You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.
Alzheimer's Association 24/7 Helpline800-272-390024 hours a day, 365 days a yearFree, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
988 Suicide & Crisis Lifeline98824/7Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
Alzheimer's Foundation of America (AFA) Helpline866-232-84849:00 am - 9:00 pm ET, seven days a weekLicensed social workers providing support, info and referrals. Also text message and web chat.Text: 646-586-5283
In a medical emergency, call 911.
More numbers, and what each line does, on the help page.
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Find studies
Showing 3,226–3,250 of 3,258 studies · tagged Risk Factors(page 130 of 131)· 27,380 in the whole library·How the 0–100 score works
From OpenAlex; 12,859 studies have no institution on record and are not counted here.
A note on reading research. One study is rarely the final word.
We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·Preprints.org·2026-09-14
Traumatic brain injury (TBI), chronic traumatic encephalopathy (CTE), and Alzheimer's disease (AD) share several neuropathophysiological mechanisms, including axonal injury, neuroinflammation, and abnormal protein aggregation, which may contribute to overlapping clinical manifestations. 1 key finding →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-10-11
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. 4 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·bioRxiv·2026-07-23
Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders, yet the environmental drivers that accelerate its progression remain poorly defined. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-02-05
Higher exposure to PM 2.5 was associated with cerebral arteriolosclerosis and atherosclerosis at death, consistent with the known vascular toxicity of this pollutant. 5 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-02-22
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. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-03-04
Ambient air pollution has been associated with increased incidence of chronic disease and is estimated to contribute towards 4.2 million early deaths annually. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-05-13
The Middle East and North Africa (MENA) region represents the area of greatest projected growth in instances of Alzheimer’s disease and related dementias (ADRDs) globally, yet, it remains virtually uncharacterized in health studies of aging and ADRDs. 4 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-08-04
Neuroticism, a personality trait characterized by the predisposition to experience intense and frequent negative emotions, has been associated with an increased risk of Alzheimer’s disease (AD). 5 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·PsyArXiv·2026-07-23
INTRODUCTIONLittle is understood about the extent to which lifestyle factors can advance or delay the risk of developing dementia, and whether that is dependent on non-modifiable factors, e.g. sex and genetic susceptibility.METHODSAmong 224,516 UK Biobank participants aged ≥50 years at baseline, Cox regression examined the relations of apolipoprotein E gene (APOE) genotypes, and lifestyle with incident dementia. 3 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-10-06
Vascular risk factors were associated with CSVD burden and progression, and WMH and PVS progression were further associated with cortical atrophy and cognitive decline, underscoring the interconnected contributions of vascular risk, CSVD, and neurodegeneration to cognitive aging and dementia risk. 5 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-07-31
In a contemporary, diverse cohort, most established dementia risk algorithms had limited power in discriminating amyloid positivity, pTau-217 positivity, and current cognitive status despite acceptable calibration. 3 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-07-06
In SPRINT, intensive vs standard SBP control yielded a significantly larger 4-year absolute risk reduction in dementia among APOE ε4 carriers (−1.7%) than non-carriers (0.2%; P-interaction = .045); the relative-scale interactions were directionally consistent but not significant. 3 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-07-06
Lifetime TBI exposure is associated with increased likelihood and long-term risk of psychiatric disorders in individuals with dementia, stroke, and Parkinson’s disease, with mood disorders being the most consistent outcome across conditions. 4 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-02-09
Both classes act on neuronal calcium signaling, raising the question of whether their combined use is associated with greater cognitive risk than gabapentin alone. 5 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·Research Square·2026-10-11
Patients with peripheral artery disease (PAD), chronic limb-threatening ischemia (CLTI), and/or diabetic foot ulcer (DFU) are at increased risk for limb loss and death. 3 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-10-14
Of 22,025,599 individuals screened, 2,051,275 were eligible; matched cohorts ranged from 10,113 to 857,773, with median follow-up of 4.7 to 7.2 years. 5 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-04-06
The prevalence of dementia and Parkinson’s disease in Russia varies widely depending on diagnostic method, age group, and study design. 2 key findings →
10 of the 3,247 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.
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 tierup to 10 pts
Journal's citation recordup to 4 pts
Study designup to 12 pts
Strength of evidenceup to 5 pts
Peer-review validationup to 10 pts
How recentup to 5 pts
Sample sizeup to 4 pts
Effect reportedup to 3 pts
Studied in peopleup to 3 pts
Randomised / blindedup to 2 pts
Times citedup to 7 pts
Citations per yearup to 5 pts
Impact for its field and yearup to 6 pts
Cited by studies hereup to 6 pts
Still being citedup to 4 pts
Senior author's track recordup to 4 pts
Institution's track recordup to 3 pts
Multi-centre collaborationup to 3 pts
Indexed in PubMedup to 2 pts
Free to readup 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC
(60.6% of the library) and OpenAlex (18.6%),
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.
1,032 records (3.8% 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.