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

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.

Cerebral small vessel disease genomics and its implications across the lifespan

✓ Peer-reviewed alzhub usefulness score 70 out of 100. Nature communications 2020-12-08

White matter hyperintensities (WMH) are the most common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main known risk factor. 1 key finding →

Evidence: moderate

These data support the use of cNfL as a biomarker of neuroaxonal damage and indicate that age-specific and sex-specific (and in some cases disease-specific) reference values may be needed. 4 key findings →

Participants: 2,795 Evidence: moderate

Between April 30, 2020, and May 9, 2022, we randomly allocated 204 participants (109 [53%] women and 95 [47%] men) to the intervention group and 98 (60 [61%] women and 38 [39%] men) to the control group. 218 (72%) participants at 6 months and 178 (59%) at 12 months provided cost data. 2 key findings →

Design: RCT Participants: 302 Evidence: high

IER is as effective as CER with regard to weight loss, insulin sensitivity and other health biomarkers, and may be offered as an alternative equivalent to CER for weight loss and reducing disease risk. 1 key finding →

Evidence: high

APPLE-Tree is an accessible intervention associated with small improvements in cognition, although these results were not statistically significant. 1 key finding →

Design: RCT Participants: 746 Evidence: null result

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

TDP-43 loss and ALS-risk SNPs drive mis-splicing and depletion of UNC13A

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Nature 2022-02-23

Variants of UNC13A, a critical gene for synapse function, increase the risk of amyotrophic lateral sclerosis and frontotemporal dementia 1-3 , two related neurodegenerative diseases defined by mislocalization of the RNA-binding protein TDP-43 4,5 . 2 key findings →

Evidence: low

APPLE-Tree has a high probability of being cost-effective for a 1-point NTB gain, a difference previously associated with a three-fold reduction in 5-year dementia risk. 3 key findings →

Design: RCT Participants: 746 Evidence: moderate

A total of 346 of 374 (92.5%) intervention arm participants received some intervention (reach), and 305 of 374 (81.6%) attended ≥5 main sessions (predefined as adhering: dose). 5 key findings →

Design: randomized controlled trial Participants: 346 Evidence: high

One hundred sixteen participants consented and 93 (46 waitlist control, 47 intervention) were included in the analyses. 3 key findings →

Design: RCT Participants: 93 Evidence: null result

We used records of 2 784 138 patients for the calculation of cumulative incidence and of 3 872 451 patients for the calculation of period prevalence and median age at diagnosis of these conditions. 5 key findings →

Participants: 138 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

Thirty-four reviews were included, published between 2009 and 2023. 5 key findings →

Design: systematic review Evidence: high

Although mutations within the TREM2 gene have been robustly associated with Alzheimer's disease, it is not known whether alterations in the regulation of this gene are also involved in pathogenesis. 3 key findings →

Design: meta-analysis Evidence: high

Controversies and priorities in amyotrophic lateral sclerosis

✓ Peer-reviewed alzhub usefulness score 56 out of 100. The Lancet. Neurology 2013-03-01

Two decades after the discovery that 20% of familial amyotrophic lateral sclerosis (ALS) cases were linked to mutations in the superoxide dismutase-1 (SOD1) gene, a substantial proportion of the remainder of cases of familial ALS have now been traced to an expansion of the intronic hexanucleotide repeat sequence in C9orf72. 1 key finding →

Evidence: low

Amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) constitutes a devastating disease spectrum characterized by 43-kDa TAR DNA-binding protein (TDP-43) pathology. 4 key findings →

Evidence: low

In our dataset search, we identified 108 910 people with a record indicating dementia at any time. 5 key findings →

Design: cohort study Participants: 9,819 Evidence: moderate

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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