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NEUROLOGY 2004;63:1399-1402
© 2004 American Academy of Neurology

APOE {epsilon}4 and cognitive decline in older stroke patients with early cognitive impairment

C. G. Ballard, MRC Psych, C. M. Morris, PhD, H. Rao, PhD, J. T. O’Brien, FRC Psych, R. Barber, MRC Psych, S. Stephens, BSc, E. Rowan, PhD, A. Gibson, BSc, R. N. Kalaria, FRC Path and R. A. Kenny, FRCP

From the Institute for Ageing and Health, Newcastle, UK.

Address correspondence and reprint requests to Dr. C.G. Ballard, Institute for Ageing and Health, Wolfson Research Centre, Newcastle General Hospital, Westgate Rd., Newcastle upon Tyne, NE4 6BE, UK; e-mail: c.g.ballard{at}ncl.ac.uk

Background: Dementia is common post stroke, but the potential role of early cognitive impairment and APOE {epsilon}4 as risk factors is unclear.

Method: Stroke survivors older than 75 years without dementia at 3 months post stroke received a detailed neuropsychological evaluation at 3 and 15 months post stroke, which included the Cambridge Assessment of Mental Disorders in the Elderly (CAMCOG). Early cognitive impairment was diagnosed using the criteria for cognitive impairment/no dementia (vascular CIND). APOE genotype was determined using a standardized method.

Results: One hundred thirty-seven older stroke patients without dementia (mean age 80.6 ± 4.3, mean CAMCOG score 83.5 ± 10.4, 68 women) participated in the study, of whom 40 met the criteria for CIND. Stroke patients with one or more APOE {epsilon}4 alleles were significantly more likely to have CIND (14/40 vs 17/97, odds ratio = 2.5, 95% CI 1.1 to 5.8). Over the 1 year of follow-up, CIND patients with one or more APOE {epsilon}4 alleles had a mean decline on the total CAMCOG of 2.7 points compared with an improvement of >4 points among patients without APOE {epsilon}4 (T = 2.9 p = 0.006). CIND patients with an APOE {epsilon}4 allele also experienced greater decline in memory (T = 2.5, p = 0.015).

Conclusion: In older stroke patients with early cognitive impairment, the presence of an APOE {epsilon}4 allele is associated with greater progression of cognitive decline. This has implications for interventions aimed at the secondary prevention of dementia in stroke patients.

Received October 31, 2003. Accepted in final form June 7, 2004.




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