High normal fasting blood glucose is associated with dementia in Chinese elderly.

BACKGROUND: Diabetes is a risk factor for mild cognitive impairment (MCI) and dementia. However, the association between high normal fasting blood glucose (FBG) and dementia has not been studied. METHODS: Polytomous logistic regression was used to assess the association of dementia and MCI with FBG in an age- and sex-matched sample of 32 dementia patients, 27 amnestic MCI (aMCI) patients, and 31 normal controls (NC). Analyses were repeated for those with normal FBG. Correlations between FBG and cognitive test scores were obtained. RESULTS: Controlling for age, gender, education, body mass index, Hachinski Ischemic Score, magnetic resonance imaging (MRI) stroke, and normalized brain, hippocampal, and white matter hyperintensity MRI volumes; higher FBG was associated with dementia versus aMCI status (OR = 3.13; 95% CI, 1.28-7.69). This association remained (OR = 7.75; 95% CI, 1.10-55.56) when analyses were restricted to subjects with normal FBG. When dementia patients were compared with NC adjusting for age, gender, and education, a significant association with FBG also was seen (OR = 1.83; 95% CI, 1.09-3.08), but it was lost when vascular covariates were added to the model. FBG was not associated with aMCI status versus NC. Higher FBG was correlated with poorer performance on the Trailmaking Test Part B (P = .003). The percentage of dementia patients with high normal FBG (90%) was significantly higher than that of aMCI patients with high normal FBG (32.9%) (χ(2) = 13.9, P < .001). CONCLUSIONS: Higher FBG was associated with dementia (vs. aMCI) independent of vascular risk factors and MRI indicators of vascular disease, and remained a significant risk factor when analyses were restricted to subjects with normal FBG. The results of this cross-sectional study suggest that a high normal level of FBG may be a risk factor for dementia.

Effects of apolipoprotein E-epsilon4 and -epsilon2 in amnestic mild cognitive impairment and dementia in Shanghai: SCOBHI-P.

OBJECTIVE: To determine apolipoprotein E (APOE)-epsilon4 and -epsilon2 frequencies and risk of mild cognitive impairment (MCI) and dementia in Shanghai, China. METHODS: A total of 34 MCI and 34 dementia cases were recruited from an urban Memory Disorders Clinic and 32 controls were recruited from a residential community served by the clinic. Apolipoprotein E was genotyped using standard methods. RESULTS: Among controls, frequencies were epsilon2, 0.11; epsilon3, 0.84; and epsilon4, 0.05; among MCI, 0.05, 0.77, and 0.18; and for dementia, 0.02, 0.84, and 0.15, respectively. In education-adjusted models, the odds ratio (OR) = 5.6 for dementia (95% CI = 1.09-29.3) and 4.7 for MCI (95% CI = 0.90-25.2) associated with any epsilon4 allele. The epsilon2 allele was inversely associated with dementia (OR = 0.12, 95% CI = 0.013-0.997) and MCI (OR = 0.38, 95% CI = 0.08-1.61). CONCLUSIONS: APOE-epsilon4 increases and -epsilon2 decreases the risk of dementia vs normal cognition. Similar trends were observed for amnestic mild cognitive impairment (aMCI).

Early-life risk factors for Alzheimer disease.

Research findings obtained over the past 20 years suggest that Alzheimer disease (AD) may have its origins in early life. In this review, we consider the evidence for early-life risk factors for this illness. We propose that risk factors that predict neuropathology are largely distinct from those related to the clinical expression of Alzheimer disease. Early-life risk factors for pathology include genes, chromosomal abnormalities, head injury, insulin resistance, and inflammation. With regard to risk factors for clinical expression of Alzheimer disease, six general groups of childhood exposures are reviewed: (1) perinatal conditions, (2) early-life brain development, (3) early-life body growth, (4) early-life socioeconomic conditions, (5) environmental enrichment, and (6) cognitive reserve. The literature reviewed suggests that risk of Alzheimer disease is probably not determined in any single time period but results from the complex interplay between genetic and environmental exposures throughout the life course. Enhancement or preservation of brain or cognitive reserve could delay the onset of Alzheimer disease and in some cases prevent the disease from occurring altogether.