Area Deprivation Index (ADI) is a measurement of neighborhood disadvantage. Evidence suggests that living in a disadvantaged neighborhood has a negative impact on health outcomes independent of socioeconomic status, including increased risk for Alzheimer's disease (AD). However, less is known about the biological mechanisms that drive these associations. We examined how ADI influences structural imaging variables and cognitive performance in community-dwelling older adults. We hypothesized that greater neighborhood disadvantage would predict atrophy and worse cognitive trajectory over time.

Participants included the legacy cohort from the Vanderbilt Memory and Aging Project (n=295, 73±7 years of age, 16±3 years of education, 42% female, 85% non-Hispanic White) who lived in the state of Tennessee. T1-weighted and T2-weighted fluid-attenuated inversion recovery brain MRIs and a comprehensive neuropsychological assessment were acquired at baseline, 18-month, 3-year, 5-year and 7-year follow-up time (mean follow-up time=5.2 years). Annual change scores were calculated for all neuropsychological and structural MRI outcome variables. Baseline state ADI was calculated using the University of Wisconsin School of Medicine and Public Health Neighborhood Atlas (Kind & Buckingham, 2018) and was based on deciles where 1 represents the least deprived area and 10 represents the most. Mixed effects regression models related baseline ADI to longitudinal brain structure (volume, thickness, white matter hyperintensities) and neuropsychological trajectory (one test per model). Analyses adjusted for age, sex, race/ethnicity, education, Framingham Stroke Risk Profile score, (apolipoprotein) APOE-e4 status, cognitive status, and intracranial volume (for MRI outcomes). Models were repeated testing interactions with APOE-e4 status, sex, and cognitive status. A false discovery rate (FDR) correction for multiple comparisons was performed.

On average, the sample was from relatively less disadvantaged neighborhoods in Tennessee (ADI state decile=2.4±1.8). Greater neighborhood disadvantage at study entry predicted more thinning of an AD-signature composite over time (ß=-0.002, p=0.005, pFDR=0.06); however, all other models testing MRI and neuropsychological outcomes were null (p-values>0.05, pFDR-values>0.51). Baseline ADI interacted with sex on longitudinal cortical thinning captured on the AD-signature composite (ß=0.004, p=0.006, pFDR=0.08) as well as several longitudinal cognitive outcomes including an executive function composite score (ß=0.033, p<0.001, pFDR=0.01), naming (ß=0.10, p=0.01, pFDR=0.12), visuospatial functioning (ß=0.083, p=0.02, pFDR=0.09), and an episodic memory composite score (ß=0.021, p=0.02, pFDR=0.07). In stratified models by sex, greater ADI predicted greater cortical thinning over time and worse longitudinal neuropsychological performance among men only. All stratified models in women were null except for executive function composite score, which did not survive correction for multiple comparisons (ß=-0.013, p=0.03, pFDR=0.61). Interactions by APOE-e4 and cognitive status were null (p-values>0.06, pFDR-values>0.61).

Among community-dwelling older adults, greater neighborhood disadvantage predicted greater cortical thinning over the mean 5-year follow-up in anatomical regions susceptible to AD-related neurodegeneration. Neighborhood disadvantage also interacted with sex on cortical thickness and several cognitive domains, with stronger effects found among men versus women. By contrast, there were no interactions between neighborhood disadvantage and genetic risk for AD or cognitive status. This study provides valuable evidence for sociobiological mechanisms that may underlie health disparities in aging adults whereby neighborhood deprivation is linked with neurodegeneration over time.

Novel blood-based biomarkers for Alzheimer's disease (AD) could transform AD diagnosis in the community; however, their interpretation in individuals with medical comorbidities is not well understood. Specifically, kidney function has been shown to influence plasma levels of various brain proteins. This study sought to evaluate the effect of one common marker of kidney function (estimated glomerular filtration rate (eGFR)) on the association between various blood-based biomarkers of AD/neurodegeneration (glial fibrillary acidic protein (GFAP), neurofilament light (NfL), amyloid-b42 (Ab42), total tau) and established CSF biomarkers of AD (Ab42/40 ratio, tau, phosphorylated-tau (p-tau)), neuroimaging markers of AD (AD-signature region cortical thickness), and episodic memory performance.

Vanderbilt Memory and Aging Project participants (n=329, 73±7 years, 40% mild cognitive impairment, 41% female) completed fasting venous blood draw, fasting lumbar puncture, 3T brain MRI, and neuropsychological assessment at study entry and at 18-month, 3-year, and 5-year follow-up visits. Plasma GFAP, Ab42, total tau, and NfL were quantified on the Quanterix single molecule array platform. CSF biomarkers for Ab were quantified using Meso Scale Discovery immunoassays and tau and p-tau were quantified using INNOTEST immunoassays. AD-signature region atrophy was calculated by summing bilateral cortical thickness measurements captured on T1-weighted brain MRI from regions shown to distinguish individuals with AD from normal cognition. Episodic memory functioning was measured using a previously developed composite score. Linear mixed-effects regression models related predictors to each outcome adjusting for age, sex, education, race/ethnicity, apolipoprotein E-e4 status, and cognitive status. Models were repeated with a blood-based biomarker x eGFR x time interaction term with follow-up models stratified by chronic kidney disease (CKD) staging (stage 1/no CKD: eGFR>90 mL/min/1.73m2, stage 2: eGFR=60-89 mL/min/1.73m2; stage 3: eGFR=44-59mL/min/1.73m2 (no participants with higher than stage 3)).

Cross-sectionally, GFAP was associated with all outcomes (p-values<0.005) and NfL was associated with memory and AD-signature region cortical thickness (p-values<0.05). In predictor x eGFR interaction models, GFAP and NfL interacted with eGFR on AD-signature cortical thickness, (p-values<0.004) and Ab42 interacted with eGFR on tau, p-tau, and memory (p-values<0.03). Tau did not interact with eGFR. Stratified models across predictors showed that associations were stronger in individuals with better renal functioning and no significant associations were found in individuals with stage 3 CKD. Longitudinally, higher GFAP and NfL were associated with memory decline (p-values<0.001). In predictor x eGFR x time interaction models, GFAP and NfL interacted with eGFR on p-tau (p-values<0.04). Other models were nonsignificant. Stratified models showed that associations were significant only in individuals with no CKD/stage 1 CKD and were not significant in participants with stage 2 or 3 CKD.

In this community-based sample of older adults free of dementia, plasma biomarkers of AD/neurodegeneration were associated with AD-related clinical outcomes both cross-sectionally and longitudinally; however, these associations were modified by renal functioning with no associations in individuals with stage 3 CKD. These results highlight the value of blood-based biomarkers in individuals with healthy renal functioning and suggest caution in interpreting these biomarkers in individuals with mild to moderate CKD.

Chest tube drainage placement, a standard procedure in video-assisted thoracoscopic surgery, was reported to cause perioperative complications like pain and increased risk of infection. The present study was designed to evaluate the necessity of chest tube drainage inpaediatric thoracoscopic surgery.

Thirty children admitted to our hospital from April 2018 to April 2020 were included in the current study and were grouped as the tube group (children receiving video-assisted thoracoscopic surgery with chest tube drainage) and the non-tube group (children receiving video-assisted thoracoscopic surgery without chest tube drainage). Laboratory hemogram index, length of hospitalisation, post-operative performance of involved children, and psychological acceptance of indicated therapy by guardians of the involved children were investigated.

Laboratory examination revealed that the mean corpuscular haemoglobin concentration in the non-tube group was significantly higher than that in the tube group on post-operative day 1 (p < 0.05). Children in the non-tube group had a shorter length of hospitalisation (7–9 days) than that of patients from the tube group. Additionally, the frequency of crying of children was decreased and psychological acceptance by patients’ guardians was improved in the non-tube group when compared with the tube group.

This study showed that chest tube drainage placement may not be necessary in several cases of paediatric video-assisted thoracoscopic surgery. Rapid recovery with decreased perioperative complications in children operated by video-assisted thoracoscopic surgery without tube placement could also reduce the burden of the family and society both economically and psychologically.

To assess the association between total alcohol intake, specific alcoholic beverages and sleep quality in a community-based cohort.

A cross-sectional study.

The Kailuan community, China.

Included were 11 905 participants who were free of a history of CVD, cancer, Parkinson’s disease, dementia and head injury in or prior to 2012. Alcohol consumption (amount and frequency intake) and alcoholic beverage type were collected in 2006 (baseline) and 2012. Participants were grouped into non-, light- (women: 0–0·4 serving/d; men: 0–0·9 serving/d), moderate- (women: 0·5–1·0 serving/d; men: 1·0–2·0 servings/d) and heavy- (women: >1·0 servings/d; men: >2·0 servings/d) drinkers. Overall sleep quality was measured in 2012 and included four sleep parameters (insomnia, daytime sleepiness, sleep duration, snoring/obstructive sleep apnoea).

We observed a dose–response association between higher alcohol consumption in 2006 and worse sleep quality in 2012 (Ptrend < 0·001), after adjusting for age, sex, socio-economic status, smoking status, physical activity, obesity, plasma lipid profiles, diabetes and hypertension. A similar association was observed when alcohol consumption in 2012 was used as exposure. Alcohol was associated with higher odds of having short sleep duration (adjusted OR for heavy- v. non-drinkers = 1·31; 95 % CI: 1·09, 1·57) and snoring (adjusted OR for heavy- v. non-drinkers: 1·38; 95 % CI: 1·22, 1·57). Consumption of hard liquor, but not beer or wine, was significantly associated with poor sleep quality.

Higher alcohol consumption was associated with poorer sleep quality and higher odds of having snoring and short sleep duration.

The pathophysiology of obsessive-compulsive disorder (OCD) remains unclear despite extensive neuroimaging work on the disorder. Exposure to medication and comorbid mental disorders can confound the results of OCD studies. The goal of this study was to explore differences in brain functional connectivity (FC) within the cortico-striato-thalamo-cortical (CSTC) loop of drug-naïve and drug-free OCD patients and healthy controls (HCs).

A total of 29 drug-naïve OCD patients, 22 drug-free OCD patients, and 25 HCs matched on age, gender and education level underwent functional magnetic resonance imaging scanning at resting state. Seed-based connectivity analyses were conducted among the three groups. The Yale Brown Obsessive Compulsive Scale and clinical inventories were used to assess the clinical symptoms.

Compared with HCs, the drug-naïve OCD patients had reduced FC within the limbic CSTC loop. In the drug-naïve OCD participants, we also found hyperconnectivity between the supplementary motor area and ventral and dorsal putamen (p < 0.05, corrected for multiple comparisons).

Exposure to antidepressants such as selective serotonin reuptake inhibitors may affect the function of some brain regions. Future longitudinal studies could help to reveal the pharmacotherapeutic mechanisms in these loops.

Growing evidence has indicated that right ventrolateral prefrontal cortex (RVLPFC) is critical in down-regulating emotional responses to social exclusion, and that depression is accompanied by social emotional dysregulation associated with reduced lateral prefrontal engagement. This study used anodal transcranial direct current stimulation (tDCS) to examine whether stimulating RVLPFC could improve emotional down-regulation of social exclusion in individuals with high depressive mood (DM).

A total of 96 high and 94 low DM individuals received active or sham tDCS while viewing social exclusion or individual negative pictures under no-reappraisal (passive viewing) and reappraisal conditions. Participants rate their negative emotional experience following the presentation of each image. Pupil diameter and visual fixation duration were also recorded during the task.

It was found that tDCS-activated RVLPFC induced a stronger regulation effect on social exclusion than individual negative emotions. The effect of tDCS on regulation of social exclusion was more pronounced in low v. high DM individuals.

These findings demonstrate the specific role of RVLPFC on social emotion regulation, which has implications for refining target areas for the treatment of social emotion dysregulation in depression. However the findings do not suggest that high DM individuals benefit from a single-tDCS session on the emotion regulation of social exclusion. Thus we suggest to use multiple tDCS sessions or transcranial magnetic stimulation to further explore the therapeutic proposal in the future.