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.

Treatment of cognitive impairment after poststroke depression : a double-blind treatment trial

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Stroke 2000-07-01

Patients with poststroke major depression have a greater severity of cognitive impairment than nondepressed patients even when matched for size and location of stroke lesion. 4 key findings →

Participants: 33 Evidence: low

Huntington's disease (HD) is a fatal inherited neurodegenerative disorder characterized by personality changes, motor impairment, and subcortical dementia. 4 key findings →

Evidence: low

Genetic mutations in the tau gene on chromosome 17 are known to cause frontotemporal dementias. 2 key findings →

Evidence: low

To provide a detailed description of the recommendations of a Palliative Care Service (PCS) and to describe the impact of these recommendations on the care of terminally ill patients in an academic medical center, we describe data from all consecutive patients referred by their attending physicians to the PCS of an academic teaching hospital over a 15-month period. 1 key finding →

Participants: 325 Evidence: low

Participants chose to forego more invasive or long-term treatments at a higher rate than less invasive, short-term treatments in all health states. 1 key finding →

Participants: 342 Evidence: low

Progressive cerebrovascular atherosclerosis and consecutive stroke are among the most common causes of dementia. 1 key finding →

Participants: 186 Evidence: low

Galantamine: a review of its use in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Drugs 2000-11-01

Recipients of galantamine 16 or 24 mg/day achieved significant improvements in cognitive and global symptoms relative to placebo recipients in large (n = 285 to 978 patients with mild to moderate AD) well-designed trials of 3 to 6 months' duration. 4 key findings →

Participants: 285 Evidence: low

Earlier studies have shown elevated levels of tau protein and decreased levels of amyloid beta42 in cerebrospinal fluid (CSF) from patients with Alzheimer's disease (AD). 3 key findings →

Participants: 17 Evidence: low

Potential cerebrospinal fluid (CSF) markers for Alzheimer's disease (AD) include tau protein, the 42 amino-acid form of amyloid beta (amyloid beta(1-42)) and apolipoprotein E (apoE). 2 key findings →

Participants: 26 Evidence: low

Functional MRI has recently been used to examine activation associated with aging and dementia, yet little is known regarding the effect of cerebral atrophy on fMRI signal. 5 key findings →

Participants: 16 Evidence: low

Tau polymerization into the filaments that compose neurofibrillary tangles is seminal to the development of many neurodegenerative diseases. 2 key findings →

Evidence: low

Fatty acid differences, including docosahexaenoic acid (DHA; 22:6n-3) have been shown in the brains of Alzheimer's patients (AD) as compared with normal age-matched individuals. 5 key findings →

Evidence: low

We have previously shown that Alzheimer disease (AD) brain exhibits terminal deoxynucleotidyl transferase dUTP nick end-labeling (TUNEL) for DNA damage and morphological evidence for apoptosis. 5 key findings →

Evidence: low

Cholinesterase inhibitor therapy stabilizes symptoms of Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Alzheimer disease and associated disorders 2000-01-01

Cholinesterase inhibitors tested in clinical trials in Europe, the United States, and Japan include fewer than 10 drugs; however, most of these compounds have advanced to clinical phase III trials. 1 key finding →

Participants: 8,000 Evidence: low

Many neurodegenerative diseases are associated with the abnormal sequestration of disease-specific proteins in the brain, but the events that initiate this process remain unclear. 4 key findings →

Evidence: low

Dietary intake of fatty acids may be related to dementia and cognitive function through a number of plausible mechanisms, such as atherosclerosis and thrombosis, inflammation, via an effect on brain development and membrane functioning, or via accumulation of beta-amyloid. 4 key findings →

Participants: 476 Evidence: low

Deposition of beta-amyloid (A beta), a metabolite of approximately 4 kd of the amyloid precursor protein, is a critical pathological feature in Alzheimer disease. 5 key findings →

Evidence: low

Twelve cases of dementia were diagnosed among individuals with scores below cutoff point and one among subjects with high scores. 2 key findings →

Design: clinical trial Participants: 1,611 Evidence: low

Evidence is reviewed for a developmentally-emerging behavioral phenotype in individuals with Down syndrome that includes significant delay in nonverbal cognitive development accompanied by additional, specific deficits in speech, language production, and auditory short-term memory in infancy and childhood, but fewer adaptive behavior problems than individuals with other cognitive disabilities. 1 key finding →

Evidence: low

Are hereditary hemochromatosis mutations involved in Alzheimer disease?

✓ Peer-reviewed alzhub usefulness score 43 out of 100. American journal of medical genetics 2000-07-01

Mutations in the class I-like major histocompatibility complex gene called HFE are associated with hereditary hemochromatosis (HHC), a disorder of excessive iron uptake. 3 key findings →

Participants: 26 Evidence: low

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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