nitrogen-dioxide and Dementia--Vascular

Evidence on the association between air pollution and dementia is accumulating but still inconclusive, and the potential effect modification by genetics is unclear. We investigated the joint effects of air pollution exposure and genetic risk on incident dementia in a prospective cohort study, the UK Biobank study. Land use regression models were used to estimate exposure to ambient particulate matter (PM) in 3 fraction sizes (PM with diameter < 2.5 μm (PM2.5), coarse particles (PM with diameter 2.5-10 μm (PMc)), and PM with diameter < 10 μm (PM10)), PM2.5 absorbance, nitrogen dioxide levels, and nitrogen oxide levels at each individual's baseline residence. A polygenic risk score was calculated as a quantitative measure of genetic dementia risk. Incident cases of dementia were ascertained through linkage to health administrative data sets. Among the 227,840 participants included in the analysis, 3,774 incident dementia cases (including 1,238 cases of Alzheimer disease and 563 cases of vascular dementia) were identified. After adjustment for a variety of covariates, including genetic factors, positive associations were found between exposure to air pollution-particularly PM10, PM2.5 absorbance, and nitrogen dioxide-and incident all-cause dementia and Alzheimer disease but not vascular dementia. No significant interaction between air pollution and genetics was found, either on the multiplicative scale or on the additive scale. Exposure to air pollution was associated with a higher risk of developing dementia regardless of genetic risk.

Topics: Air Pollutants; Air Pollution; Alzheimer Disease; Dementia, Vascular; Environmental Exposure; Humans; Nitrogen Dioxide; Particulate Matter; Prospective Studies; Risk Factors

Little is known about the role of air pollution in how people with dementia use mental health services.. We examined longitudinal associations between air pollution exposure and mental health service use in people with dementia.. In 5024 people aged 65 years or older with dementia in South London, high resolution estimates of nitrogen dioxide (NO. In the first year of follow-up, increased exposure to all air pollutants was associated with an increase in the use of CMHTs in a dose-response manner. These associations were strongest when we compared the highest air pollution quartile (quartile 4: Q4) with the lowest quartile (Q1) (eg, NO. Residential air pollution exposure is associated with increased CMHT usage among people with dementia.. Efforts to reduce pollutant exposures in urban settings might reduce the use of mental health services in people with dementia, freeing up resources in already considerably stretched psychiatric services.

Topics: Air Pollutants; Air Pollution; Dementia, Vascular; Environmental Exposure; Humans; Mental Health Services; Nitrogen Dioxide; Particulate Matter; Retrospective Studies

Evidence regarding the association of specific air pollutants with vascular dementia (VaD) risk is limited. In this nested case-control study, we enrolled 831 adults aged >65 years with VaD (International Classification of Diseases, Ninth Revision, Clinical Modification code 290.4x) newly diagnosed during 2005-2013; 3324 controls were age-, sex-, and VaD diagnosis year-matched with the study patients. Both patients with VaD and controls were selected from among a cohort of one million beneficiaries of Taiwan's National Health Insurance program, all of whom were registered in 2005. Exposure to the mean daily air pollutant concentration, derived from 76 fixed air quality monitoring stations, in 3, 5, and 7 years before VaD diagnosis was assessed using the spatial analysis method (i.e., ordinary kriging) on ArcGIS. A logistic regression model was used to calculate covariate-adjusted odds ratios (ORs) of VaD in relation to specific air pollutants. After potential confounders and other air pollutants were controlled for, high concentrations of coarse particulate matter (10 µm or less in diameter) and carbon monoxide (CO) were sporadically associated with higher OR of VaD. The most prominent association was observed for nitrogen dioxide (NO

Topics: Aged; Aged, 80 and over; Air Pollutants; Air Pollution; Carbon Monoxide; Case-Control Studies; Cohort Studies; Dementia, Vascular; Female; Humans; Male; Nitrogen Dioxide; Odds Ratio; Particulate Matter; Taiwan; Vehicle Emissions

Recent epidemiological literatures reported that NO(2) is a potential risk factor of ischemic stroke in polluted area. Meanwhile, our previous in vivo study found that NO(2) could delay the recovery of nerve function after stroke, implying a possible risk of vascular dementia (VaD) with NO(2) inhalation, which is often a common cognitive complication resulting from stroke. However, the effect and detailed mechanisms have not been fully elucidated. In the present study, synaptic mechanisms, the foundation of neuronal function and viability, were investigated in both model rats of ischemic stroke and healthy rats after NO(2) exposure. Transmission electron microscope (TEM) observation showed that 5 mg m(-3) NO(2) exposure not only exacerbated the ultrastructural impairment of synapses in stroke model rats, but also induced neuronal damage in healthy rats. Meantime, we found that the expression of synaptophysin (SYP) and postsynaptic density protein 95 (PSD-95), two structural markers of synapses in ischemic stroke model were inhibited by NO(2) inhalation; and so it was with the key proteins mediating long-term potentiation (LTP), the major form of synaptic plasticity. On the contrary, NO(2) inhalation induced the expression of nearly all these proteins in healthy rats in a concentration-dependent manner. Our results implied that NO(2) exposure could increase the risk of VaD through inducing excitotoxicity in healthy rats but weakening synaptic plasticity directly in stroke model rats.

Topics: Air Pollutants; Animals; Dementia, Vascular; Disease Models, Animal; Disks Large Homolog 4 Protein; Hippocampus; Intracellular Signaling Peptides and Proteins; Male; Membrane Proteins; Neuronal Plasticity; Nitrogen Dioxide; Protein Kinases; Rats; Rats, Wistar; Risk Factors; Stroke; Synapses; Synaptophysin; Transcription Factors