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.

Immunotherapeutics targeting amyloid-β (Aβ) have had mixed results in clinical trials. 3 key findings →

Participants: 5,554 Evidence: high

The efficacy and safety of anti-amyloid mAbs in AD may differ based on patients' demographic and genetic factors. 4 key findings →

Design: systematic review Participants: 5,633 Evidence: high

A total of 210 participants were enrolled and 82% completed 26 weeks of treatment. 5 key findings →

Design: clinical trial Participants: 210 Evidence: high

No significant difference in ADAS-Cog13, CDR Sum of Boxes (CDR-SOB), or FAQ scores were found between treatment groups at 3 and 6 months. 5 key findings →

Evidence: high

Between Dec 8, 2009, and Dec 23, 2011, we randomly allocated 278 patients to treatment: 133 to placebo and 145 to idalopirdine. 132 patients in the placebo group and 140 in the experimental group were included in the final analysis. 5 key findings →

Design: clinical trial Participants: 278 Evidence: high

Among 14 placebo-controlled trials of elderly patients with dementia reporting a total global outcome score that includes symptoms such as psychosis, mood alterations, and aggression, small but statistically significant effects sizes ranging from 0.12 and 0.20 were observed for aripiprazole, olanzapine, and risperidone. 5 key findings →

Design: systematic review Participants: 1,000 Evidence: high

The risk-benefit profile of anti-Aβ monoclonal antibodies (mAbs) in Alzheimer's disease (AD) remains unclear, especially concerning their safety and overall effects on AD progression and cognitive function. 4 key findings →

Design: meta-analysis Participants: 14,980 Evidence: high

In participants with prodromal to mild AD in this randomized clinical trial, semorinemab did not slow clinical AD progression compared with placebo throughout the 73-week study period but did demonstrate an acceptable and well-tolerated safety profile. 3 key findings →

Design: clinical trial Participants: 422 Evidence: high

ARIA was detected more often on MRI scans when every scan was reviewed by trained neuroradiologists and results adjudicated. 4 key findings →

Participants: 242 Evidence: high

Three donepezil, two galantamine, one rivastigmine, and two memantine trials, comprising 3093 patients on the study drugs and 2090 patients on placebo, met the selection criteria. 2 key findings →

Design: systematic review Participants: 3,093 Evidence: high

We aimed to assess whether continued treatment with antipsychotics in people with AD is associated with an increased risk of mortality. 5 key findings →

Participants: 165 Evidence: high

Group 3 showed less decrease in the SIB score at 12 and 24 weeks compared with group 1 (P < 0.05). 5 key findings →

Design: clinical trial Participants: 31 Evidence: high

No clinically important adverse events were associated with treatment. 2 key findings →

Design: clinical trial Participants: 432 Evidence: high

These results show that in addition to APOE ε4 allele count, severity of Aβ neuropathology and comorbid cerebrovascular pathology may be relevant for clinicians prescribing anti-Aβ monoclonal antibodies for early AD and developing individualized safety monitoring plans. 2 key findings →

Design: clinical trial Participants: 985 Evidence: high

Cumulative use of strong anticholinergics and incident dementia: a prospective cohort study

✓ Peer-reviewed alzhub usefulness score 77 out of 100. JAMA internal medicine 2015-03-01

The most common anticholinergic classes used were tricyclic antidepressants, first-generation antihistamines, and bladder antimuscarinics. 4 key findings →

Design: cohort study Participants: 3,434 Evidence: moderate

No significant difference was seen in cognitive and functional decline between early and delayed treatment groups. 4 key findings →

Design: clinical trial Participants: 85 Evidence: high

SC gantenerumab at doses of up to 1,200 mg Q4W were well tolerated in participants with mild AD dementia. 2 key findings →

Design: open-label trial Participants: 225 Evidence: low

Antipsychotic use compared with non-use in adults with dementia was associated with increased risks of stroke, venous thromboembolism, myocardial infarction, heart failure, fracture, pneumonia, and acute kidney injury, but not ventricular arrhythmia. 5 key findings →

Design: cohort Participants: 173,910 Evidence: moderate

Modified titration of donanemab reduces ARIA risk and maintains amyloid reduction

✓ Peer-reviewed alzhub usefulness score 76 out of 100. Alzheimer's & Dementia 2025-04-02

Gradual up-titration of dose significantly reduced ARIA-E risk while demonstrating comparable pharmacokinetics/pharmacodynamics compared to standard dosing. 5 key findings →

Design: phase-3-trial Participants: 843 Evidence: moderate

The experimental paradigm was feasible and acceptable. 3 key findings →

Design: randomized controlled trial Participants: 95 Evidence: high

Our analysis found that lecanemab showed significant positive statistical efficacy with respect to cognition, function, and behavior in patients with early AD though the actual clinical significance is yet to be established. 2 key findings →

Design: systematic review Evidence: high

Use of lecanemab for the treatment of Alzheimer's disease: A systematic review

✓ Peer-reviewed alzhub usefulness score 76 out of 100. Brain and behavior 2024-06-01

According to studies, lecanemab lessens clinical deterioration and reduces brain amyloid-beta plaques (difference,.45; 95% confidence interval,.67 to.23; p < .001). 1 key finding →

Design: meta-analysis Evidence: high

The safety profile was similar for 20 μg treatment and placebo patients. 5 key findings →

Design: post-hoc analysis Evidence: high

From across this tag

10 of the 468 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.

↑ 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