Semantic memory and language dysfunction in early Alzheimer's disease: a review
Article first published online: 1 FEB 2012
Copyright © 2012 John Wiley & Sons, Ltd.
International Journal of Geriatric Psychiatry
Volume 27, Issue 12, pages 1209–1217, December 2012
How to Cite
Verma, M. and Howard, R. J. (2012), Semantic memory and language dysfunction in early Alzheimer's disease: a review. Int. J. Geriat. Psychiatry, 27: 1209–1217. doi: 10.1002/gps.3766
- Issue published online: 7 NOV 2012
- Article first published online: 1 FEB 2012
- Manuscript Accepted: 7 DEC 2011
- Manuscript Received: 28 MAY 2011
- Alzheimer's disease;
- semantic memory;
- category fluency
Language impairment in Alzheimer's disease occurs early, and language function deteriorates with progression of the illness to cause significant disability. This review focuses on language dysfunction in Alzheimer's disease and the contribution of semantic memory impairment.
Electronic publication databases were searched for literature relevant to the review. Additionally, individual references were examined to elicit further studies not found by online search.
Language impairment in Alzheimer's disease initially affects verbal fluency and naming before breakdown in other facets. Naming and fluency require integrity of semantic concepts, and dysfunction may be a marker of primary semantic memory impairment rather than overall cognitive decline. Research suggests the presence of semantic loss several years prior to diagnosis. Imaging studies indicate an altered connectivity state with respect to language networks, and this is associated with potential semantic failure. This state may also be present in individuals with established risk factors for Alzheimer's disease. Compensatory recruitment of alternative cortical areas to supplement language function appears to occur and may be a target for future intervention.
Identifying and classifying the nature and degree of language impairment more closely could aid in developing targeted therapies. Treatments already established in other aphasic states, such as post-stroke, may be especially relevant. The nature of these and the protective nature of cognitive reserve are potential therapeutic avenues. Copyright © 2012 John Wiley & Sons, Ltd.