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Background Population aging will lead to a dramatic increase in dementia prevalence, which will disproportionally affect racial minorities. The presence of racial differences in dementia prevalence has been widely reported in United States, but there are no relevant studies on this topic in low-middle income countries (LMIC). Methods In a cross-sectional survey, 2,944 older Cubans were recruited at a community-based level aimed to identify the effects of self-identified race and genetic admixture on cognitive performance. Dementia diagnosis was established using 10/66 Dementia and DSM-IV criteria. APOE-ε4 genotype was determined in 2,511 (85%) and genetic admixture was completed for all dementia cases and in a randomly selected sample of cognitive healthy participants (218 dementia cases and 367 participants without dementia). Results The overall prevalence of dementia was 8.7%, without large or statistically significant differences on dementia prevalence (p=0.12) by self-identified race. Mean cognitive scores were similar across racial groups (p=0.46). After controlling for age, sex and education, greater proportion of African ancestry was not associated with cognitive performance (p=0.17). Conclusions We found no evidence of an independent effect of self-identified race and/or population ancestry on dementia prevalence or cognitive performance. This suggests that observed differences in dementia prevalence among diverse populations may be driven primarily by social determinants of health.

Introduction Apolipoprotein E (APOE) is considered the major susceptibility gene for developing Alzheimer's disease. However, the strength of this risk factor is not well established across diverse Hispanic populations. Methods We investigated the associations among APOE genotype, dementia prevalence, and memory performance (immediate and delayed recall scores) in Caribbean Hispanics (CH), African Americans (AA), Hispanic Americans (HA) and non‐Hispanic White Americans (NHW). Multivariable logistic regressions and negative binomial regressions were used to examine these associations by subsample. Results Our final dataset included 13,516 participants (5198 men, 8318 women) across all subsamples, with a mean age of 74.8 years. Prevalence of APOE ε4 allele was similar in CHs, HAs, and NHWs (21.8%–25.4%), but was substantially higher in AAs (33.6%; P < 0.001). APOE ε4 carriers had higher dementia prevalence across all groups. Discussion APOE ε4 was similarly associated with increased relative risk of dementia and lower memory performance in all subsamples.

ObjectiveIn an admixed population of older Cubans, the incidence and association of APOE and sociodemographic risk factors with dementia incidence was estimated.MethodsA single-phase survey (baseline) of all over 65-year-olds residing in seven catchment areas in Cuba (n=2944) was conducted between 2003 and 2007. Dementia diagnosis was established according to DSM-IV and 10/66 criteria. APOE genotype was determined in 2520 participants. An incidence wave was conducted 4.5 years after cohort inception in order to estimate incidence and associations with sociodemographic risk factors of the APOE ε4 genotype.ResultsThe incidence rate of DSM IV dementia was 9.0 per 1000 person-years (95% CI 7.2-11.3) and of 10/66 dementia was 20.5 per 1000 person-years (95% CI, 17.6-23.5). Older age, a family history of dementia and APOE ε4 genotype were independent risk factors for incident 10/66 dementia. APOE genotype was associated cross-sectionally with dementia prevalence, but the effect on the incidence of dementia was attenuated, and only apparent among those in the youngest age group.ConclusionThe incidence of dementia in the older Cuban population is relatively high and similar to levels reported in Europe and North-America. The study showed that the relationship between APOE ε4 and incident dementia is stronger in the younger-old than the older-old and that this change must be taken into account in models of dementia.

Dural arteriovenous fistulas (DAVFs) represent 10–15% of intracranial arteriovenous malformations. Of these, only 12–29% cause intracranial hemorrhage. The presentation of DAVF as a subdural hematoma (SDH) and intraparenchymal hemorrhage (IPH) is infrequent; additionally, behavioral changes are not common among these patients. We report, for the first time in our country, the case of a 23-year-old man with no history of head injury, in which a brain computed tomography (CT) scan revealed SDH and IPH with behavioral disturbances. The angiotomography showed ecstatic venous vessels, indicating the presence of a DAVF, which was later confirmed by cerebral angiography. Endovascular therapy, which followed the clinical diagnosis, resulted in satisfactory evolution two years after treatment. A review of the literature concerning cases with DAVF and behavioral disturbances is presented. DAVF may lead to cognitive impairment, behavioral changes, and dementia as a result of diffuse white matter and thalamus modifications related to venous ischemia, and it should be considered as a reversible cause of vascular dementia.