Get help now — free helplines

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 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call 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) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed 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.

Find studies

Showing 1–25 of 100 studies with an author at University College London (GB) · tagged Risk Factors (page 1 of 4) · 29,380 in the whole library · How the 0–100 score works

Download bibliography of these 100 studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

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.

Study-level data from 14 studies, 2,310,330 individuals, and 102,174 dementia case patients were included. 3 key findings →

Design: meta-analysis Participants: 2,310,330 Evidence: high

In a large placebo-controlled randomized trial, we found that pantoprazole is not associated with any adverse event when used for 3 years, with the possible exception of an increased risk of enteric infections. 5 key findings →

Design: randomized controlled trial Participants: 8,791 Evidence: high

In analyses that addressed bias due to reverse causation, physical inactivity was not associated with all-cause dementia or Alzheimer's disease, although an indication of excess dementia risk was observed in a subgroup of physically inactive individuals who developed cardiometabolic disease. 2 key findings →

Design: meta-analysis Participants: 404 Evidence: high

Association of Lifestyle and Genetic Risk With Incidence of Dementia

✓ Peer-reviewed alzhub usefulness score 78 out of 100. JAMA 2019-08-01

Among older adults without cognitive impairment or dementia, both an unfavorable lifestyle and high genetic risk were significantly associated with higher dementia risk. 5 key findings →

Design: cohort study Participants: 383 Evidence: moderate

Association Between Age at Diabetes Onset and Subsequent Risk of Dementia

✓ Peer-reviewed alzhub usefulness score 77 out of 100. JAMA 2021-04-01

Among 10 095 participants (67.3% men; aged 35-55 years in 1985-1988), a total of 1710 cases of diabetes and 639 cases of dementia were recorded over a median follow-up of 31.7 years. 3 key findings →

Design: cohort study Participants: 95 Evidence: moderate

The overall weighted PAF for potentially modifiable risk factors for dementia was 39·5% (95% CI 37·5-41·6) in China (n=2162 participants), 41·2% (39·1-43·4) in India (n=2004), and 55·8% (54·9-56·7) in our Latin American sample (n=12 865). 2 key findings →

Design: meta-analysis Participants: 2,162 Evidence: high

Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) is a fatal neurodegenerative disorder with only a limited number of risk loci identified. 3 key findings →

Design: meta-analysis Participants: 985 Evidence: high

Where appropriate, we undertook subgroup analysis by modality (individual versus group), number of sessions and frequency, setting (community versus care home), type of control condition and dementia severity. 5 key findings →

Design: systematic review Participants: 37 Evidence: high

During 1 110 831 person-years at risk, we recorded 245 573 hospitalisations in the Finnish cohorts; the corresponding numbers in the UK study were 60 946 hospitalisations in 186 572 person-years. 4 key findings →

Design: cohort study Participants: 9,838 Evidence: moderate

The association between BMI and dementia is likely to be attributable to two different processes: a harmful effect of higher BMI, which is observable in long follow-up, and a reverse-causation effect that makes a higher BMI to appear protective when the follow-up is short. 1 key finding →

Design: cohort study Participants: 6,894 Evidence: moderate

Midlife and late-life risk factors contributed to 22.7% and 16.5% of total dementia cases, respectively. 5 key findings →

Design: meta-analysis Participants: 37,931 Evidence: high

Adherence to the Life Simple 7 ideal cardiovascular health recommendations in midlife was associated with a lower risk of dementia later in life. 4 key findings →

Design: cohort study Participants: 7,899 Evidence: moderate

The number of years of formal education completed by individuals is positively correlated with their cognitive function throughout adulthood and predicts lower risk of dementia late in life. 4 key findings →

Design: meta-analysis Evidence: high

High and increasing blood pressure from early adulthood into midlife seems to be associated with increased WMHV and smaller brain volumes at 69-71 years of age. 5 key findings →

Design: longitudinal study Participants: 5,362 Evidence: moderate

Being married is associated with reduced risk of dementia than widowed and lifelong single people, who are also underdiagnosed in routine clinical practice. 5 key findings →

Design: systematic review Participants: 15 Evidence: high

Socioeconomic differences in dementia risk can be partly explained by differences in modifiable health conditions and lifestyle factors. 5 key findings →

Design: longitudinal study Participants: 6,346 Evidence: moderate

Existing studies have included a narrow range of infectious diseases, relied on short follow-up periods, and provided little evidence for whether the increased risk is limited to specific dementia subtypes or attributable to specific microbes rather than infection burden. 5 key findings →

Design: cohort study Participants: 490 Evidence: moderate

The potential determinants of cognitive decline identified in this study, in particular modifiable risk factors, should be tested in the context of randomised controlled trials. 2 key findings →

Design: longitudinal study Participants: 626 Evidence: high

The overall unadjusted pooled odds ratio for the progression of MCI to dementia in people with diabetes/MetS was 1.67 (95% CI 1.27-2.19); the pooled odds ratio for progression in diabetes + MCI was 1.53 (95% CI 1.20-1.97) and in people with MetS + MCI was 2.95 (95% CI 1.23-7.05). 4 key findings →

Design: meta-analysis Participants: 15 Evidence: high

Of 23 558 people without pre-existing dementia, 4135 (17·6%) had an admission with delirium. 5 key findings →

Design: cohort Participants: 23,558 Evidence: moderate

↑ Change the filters

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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.

1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →

Newest studies, as a dated timeline →    Atom feed