ReviewOpen biology2020
The proteostatic effects of traffic-derived air pollution on Alzheimer's disease risk.
Review in Open biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Premature aging and metabolic diseases: the impact of telomere attrition.Frontiers in aging · 2025Review
- Association of long-term exposure to various ambient air pollutants, lifestyle, and genetic predisposition with incident cognitive impairment and dementia.BMC public health · 2024Article
- Aging, longevity, and the role of environmental stressors: a focus on wildfire smoke and air quality.Frontiers in toxicology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is an age-related neurodegenerative disease and the leading cause of dementia in the elderly. Recent decades have been marked by considerable advances in our understanding of genetic and environmental risk factors and also of the AD mechanism(s) of action. Nonetheless, there is still no cure and the myriad ways AD affects the brain is overwhelmingly complex. Such complexity is manifest in part by the fact that genetic background interacts with the environment, including traffic-derived particulate air pollution, to greatly exacerbate AD risk. Determining the mechanisms by which particulate air pollution acts as an AD risk factor has the potential to reveal yet unknown aspects of AD pathology. This review carefully peels back the layers of complexity to discern whether a unifying disease model, one with proteostasis imbalance at its core, holds up to scrutiny in light of the recent literature. While the data are compelling, it is now time for carefully designed studies to definitively determine whether particulate air pollution acts with ageing, genetic background and other sources of proteotoxic stress to disrupt the delicate proteostasis balance.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.