Association of subclinical depressive symptoms and sleep with cognition in the community-dwelling older adults.

BACKGROUND: /Purpose: This study aimed to explore the association of subclinical depressive symptoms and sleep with cognition in community-dwelling Taiwanese older adults. METHODS: This four-year prospective cohort study (2015-2019) included 379 participants aged 65 years or older from the annual senior health checkup program at National Taiwan University Hospital who were followed up two years later. Global and domain cognitive functions were assessed using validated neuropsychological tests. Depressive symptoms were evaluated using the Center for Epidemiologic Studies Depression (CES-D) Scale. Sleep quality was evaluated using the Pittsburg Sleep Quality Index (PSQI). Excessive daytime sleepiness was assessed using the Epworth Sleepiness Scale (ESS). Generalized linear mixed models were used to explore the associations of subclinical depressive symptoms and sleep variables with cognition, adjusting for important covariates. Stratification analyses were performed using the sleep variables. RESULTS: Over time, depressive symptoms were associated with poor performance of memory (߈ = 0.24, P = 0.04) and executive function (߈ = -0.24, P = 0.03). Poor sleep quality (elevated PSQI score) was associated with poor memory performance (߈ = -0.04 to -0.03, P < 0.05). Excessive daytime sleepiness (elevated ESS score) was associated with poor performance of memory (߈ = -0.02, P < 0.05) and executive function (߈ = -0.02, P = 0.001). At baseline, better sleep quality and no excessive daytime sleepiness were associated with better memory performance over time. CONCLUSION: Subclinical depressive symptoms, worse sleep quality, and excessive daytime sleepiness were differentially associated with impairment of cognitive domains (mainly memory and executive function).

Genetic polymorphisms of lipid metabolism gene SAR1 homolog B and the risk of Alzheimer's disease and vascular dementia.

BACKGROUND/PURPOSE: Lipid metabolism is involved in beta amyloid generation, which has been related with the progression of Alzheimer's disease (AD). No study has explored the association between polymorphisms of SAR1 homolog B (SAR1B) and the risk of dementia previously. METHODS: This is a case-control study. A total of 279 AD and 117 vascular dementia (VaD) patients were recruited from neurology clinics at three teaching hospitals in Taiwan from 2007 to 2010. Controls (n = 466) were recruited from the elderly health checkup program and volunteers in the hospital during the same time interval. Three common (frequency ≥ 5%) haplotype-tagging single nucleotide polymorphisms were selected from the lipid metabolism gene SAR1B to assess its association with AD and VaD. RESULTS: Homozygous variants of rs11948613 were associated with a decreased AD risk (CC vs. TT: adjusted odds ratio = 0.39, 95% confidence interval = 0.15-0.98) with a population attributable risk of 26.7%. This association decreased further in apolipoprotein E ε4 (ApoE ε4) noncarriers (adjusted odds ratio = 0.28, 95% confidence interval = 0.09-0.91). No association was found for VaD. Two common haplotypes (with a cumulative frequency of 95.7% in controls) were identified for SAR1B, and no association was found for AD or VaD. Simultaneous screening using rs11948613 and ApoE ε4 significantly improved the sensitivity of ApoE ε4 alone (from 0.40 to 0.75). CONCLUSION: SAR1B polymorphisms were associated with AD risk; results were not significant after correction for multiple tests. Simultaneous screening using SAR1B rs11948613 and ApoE ε4 status offered a better sensitivity for AD screening.

Sequence variants of the aging gene CISD2 and the risk for Alzheimer's disease.

BACKGROUND/PURPOSE: The CISD2 gene has been related to life span control and mitochondrial dysfunction in animals. In addition, inhibition of mitochondrial enzymes due to an accumulation of beta-amyloid peptide has been related to Alzheimer's disease (AD). This study aimed to explore the association between sequence variants of the CISD2 gene and risk for AD, which has not been explored previously. METHODS: This was a case-control study involving a total of 276 patients with AD who were recruited from three teaching hospitals in Taiwan from 2007 to 2010; 460 controls were recruited from elderly individuals attending for health check-ups and volunteers in the hospital during the same period of time. All participants were aged 60 years or older. Two haplotype-tagging single nucleotide polymorphisms (htSNPs), rs223330 and rs223331, were selected from the CISD2 gene to test the association between their polymorphisms and the risk for dementia, and how ApoE ɛ4 status, sex, hypertension, and type 2 diabetes mellitus might modify this association. RESULTS: rs223330 variant carriage was not associated with risk for AD [TT versus CC: adjusted odds ratio (AOR) = 0.98, 95% confidence interval (CI) = 0.59-1.62; TC versus CC: AOR = 0.72, 95% CI = 0.47-1.11]. Similar findings were observed for rs223331 (AA versus TT: AOR = 1.12; AT versus TT: AOR = 0.99). In addition, hypertension significantly modified the association between rs223331 and risk for AD (p = 0.005).Three common haplotypes (with a frequency of 99.8%) were observed for CISD2. Common CISD2 haplotypes were not associated with the risk for AD. CONCLUSION: Our findings suggested that CISD2 htSNPs are not associated with AD risk.