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.

Parkinson's disease (PD) is a complex syndrome for which there is no disease-modifying treatment on the market. 4 key findings →

Evidence: low

We developed a set of informant-based items describing performance of activities of daily living (ADL) by patients with Alzheimer's disease (AD) to identify which ADL are useful for assessment of patients in clinical trials. 4 key findings →

Participants: 45 Evidence: low

Cholesteryl ester transfer protein inhibition (CETP) has been shown to increase levels of high-density lipoprotein cholesterol (HDL-C) and reduce levels of low-density lipoprotein cholesterol (LDL-C). 4 key findings →

Design: clinical trial Evidence: low

Deep Brain Stimulation of Frontal Lobe Networks to Treat Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Journal of Alzheimer's disease : JAD 2018-01-01

The study objective was to evaluate the safety and efficacy of deep brain stimulation (DBS) at the ventral capsule/ventral striatum (VC/VS) region to specifically modulate frontal lobe behavioral and cognitive networks as a novel treatment approach for Alzheimer's disease (AD) patients. 4 key findings →

Evidence: high

In most of these nonacademic healthcare delivery systems, traditional randomized clinical trial designs to evaluate effectiveness are too rigid, too expensive, and take too long to achieve results. 5 key findings →

Participants: 75 Evidence: high

(cobalamin)-dependent pathways. Supplementation of B vitamins has been shown to effectively reduce plasma homocysteine levels. 2 key findings →

Evidence: low

The ACoE's overall cognitive assessments were significantly reliable (ICC [intraclass correlation coefficient]=0.89; P<.001). 5 key findings →

Participants: 35 Evidence: high

Development and Validation of a 18 F-Flortaucipir PET Visual Stratification Method

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Journal of Nuclear Medicine 2025-03-13

The median PPA and NPA were 83.4% and 88.9%, respectively, with lower bounds of 2-sided 95% CIs being 50% or greater for all readers. 4 key findings →

Design: clinical trial Participants: 140 Evidence: low

These findings suggest that HB-CCT via Neurotablet can effectively enhance specific cognitive abilities in PD, supporting the role of digital, home-based interventions as feasible strategies to mitigate cognitive decline. 4 key findings →

Design: post-hoc analysis Evidence: high

COG-T CHD is the first clinical trial to evaluate the efficacy of computer-based cognitive training in patients with coronary heart disease, filling an important gap in the treatment evidence for cognitive digital therapy. 2 key findings →

Design: randomized controlled trial Evidence: high

BPs of [(11)C](R)PK11195 and [(11)C]PIB were significantly higher in the parietotemporal regions of AD patients than in ten healthy controls. 3 key findings →

Design: clinical trial Evidence: low

Comparative effectiveness of behavioral interventions to mitigate the impacts of degeneration-based cognitive decline is not well understood. 4 key findings →

Evidence: high

Nonclinical data indicate that ACU193 can reduce the toxic effects of amyloid β oligomers. 3 key findings →

Design: clinical trial Evidence: high

Alzheimer's Disease: Key Insights from Two Decades of Clinical Trial Failures

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Journal of Alzheimer's disease : JAD 2022-01-01

Given the acknowledged lack of success in Alzheimer's disease (AD) drug development over the past two decades, the objective of this review was to derive key insights from the myriad failures to inform future drug development. 5 key findings →

Evidence: low

The amyloid hypothesis has been the dominant framework for Alzheimer's disease (AD) research, including the development of anti-AD therapies. 2 key findings →

Participants: 196 Evidence: low

Primary biomarker efficacy endpoints were not statistically significant in either dose group. 5 key findings →

Design: clinical trial Evidence: high

Tau neurofibrillary tangles are found in the brains of patients suffering from Alzheimer's disease and other tauopathies. 2 key findings →

Design: clinical trial Participants: 30 Evidence: low

Despite an ever-growing prevalence and increasing economic burden of Alzheimer's disease (AD) and Parkinson's disease (PD), recent advances in drug development have only resulted in minimally effective treatment. 1 key finding →

Design: clinical trial Evidence: low

From across this tag

10 of the 1,875 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.

1,034 records (3.7% 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