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.

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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.

Staging tau pathology with tau PET in Alzheimer's disease: a longitudinal study

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Translational psychiatry 2021-09-18

A biological research framework to define Alzheimer' disease with dichotomized biomarker measurement was proposed by National Institute on Aging-Alzheimer's Association (NIA-AA). 3 key findings →

Design: longitudinal study Evidence: moderate

Phosphorylation of tau protein at threonine 231 (using full-length tau, 441 amino acids, for the numbering scheme) (p-tau(231)) occurs specifically in postmortem brain tissue of patients with Alzheimer disease (AD) and can be sensitively detected in cerebrospinal fluid (CSF). 4 key findings →

Design: cross-sectional Evidence: low

We identified individuals with an incident diagnosis of PD (n=1276) and controls (n=500 406) in UK Biobank. 4 key findings →

Participants: 1,276 Evidence: moderate

The Dementia SomaSignal Test (dSST): A plasma proteomic predictor of 20‐year dementia risk

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Alzheimer s & Dementia 2025-02-01

In addition to outperforming existing plasma biomarkers, the dSST predicted mid-life dementia risk over a 20-year follow-up across two independent cohorts with different ethnic backgrounds (areas under the curve [AUCs]: dSST 0.68-0.70, dSST+age 0.75-0.81). 4 key findings →

Design: longitudinal study Participants: 11,277 Evidence: moderate

DLB and PDD boundary issues: diagnosis, treatment, molecular pathology, and biomarkers

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neurology 2007-03-01

For more than a decade, researchers have refined criteria for the diagnosis of dementia with Lewy bodies (DLB) and at the same time have recognized that cognitive impairment and dementia occur commonly in patients with Parkinson disease (PD). 1 key finding →

Evidence: low

We examined longitudinal associations between the apolipoprotein E ε4 allele (ApoE4(+) status) and several cognitive outcomes and tested effect modification by sex. 3 key findings →

Design: longitudinal study Participants: 113 Evidence: moderate

In these older adults, associations of risk factors with a given cause of death were related to specific deficits in that same organ system. 2 key findings →

Design: cohort study Participants: 5,888 Evidence: moderate

ApoE Cascade Hypothesis in the pathogenesis of Alzheimer's disease and related dementias

✓ Peer-reviewed alzhub usefulness score 58 out of 100. Neuron 2022-03-16

The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD). 5 key findings →

Evidence: low

Dementia diagnosis increasingly relies on blood-based biomarkers, yet their performance in diverse populations remains insufficiently characterized. 1 key finding →

Design: cross-sectional Participants: 605 Evidence: moderate

The protease inhibitor alpha 1-antichymotrypsin and the lipid transport protein apolipoprotein E (apoE) are intimately associated with the 42-amino-acid beta-peptide (A beta) in the filamentous amyloid deposits of Alzheimer's disease. 2 key findings →

Evidence: low

APOE epsilon4 genotype and longitudinal changes in cerebral blood flow in normal aging

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Archives of neurology 2010-01-01

Our findings suggest that APOE epsilon4-mediated risk for Alzheimer disease is associated with widespread decline in rCBF over time that precedes the onset of dementia. 3 key findings →

Design: longitudinal study Evidence: moderate

Association of olfactory dysfunction with risk for future Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Annals of neurology 2008-02-01

Although olfactory dysfunction is commonly associated with Parkinson's disease (PD), it is not known whether such dysfunction can predate the onset of clinical PD in a community-based population. 2 key findings →

Evidence: moderate

Our results show that TREM2 is responsible for an unexpectedly high number of dementia cases in our cohort, suggesting that this gene should be taken into account when mutations in other dementia genes are excluded. 4 key findings →

Evidence: moderate

In older adults, variable agreement between in vivo imaging and CERAD NP score was observed. 3 key findings →

Design: longitudinal study Evidence: moderate

Caregiving burden, stress, and health effects among family caregivers of adult cancer patients

✓ Peer-reviewed alzhub usefulness score 57 out of 100. JAMA 2012-01-01

Unlike professional caregivers such as physicians and nurses, informal caregivers, typically family members or friends, provide care to individuals with a variety of conditions including advanced age, dementia, and cancer. 1 key finding →

Evidence: low

Survival after dementia diagnosis differs by race/ethnicity, with shortest survival among whites and longest among Asian Americans. 3 key findings →

Participants: 23,032 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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    Where this research is being discussed: events