Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Wildfire smoke exposure is increasing across the U.S., but the long-term neurological effects of smoke-specific fine particulate matter (PM 2.5 ) and its carbonaceous components remain uncertain.
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Seasonally normalized 25(OH)D identifies a reproducible state of systemic vulnerability while reducing exposure misclassification caused by calendar timing of measurement.
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These findings identify restoration of hippocampal transcript fate and splice-isoform selection as a mechanism potentially underlying A. muciniphila -mediated protection against Cd neurotoxicity, and establish post-transcriptional RNA regulation as a gut-brain target for mitigating environmentally driven neurotoxicity.
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Environmental microplastics and nanoplastics (MNPs) are emerging contaminants that accumulate in human tissues, including the brain, yet their mechanistic impact on the nervous system remains poorly understood.
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Higher UGS coverage was associated with a lower risk of incident AD among older adults in urban South Korea.
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The short-wavelength content of available light declines steadily through the afternoon, well before nightfall, while the long-wavelength component remains nearly constant.
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16/100
Neuroexposome research investigates associations between physical, chemical, biological, and psychosocial factors and neurological health.
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Of 2,496 records screened, 26 studies met eligibility, comprising >84,000 older adults across 10 countries: United States, South Korea, United Kingdom, France, Spain, Sweden, Netherlands, Taiwan, Germany, and Japan.
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Transactive response DNA-binding protein 43 (TDP-43) aggregation and loss of function are hallmark features of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) among other neurodegenerative diseases.
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Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders, yet the environmental drivers that accelerate its progression remain poorly defined.
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In this prospective birth cohort study, prenatal exposure to a persistent environmental toxicant was associated with lower plasma Aβ42/40 ratio and worse cognitive performance in midlife, consistent with DDE accelerating the preclinical trajectory of AD-related biological changes decades before symptom onset.
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Direct medical and productivity-related costs associated with incident cases were estimated using a cost-of-illness (COI) framework.
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Ambient air pollution has been associated with increased incidence of chronic disease and is estimated to contribute towards 4.2 million early deaths annually.
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Exposure to the highest quintile of PM 2·5 (Rte:1·14, 95% CI:1·06-1·23), NO x (Rte:1·11, 95% CI:1·03-1·20) or NO 2 (Rte:1·08, 95% CI:0·99-1·16), compared to the lowest quintile, was associated with higher dementia risk.
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Higher exposure to PM 2.5 was associated with cerebral arteriolosclerosis and atherosclerosis at death, consistent with the known vascular toxicity of this pollutant.
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No association between cadmium exposure and dementia incidence was observed.
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Air pollution (AirP) exposure is associated with increased Alzheimer’s disease (AD) risk, yet AirP is chemically heterogeneous, complicating identification of shared pathogenic drivers.
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16/100
Our findings demonstrate differential effects of nicotine on AD risk and smoking intensity on white matter integrity, requiring triangulation with complementary methodological approaches to better inform potential long-term risks of nicotine intake on neurocognitive outcomes.
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16/100
Living in locations with higher PM2.5 (per interquartile range [IQR]=3.17μg/m3) or NO2 (per IQR=6.63ppb) was associated with greater MTL atrophy (βPM2.5 = -0.29, 95% confidence interval [CI]=[-0.41,-0.18]; βNO2 =-0.12, 95%CI=[-0.23,-0.02]).