurons might work through nonsynaptic neurotransmission in which communication between cells takes place not through connected synapses, but rather through the release of neurotransmitters from remote sites that can be trained to assume the function previously performed by the injured brain (Bach-y-Rita, 2003). In animal models, neuronal stimulation and rehabilitation can be achieved through environmental enrichment. For example, compared with animals in standard cages, animals housed in environments with access to novel objects, exercise wheels, and a large number of cage mates had significantly improved brain structure and function (Jankowsky et al., 2005). Using functional magnetic resonance imaging, individuals with early-stage AD demonstrated increased activation of several cortical areas when engaged in cognitive tasks, indicating