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 42 studies in Prevention and risk published 2019 · free to read (page 1 of 2) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

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

What “Prevention and risk” covers

Prevention and risk — What might lower the risk of dementia — and what happened when those things were properly tested.

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.

Of 2846 articles identified, 94 studies were eligible, with up to 14 529 participants for WMH, 16 012 participants for BI, 15 693 participants for CMB, and 4587 participants for PVS. 2 key findings →

Design: meta-analysis Participants: 529 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

With no effective treatments for cognitive decline or dementia, improving the evidence base for modifiable risk factors is a research priority. 1 key finding →

Design: meta-analysis Participants: 48,522 Evidence: high

There is moderate-to-strong support that PA benefits cognitive functioning during early and late periods of the life span and in certain populations characterized by cognitive deficits. 3 key findings →

Design: meta-analysis Evidence: high

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

Over a long period of observation, no evidence was found that a specific AHM drug class was more effective than others in lowering risk of dementia. 4 key findings →

Design: meta-analysis Participants: 31 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

More frequent social contact at age 60 years was associated with lower dementia risk (hazard ratio [HR] for each SD higher social contact frequency = 0.88 [95% CI 0.79, 0.98], p = 0.02); effect size of the association of social contact at 50 or 70 years with dementia was similar (0.92 [95% CI 0.83, 1.02], p = 0.13 and 0.91 [95% CI 0.78, 1.06], p = 0.23, respectively) but not statistically significant. 3 key findings →

Design: cohort Participants: 10,228 Evidence: moderate

Multimorbidity (hazard ratio [HR] 4·12 [95% CI 3·41-4·98]), frailty (HR 2·38 [95% CI 1·93-2·93]), and disability (HR 1·73 [95% CI 1·34-2·22]) were associated with increased risk of mortality; these associations were not modified by socioeconomic status. 2 key findings →

Design: cohort study Participants: 308 Evidence: moderate

The strength of evidence for an association between gait speed and cognition was demonstrated by the number and consistency of results, as well as quality of the studies. 5 key findings →

Design: meta-analysis Participants: 29,520 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

As there is currently no cure for dementia, there is an urgent need for preventive strategies. 5 key findings →

Design: case-control study Evidence: moderate

Burden of Cause-Specific Mortality Associated With PM2.5 Air Pollution in the United States

✓ Peer-reviewed alzhub usefulness score 66 out of 100. JAMA network open 2019-11-01

A cohort of 4 522 160 US veterans (4 243 462 [93.8%] male; median [interquartile range] age, 64.1 [55.7-75.5] years; 3 702 942 [82.0%] white, 667 550 [14.8%] black, and 145 593 [3.2%] other race) was followed up for a median (interquartile range) of 10.0 (6.8-10.2) years. 5 key findings →

Design: cohort study Evidence: moderate

Rationale and Design of the Hamburg City Health Study

✓ Peer-reviewed alzhub usefulness score 65 out of 100. European journal of epidemiology 2019-11-08

The Hamburg City Health Study (HCHS) is a large, prospective, long-term, population-based cohort study and a unique research platform and network to obtain substantial knowledge about several important risk and prognostic factors in major chronic diseases. 1 key finding →

Design: cohort study Participants: 45,000 Evidence: moderate

For the last 17 years, an increase of mortality for patients with hip fracture and a higher mortality rate in men than in women were observed. 5 key findings →

Design: cohort study Participants: 3,992 Evidence: moderate

The exact etiology of dementia is still unclear, but both genetic and lifestyle factors are thought to be key drivers of this complex disease. 1 key finding →

Participants: 6,352 Evidence: low

White matter hyperintensities (WMHs) are frequently seen on brain magnetic resonance imaging scans of older people. 1 key finding →

Evidence: low

An update on genetic frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Journal of neurology 2019-05-22

Grey matter changes on MRI and hypometabolism on FDG-PET are seen at least 10 years before symptom onset with white matter abnormalities seen earlier, but the pattern and exact timing of changes differ between different genetic groups. 5 key findings →

Evidence: low

The incidence of stroke and dementia are diverging across the world, rising for those in low- and middle-income countries and falling in those in high-income countries. 3 key findings →

Evidence: low

MBI may be an earlier marker of neurodegenerative disease than MCI, captured at the stage of subjective cognitive decline or before, raising the possibility that MBI represents a novel target for dementia clinical trials or prevention strategies. 3 key findings →

Participants: 9,931 Evidence: low

The deep-learning time-to-event model predicted individual subjects' progression to AD dementia with a concordance index of 0.762 on 439 Alzheimer's Disease Neuroimaging Initiative testing MCI subjects with follow-up duration from 6 to 78 months (quartiles: [24, 42, 54]) and a concordance index of 0.781 on 40 Australian Imaging Biomarkers and Lifestyle Study of Aging testing MCI subjects with follow-up duration from 18 to 54 months (quartiles: [18, 36, 54]). 2 key findings →

Participants: 2,146 Evidence: low

↑ 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.

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 27,380 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.

See the full, machine-readable breakdown of this library's coverage →

Newest studies, as a dated timeline →    Atom feed