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.

Physical and cognitive exercise may prevent or delay dementia in later life but the neural mechanisms underlying these therapeutic benefits are largely unknown. 3 key findings →

Participants: 100 Evidence: low

Reduction in hippocampal and amygdala volume measured via structural magnetic resonance imaging is an early marker of Alzheimer's disease (AD). 4 key findings →

Design: case-control study Evidence: moderate

Neuropsychiatric symptoms (NPS) are common in dementia and in predementia syndromes such as mild cognitive impairment (MCI). 2 key findings →

Evidence: low

Use of potentially inappropriate medications in Australian nursing home residents with advanced dementia is common. 3 key findings →

Design: randomized controlled trial Participants: 65 Evidence: high

Diagnostic criteria for vascular cognitive disorders: a VASCOG statement

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Alzheimer disease and associated disorders 2014-07-01

The proposed criteria for VCD provide a coherent approach to the diagnosis of this diverse group of disorders, with a view to stimulating clinical and pathologic validation studies. 1 key finding →

Evidence: low

A total of 158 participants were included, with an average age of 75.2 years (SD 7.65). 60.8% (n=96) of patients had AD, and 39.2% (n=62) had LBD. 4 key findings →

Design: cohort study Participants: 96 Evidence: moderate

Making time for brain health: recognising temporal inequity in dementia risk reduction

✓ Peer-reviewed alzhub usefulness score 53 out of 100. The Lancet Healthy Longevity 2025-10-01

Time is an under-recognised social determinant of brain health, and is potentially as important as education or income for dementia risk. 5 key findings →

Design: longitudinal study Evidence: moderate

Research increasingly suggests that subjective cognitive decline (SCD) in older adults, in the absence of objective cognitive dysfunction or depression, may be a harbinger of non-normative cognitive decline and eventual progression to dementia. 3 key findings →

Evidence: low

This study included 3540 participants with RVC data and 489 with WMH data (median [IQR] age: 73.2 [71.4-76.3] and 72.5 [71.2-75.4] years; female: 52.9% and 47.6%) over a median follow-up of 7.4 [IQR 5.5-8.5] and 3.8 [IQR 2.9-5.3] years, respectively. 5 key findings →

Design: cross-sectional Participants: 3,540 Evidence: moderate

Vascular Cognitive Impairment and Dementia (VCID), the second most common form of dementia, is becoming increasingly prevalent worldwide. 5 key findings →

Evidence: low

Among 403 participants (mean age 56.4 ± 5.7 years, 62.5% female), the median number of dementia risk factors was 5.0; hyperlipidaemia (92.5%), low cognitive activity (72.5%), obesity (57.6%), and hypertension (52.7%) were the most prevalent. 5 key findings →

Design: cross-sectional Participants: 403 Evidence: low

Dream recall status was associated with blood p ‐tau217 levels, APOE ε4 carriage, and future cognitive decline among older individuals cognitively healthy at baseline. 5 key findings →

Design: longitudinal study Evidence: moderate

The item-bank included 180 symptoms, most of which focus group nurses (n = 17) identified as occurring in advanced dementia. 5 key findings →

Participants: 17 Evidence: moderate

Recent advancements in molecular biomarkers and therapeutic options for Alzheimer's disease have brought into focus the need for greater progress in the second most common cause of dementia, vascular cognitive impairment and dementia (VCID). 5 key findings →

Evidence: low

Cytoplasmic mislocalisation and nuclear depletion of TDP-43 are pathological hallmarks of amyotrophic lateral sclerosis (ALS), including mutations in the C9ORF72 gene that characterise the most common genetic form of ALS (C9ALS). 3 key findings →

Evidence: low

Blood biomarkers for Alzheimer disease across ethnoracial groups and healthcare settings: a systematic review and meta-analysis

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-05-18

Blood-based biomarkers could transform Alzheimer disease (AD) detection by enabling scalable, less invasive assessment of underlying pathology, yet their applicability across globally diverse populations remains uncertain. 4 key findings →

Design: meta-analysis Evidence: high

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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