Background. Subjective memory impairment (SMI) is common in older populations but its aetiology and clinical significance is uncertain. Depression has been reported to be strongly associated with SMI. Associations with objective cognitive impairment are less clear cut. Other factors suggested to be associated with SMI include poor physical health and the apolipoprotein E (APOE) ε4 allele. Studies of SMI have been predominantly confined to white Caucasian populations.Method. A community study was carried out in a UK African-Caribbean population aged 55–75, sampled from primary care lists. Twenty-three per cent were classified with SMI. Depression was defined using the 10-item Geriatric Depression Scale. Other aetiological factors investigated were education, objective cognitive function, APOE genotype, disablement and vascular disease/risk. The principal analysis was restricted to 243 participants scoring > 20 on the Mini-Mental State Examination (85%). A second analysis included all 290 participants.Results. Depression, self-reported physical impairment and APOE ε4 were associated with SMI. The association between SMI and physical impairment was not explained by depression, vascular disease/risk, or disability/handicap. The association between ε4 and SMI increased as MMSE scores decreased and was particularly strong in those with depression. The ε4 allele was present in 69% (95% CI 41–89%) of those with depression and SMI compared with 28% (20–36%) of those with neither.Conclusions. Depression may not be a sufficient explanation for subjective memory complaints. Memory complaints in the presence of depression are associated with high prevalence of ε4 and therefore, presumably, a raised risk of subsequent dementia.

To explore whether antithrombotic medication may protect against cognitive decline, tests of verbal memory, attention, abstract reasoning, verbal fluency, and mental flexibility were administered to 405 men at risk of cardiovascular disease. These subjects were a subgroup of those who had been participating in a randomised double blind factorial trial of low dose aspirin (75 mg daily) and low intensity oral anticoagulation with warfarin (international normalised ratio of 1.5) at 35 general practices across the United Kingdom for at least five years, were at least 55 years old at trial entry, and had been randomly allocated to one of four groups: active warfarin and active aspirin, active warfarin and placebo aspirin, placebo warfarin and active aspirin, and double placebo. Verbal fluency and mental flexibility were significantly better in subjects taking antithrombotic medication than in subjects taking placebo. Aspirin may have contributed more than warfarin to any beneficial effect. These results provide tentative evidence that antithrombotic medication may protect cognitive function in men at risk of cardiovascular disease. (3 Neurol Neurosurg Psychiatry 1997;62:269-272) Keywords: cognitive; aspirin; warfarin; cardiovascular; antithrombotic A growing body of evidence suggests an association between cardiovascular risk factors and cognitive impairment during aging. These risk factors include hypertension, diabetes, hypercholesterolaemia, and cardiac disease such as atrial fibrillation and angina, all of which may promote neuropathological changes resulting from microthromboses in cerebral blood vessels. Antithrombotic medication may therefore protect cognitive function. In a randomised placebo controlled trial, Meyer et alI found that aspirin improved cognitive function in patients with multi-infarct dementia. Little is known, however, about the effect of antithrombotic medication on cognitive function in those without frank dementia. Population based studies have either reported no association2 or a modest trend towards protection of cognitive function3 from medication (non-steroidal anti-inflammatory drugs and aspirin). However, these authors relied on recall of use of medication and, in both studies, employed a single, global measure of current cognitive status.In the present study we measured cognitive function in patients already enrolled in a double blind placebo controlled factorial trial of low dose aspirin and low intensity oral anticoagulation with warfarin for their effect on the prevention of coronary and cerebral thrombosis. The purpose was to assess whether those who were on active treatment showed differences in cognitive performance compared with those who were receiving placebo. Because this cognitive study was conducted after the trial was already in progress, no baseline cognitive test data are available for comparison. Nevertheless, we were able to take advantage of the randomised design and detailed monitoring during a five year interval. The content of our neuropsychological te...

No abstract