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.

Rural practitioners' experiences in dementia diagnosis and treatment

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Aging & mental health 2004-09-01

When diagnosis of dementia occurs earlier in the disease process, more time is available for treatment aimed at maintaining patient function and delaying decline, and for family education about the disease and its management. 5 key findings →

Evidence: low

We examined the real-world utilization and persistence of rapid acting insulin (RAI) in elderly patients with type 2 diabetes who added RAI to their drug (OAD) regimen. 2 key findings →

Participants: 3,734 Evidence: low

Lecanemab use for early Alzheimer disease in Canada

✓ Peer-reviewed alzhub usefulness score 37 out of 100. Canadian Medical Association Journal 2026-06-28

Lecanemab is a humanized monoclonal antibody that binds soluble brain amyloid-β protein, promoting its removal and slowing the underlying process of Alzheimer disease. 1 This mechanism aligns with the amyloid hypothesis, a debated model of Alzheimer disease pathogenesis.1 Only patients with mild cognitive impairment (MCI) or mild dementia due to Alzheimer disease are eligible for lecanemab treatment. 1 key finding →

Evidence: low

Tau aggregation driven by microtubule-associated protein tau (MAPT) mutations is central to frontotemporal dementia pathology, yet no disease-modifying therapies effectively target mutant tau. 4 key findings →

Evidence: low

GRc exerted neuroprotective effects in VaD by targeting Stat3 and driving its dual-phosphorylation. 2 key findings →

Evidence: low

Alzheimer's Disease (AD) is the most common dementia, affecting mainly older adults, particularly over 65. 2 key findings →

Evidence: low

The amyloid hypothesis is the predominant model of Alzheimer's disease (AD) pathogenesis, suggesting that amyloid beta (Aβ) peptide is the primary driver of neurotoxicity and a cascade of pathological events in the central nervous system. 1 key finding →

Evidence: low

Lecanemab, an amyloid-targeting monoclonal antibody, was recently approved for early symptomatic Alzheimer's disease in South Korea. 5 key findings →

Participants: 112 Evidence: low

The advent of disease-modifying therapies for neurodegenerative diseases may result in a growing demand for nuclear neuroimaging procedures presenting opportunities but also challenges to the nuclear medicine community. 1 key finding →

Evidence: low

Deregulation of amyloid precursor protein (APP) processing with increased production of amyloid beta-peptide (Abeta) is considered to be a key pathogenic event in Alzheimer's disease (AD). 4 key findings →

Design: clinical trial Evidence: low

The authors of this mini-review list the key benefits (e.g., positive results of the reviewed randomized clinical trials studies for the improvement of cognitive decline in AD) and limitations (e.g., low awareness of benefits of TCM in Europe) of Chinese medicine therapy for the treatment of AD. 2 key findings →

Evidence: high

The cognitive deficits in Down syndrome (DS) are attributed to an excessive hippocampal inhibition, which obstructs neuronal plasticity and normal learning and memory, a view which is largely based on studies of Ts65Dn mice, the best characterized mouse model of DS. 1 key finding →

Evidence: low

The COVID-19 pandemic and the social unrest pervading U.S. cities in response to the killings of George Floyd and other Black citizens at the hands of police are historically significant. 2 key findings →

Evidence: low

Primary analysis calculated the impact of increasing the use of mirabegron from 4.5% to 5.3%, 7.1%, and 9.4% in years 1, 2, and 3, respectively, among oral pharmacological OAB treatments that included generic and branded antimuscarinics: oxybutynin, tolterodine, trospium, darifenacin, fesoterodine, and solifenacin. 5 key findings →

Evidence: moderate

Atypical antipsychotics are associated with incident diabetes in older adults without schizophrenia or bipolar disorder QUESTION Question: Is atypical antipsychotic use associated with incident diabetes or hyperlipidaemia in older people without schizophrenia or bipolar disorder? 1 key finding →

Participants: 75 Evidence: low

Extensive understanding of a drug’s real‐world target population can inform generalizability of clinical trial results and highlight unaddressed risk. 3 key findings →

Evidence: moderate

From across this tag

10 of the 3,106 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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