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.

We aimed to summarise current evidence on different antidiabetic drugs to delay cognitive impairment, including mild cognitive impairment, dementia, Alzheimer's disease (AD) and vascular dementia, among subjects with type 2 diabetes mellitus (T2DM). 4 key findings →

Design: meta-analysis Evidence: high

Dose-response relationship between computerized cognitive training and cognitive improvement

✓ Peer-reviewed alzhub usefulness score 71 out of 100. NPJ digital medicine 2024-08-15

Although computerized cognitive training (CCT) is an effective digital intervention for cognitive impairment, its dose-response relationship is understudied. 2 key findings →

Design: cohort study Participants: 8,709 Evidence: moderate

The mean age was 70.9 years (standard deviation, 5.9), 57.2% were women, 40.6% were illiterate, and 88.3% were farmers. 2 key findings →

Participants: 5,765 Evidence: high

Overall age-adjusted and sex-adjusted prevalence was estimated to be 6·0% (95% CI 5·8-6·3) for dementia, 3·9% (3·8-4·1) for Alzheimer's disease, 1·6% (1·5-1·7) for vascular dementia, and 0·5% (0·5-0·6) for other dementias. 2 key findings →

Design: cross-sectional Evidence: low

Neuropsychiatric symptoms (NPSs) are common in patients with Alzheimer's disease (AD) and are associated with accelerated cognitive impairment and earlier deaths. 2 key findings →

Evidence: low

A safe and effective medicine, huperzine Alpha remarkably improves the cognition, behavior, ADL,and mood of AD patients. 2 key findings →

Participants: 100 Evidence: low

Microglia-mediated neuroinflammation plays a crucial role in the pathogenesis of Parkinson's disease (PD). 4 key findings →

Evidence: low

Animal studies indicate that Dang Gui Shao Yao San (DGSYS) may enhance cognitive function in VaD models through mechanisms such as antioxidation and the enhancement of cerebral blood flow. 4 key findings →

Design: systematic review Evidence: high

Our results revealed disease severity-related alterations of the thalamo-default mode network and thalamocortical connectivity in AD and MCI patients. 4 key findings →

Participants: 35 Evidence: low

Bibliometric analysis is crucial in identifying research gaps and trends and guiding future studies to address unmet needs in understanding and modeling human physiology and pathology. 1 key finding →

Design: systematic review Evidence: low

Triggering receptor expressed on myeloid cells 2 (TREM2) is an immune receptor expressed on the surface of microglia, macrophages, dendritic cells, and osteoclasts. 4 key findings →

Evidence: low

Alzheimer's disease (AD) is a progressive neurodegenerative disorder, accompanied by memory loss and cognitive impairments, and there is no effective treatment for it at present. 3 key findings →

Evidence: low

Individuals with Down syndrome (DS) will inevitably develop Alzheimer disease (AD) neuropathology sometime after middle age, which may be attributable to genes triplicated in individuals with DS. 1 key finding →

Evidence: low

Neurofibrillary tangles (NFTs), composed of truncated and hyperphosphorylated tau, are a common feature of numerous aging-related neurodegenerative diseases, including Alzheimer's disease (AD). 2 key findings →

Evidence: low

Here, we observed significant compromise in macroautophagy/autophagy in the brains of mlkl knockout (KO) mice, as evidenced by the downregulation of BECN1/Beclin1 and ULK1 (unc-51 like autophagy activating kinase 1). 5 key findings →

Evidence: low

Recent studies indicate that the deposition of β-amyloid peptide (Aβ) is related to the pathogenesis of Alzheimer disease (AD); however, the underlying mechanism is still not clear. 4 key findings →

Evidence: low

Systematic Pan-Cancer Analysis Identifies TREM2 as an Immunological and Prognostic Biomarker

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Frontiers in immunology 2021-02-17

Triggering receptor expressed on myeloid cells-2 (TREM2) is a transmembrane receptor of the immunoglobulin superfamily and a crucial signaling hub for multiple pathological pathways that mediate immunity. 4 key findings →

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. 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