Air pollution may increase risk of Alzheimer's disease and related dementias (ADRD) in the U.S., but the extent of this relationship is unclear. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
We observed a significant association between blood cadmium levels and AD mortality among older adults in the US. 5 key findings →
Participants: 4,064 Evidence: low
Full summary, score breakdown and related studies → Original source
Asthma participants had widespread and large-magnitude differences in several dMRI metrics, which were indicative of neuroinflammation and neurodegeneration, and which were robustly associated with GFAP and, to a lesser extent, NfL. 5 key findings →
Participants: 111 Evidence: low
Full summary, score breakdown and related studies → Original source
PM2.5 can enter the central nervous system through 2 main pathways, the blood-brain barrier and olfactory neurons. 5 key findings →
Participants: 113 Evidence: low
Full summary, score breakdown and related studies → Original source
50/100
Among the compounds detected in greater abundance in the CSF of patients with DLB compared with patients with AD, only one had a xenobiotic profile potentially related to the pathophysiology of DLB. 5 key findings →
Participants: 45 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The adjusted hazard ratio (HR) of dementia for a 5-μg/m3 increase in NO2 was 1.09 (95% CI, 1.05-1.14); the adjusted HR of dementia for a 1-μg/m3 increase in PM2.5 was 1.10 (1.04-1.17). 5 key findings →
Participants: 447 Evidence: low
Full summary, score breakdown and related studies → Original source
During a median 11.7 years follow-up, 5 905 incident cases of all-cause dementia were identified. 5 key findings →
Participants: 459 Evidence: low
Full summary, score breakdown and related studies → Original source
In a population of cognitively unimpaired adults with increased risk of AD, long-term exposure to air pollution was associated with higher levels in biomarkers of AD pathology. 5 key findings →
Participants: 156 Evidence: low
Full summary, score breakdown and related studies → Original source
Preliminary studies have shown associations between chronic pesticide exposure in occupational settings and neurological disorders. 3 key findings →
Participants: 17,429 Evidence: low
Full summary, score breakdown and related studies → Original source
614 subjects were available for investigation at follow-up. 5 key findings →
Participants: 614 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), non-AD dementia, and Parkinson's disease (PD) are increasingly common in older adults, yet all risk factors for their onset are not fully understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Air pollution is a serious environmental problem. 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
Our study shows that increasing long-term exposure to air pollution may increase the odds of depression and the use of antidepressants and benzodiazepines. 3 key findings →
Participants: 958 Evidence: low
Full summary, score breakdown and related studies → Original source
With recent findings connecting the Epstein-Barr virus to an increased risk of multiple sclerosis and growing concerns regarding the neurological impact of the coronavirus pandemic, we examined potential links between viral exposures and neurodegenerative disease risk. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
In this non-demented study population, of which 62% were cognitively normal and 38% were in mild cognitive impairment state, exposure to the highest tertile of PM10mean was associated with increased risk of amyloid-β (Aβ) positivity (odds ratio 2.19, 95% confidence interval 1.13 to 4.26) even after controlling all potential confounders. 4 key findings →
Participants: 78 Evidence: low
Full summary, score breakdown and related studies → Original source
During a 12-year period of follow-up, 4,389 incidents of all-cause dementia were identified. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
46/100
In total, 104 incident dementia and 159 incident dementia/CIND cases were identified during the 10 years of follow-up. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We had a follow-up of 71 million person-years. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Air pollution is a risk factor for cardiovascular and Alzheimer's disease (AD). 3 key findings →
Participants: 72 Evidence: low
Full summary, score breakdown and related studies → Original source
An interquartile range increase in 20-year PM2.5 was associated with a 20% higher risk of dementia (95% confidence interval [CI]: 5%, 37%) and an increased risk of mixed VaD/AD but not AD alone. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The neuropathological hallmarks of Alzheimer's disease (AD), Parkinson's disease (PD), frontotemporal lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS) are present in urban children exposed to fine particulate matter (PM2.5), combustion and friction ultrafine PM (UFPM), and industrial nanoparticles (NPs). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
The scientific literature is scarce when referring to the influence of atmospheric pollutants on neurodegenerative diseases for present and future climate change scenarios. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
45/100
We observed significant increases in all-cause hospital admissions (2.53% in PD and 2.49% in AD/dementia) attributable to high PM2.5 exposure. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Fine particulate matter (PM2.5), a major component among air pollutants, highlights as a global health concern. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The increasing amount of particulate matter (PM) in the ambient air is a pressing public health issue globally. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 238 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Urban air pollution: influences on olfactory function and pathology in exposed children and young adults
- Association between air pollution from residential wood burning and dementia incidence in a longitudinal study in Northern Sweden
- Air pollution and brain damage
- Neurotoxicity of Diesel Exhaust Particles
- Toll-like receptor 4 in glial inflammatory responses to air pollution in vitro and in vivo
- Association between air pollution and CSF sTREM2 in cognitively normal older adults: The CABLE study
- Air pollution and children: neural and tight junction antibodies and combustion metals, the role of barrier breakdown and brain immunity in neurodegeneration
- Fine Particulate Matter and Dementia Incidence in the Adult Changes in Thought Study
- Human Health and Ocean Pollution
- Health Impacts from Ambient Particle Exposure in Southern Sweden
Where “Free full text” comes from
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
How the 0–100 score works — and why some entries are capped
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 27,780 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,034 records (3.7% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →