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.
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In a medical emergency, call 911. More numbers, and what each line does, on the help page.

Find studies

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.

A non-synonymous genetic rare variant, rs75932628-T (p.R47H), in the TREM2 gene has recently been reported to be a strong genetic risk factor for Alzheimer's disease (AD). 4 key findings →

Design: meta-analysis Participants: 32,598 Evidence: high

Association of Alzheimer's disease GWAS loci with MRI markers of brain aging

✓ Peer-reviewed alzhub usefulness score 69 out of 100. Neurobiology of aging 2015-01-06

Whether novel risk variants of Alzheimer's disease (AD) identified through genome-wide association studies also influence magnetic resonance imaging-based intermediate phenotypes of AD in the general population is unclear. 4 key findings →

Design: meta-analysis Participants: 8,175 Evidence: high

Efficacy of PPAR-γ agonist pioglitazone in mild Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 69 out of 100. Neurobiology of aging 2009-11-17

To test the effects of the PPAR-γ agonist pioglitazone on cognition, regional cerebral blood flow (rCBF), and plasma levels of Aβ40 and Aβ42, we conducted a 6-month, randomized, open-controlled trial in patients with mild Alzheimer disease (AD) accompanied with type II diabetes mellitus. 2 key findings →

Participants: 21 Evidence: high

Cardiovascular risk and memory in non-demented elderly women

✓ Peer-reviewed alzhub usefulness score 69 out of 100. Neurobiology of aging 2008-09-21

These findings suggest that subtle elevation of CHD risk may negatively affect memory functioning even in otherwise healthy, non-demented older women without a history of heart disease. 3 key findings →

Participants: 375 Evidence: high

Enlarged perivascular spaces and plasma Aβ42/Aβ40 ratio in older adults without dementia

✓ Peer-reviewed alzhub usefulness score 68 out of 100. Neurobiology of aging 2023-04-14

Dilation of perivascular spaces (PVS) in the brain may indicate poor fluid drainage due to the accumulation of perivascular cell debris, waste, and proteins, including amyloid-beta (Aβ). 2 key findings →

Design: longitudinal study Participants: 56 Evidence: moderate

Sex and age differences in atrophic rates: an ADNI study with n=1368 MRI scans

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Neurobiology of aging 2010-08-01

We set out to determine factors that influence the rate of brain atrophy in 1-year longitudinal magnetic resonance imaging (MRI) data. 1 key finding →

Design: longitudinal study Participants: 363 Evidence: moderate

Effects of ω-3 fatty acids on cognitive performance: a meta-analysis

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Neurobiology of aging 2012-02-03

Higher intake of omega-3 fatty acids (n-3 FAs) is associated with a reduced risk of Alzheimer's disease (AD) and milder forms of cognitive impairment (e.g. cognitive impairment no dementia [CIND]); however, findings from interventional trials are inconsistent. 4 key findings →

Design: meta-analysis Participants: 934 Evidence: high

Homozygous mutations in exon 2 of TREM2, a gene involved in Nasu-Hakola disease, can cause frontotemporal dementia (FTD). 4 key findings →

Design: meta-analysis Evidence: high

There is evidence from a population-based study of an inverse relationship between monounsaturated fatty acids (MUFA) energy intake and age-related cognitive decline (ARCD), while high polyunsaturated fatty acids (PUFA) intake was positively associated with cognitive impairment in elderly subjects. 2 key findings →

Design: longitudinal study Participants: 704 Evidence: high

Identifying which neuropsychological measures detect early cognitive changes associated with Alzheimer disease (AD), brain pathology would be helpful clinically for the diagnosis of early AD and for the design of clinical trials. 3 key findings →

Design: longitudinal study Participants: 233 Evidence: moderate

Recent studies have found an association between a variant in triggering receptor expressed on myeloid cells 2 (TREM2) (rs75932628-T) and both Alzheimer's disease (AD) and cognitive function in individuals aged 80-100 years. 2 key findings →

Design: longitudinal study Participants: 1,148 Evidence: moderate

Longitudinal MRI findings from the vitamin E and donepezil treatment study for MCI

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Neurobiology of aging 2007-04-23

The vitamin E and donepezil trial for the treatment of amnestic mild cognitive impairment (MCI) was conducted at 69 centers in North America; 24 centers participated in an MRI sub study. 2 key findings →

Participants: 131 Evidence: low

Midlife hypertension is associated with later development of cognitive impairment, vascular dementia (VsD), and possibly Alzheimer's disease (AD). 5 key findings →

Design: longitudinal study Evidence: moderate

White matter hyperintensities (WMHs) are commonly assumed to represent non-specific cerebrovascular disease comorbid to neurodegenerative processes, rather than playing a synergistic role. 4 key findings →

Design: longitudinal study Participants: 571 Evidence: moderate

Aerobic glycolysis and tau deposition in preclinical Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Neurobiology of aging 2018-03-20

Research of the human brain metabolism in vivo has largely focused on total glucose use (via fluorodeoxyglucose positron emission tomography) and, until recently, did not examine the use of glucose outside oxidative phosphorylation, which is known as aerobic glycolysis (AG). 2 key findings →

Design: longitudinal study Participants: 42 Evidence: moderate

Olfactory identification deficits and MCI in a multi-ethnic elderly community sample

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Neurobiology of aging 2008-10-28

Odor identification deficits occur in Alzheimer's disease (AD) and mild cognitive impairment (MCI), and predict clinical conversion from MCI to AD. 4 key findings →

Design: longitudinal study Participants: 571 Evidence: moderate

Brain tissue volumes in relation to cognitive function and risk of dementia

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Neurobiology of aging 2008-05-23

We investigated in a population-based cohort study the association of global and lobar brain tissue volumes with specific cognitive domains and risk of dementia. 3 key findings →

Design: cohort study Participants: 490 Evidence: moderate

Hippocampal formation glucose metabolism and volume losses in MCI and AD

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Neurobiology of aging 2001-07-01

We used MRI volume sampling with coregistered and atrophy corrected FDG-PET scans to test three hypotheses: 1) hippocampal formation measures are superior to temporal neocortical measures in the discrimination of normal (NL) and mild cognitive impairment (MCI); 2) neocortical measures are most useful in the separation of Alzheimer disease (AD) from NL or MCI; 3) measures of PET glucose metabolism (MRglu) have greater diagnostic sensitivity than MRI volume. 2 key findings →

Design: cross-sectional Evidence: low

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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 27,380 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