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.

The temporal evolutions and relative orderings of Alzheimer disease biomarkers, including CSF amyloid-β42 (Aβ42), Aβ40, total tau (Tau) and phosphorylated tau181 (pTau181), standardized uptake value ratio (SUVR) from the molecular imaging of cerebral fibrillar amyloid-β with PET using the 11C-Pittsburgh Compound-B (PiB), MRI-based hippocampal volume and cortical thickness and cognition have been hypothesized but not yet fully tested with longitudinal data for all major biomarker modalities among cognitively normal individuals across the adult lifespan starting from 18 years. 4 key findings →

Design: longitudinal study Participants: 2,609 Evidence: moderate

The treatment of ischaemic stroke with neuroprotective drugs has been unsuccessful, and whether these compounds can be used to reduce disability after recurrent stroke is unknown. 4 key findings →

Participants: 20,332 Evidence: high

The aim of the reported trial was to investigate the safety and efficacy of memantine in mild to moderate vascular dementia (VaD). 4 key findings →

Design: randomized controlled trial Participants: 579 Evidence: high

Long-term Effects of Cholinesterase Inhibitors on Cognitive Decline and Mortality

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Neurology 2021-03-19

Patients with Alzheimer dementia from the Swedish Dementia Registry starting on ChEIs within 3 months of the dementia diagnosis were included and compared to nontreated patients with Alzheimer dementia. 4 key findings →

Participants: 11,652 Evidence: moderate

Although both overt hyper- and hypothyroidism are known to lead to cognitive impairment, data on the association between subclinical thyroid dysfunction and cognitive function are conflicting. 4 key findings →

Participants: 6,410 Evidence: low

There are 9.9 million new cases of dementia in the world every year. 4 key findings →

Design: randomized controlled trial Participants: 52 Evidence: high

The Montreal Cognitive Assessment (MoCA) is an increasingly used screening tool for cognitive impairment. 4 key findings →

Design: case-control study Participants: 710 Evidence: moderate

Effect of TTP488 in patients with mild to moderate Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 65 out of 100. BMC neurology 2014-01-15

A previous report describes decreased decline in ADAS-cog (delta = 3.1, p = 0.008 at 18 months, ANCOVA with multiple imputation), relative to placebo, following a 5 mg/day dose of TTP488. 4 key findings →

Design: clinical trial Participants: 399 Evidence: high

Lipid-lowering medications (LLMs) and especially statin drugs can delay cognitive decline and dementia onset in individuals with and without mild cognitive impairment (MCI) at baseline. 4 key findings →

Design: longitudinal study Evidence: high

Low cardiac index is associated with incident dementia and Alzheimer disease: the Framingham Heart Study

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Circulation 2015-02-19

Cross-sectional epidemiological and clinical research suggests that lower cardiac index is associated with abnormal brain aging, including smaller brain volumes, increased white matter hyperintensities, and worse cognitive performances. 4 key findings →

Design: cross-sectional Participants: 184 Evidence: moderate

Neurofilament light (NfL) is a marker of neuroaxonal injury, a prominent feature of Alzheimer's disease. 4 key findings →

Design: cross-sectional Participants: 1,149 Evidence: moderate

Predicting Alzheimer's disease progression using deep recurrent neural networks

✓ Peer-reviewed alzhub usefulness score 65 out of 100. NeuroImage 2020-08-04

Early identification of individuals at risk of developing Alzheimer's disease (AD) dementia is important for developing disease-modifying therapies. 4 key findings →

Design: cross-sectional Participants: 1,677 Evidence: moderate

Physical Frailty, Genetic Predisposition, and Incident Parkinson Disease

✓ Peer-reviewed alzhub usefulness score 65 out of 100. JAMA neurology 2023-05-01

Cross-sectional evidence implicates high prevalent frailty in patients with Parkinson disease (PD), whereas the longitudinal association remains unknown. 4 key findings →

Design: cohort study Participants: 101 Evidence: moderate

Hippocampal morphological change is one of the main hallmarks of Alzheimer's disease (AD). 4 key findings →

Design: longitudinal study Participants: 261 Evidence: moderate

A total of 16 084 European adults from 8 cohort studies (mean age range, 56.9±12.3-82.1±4.2 years) of the European Eye Epidemiology (E3) consortium. 4 key findings →

Design: meta-analysis Participants: 16 Evidence: high

Choroid plexus (ChP) is emerging as a key brain structure in the pathophysiology of neurodegenerative disorders. 4 key findings →

Design: longitudinal study Participants: 135 Evidence: moderate

Alzheimer's disease (AD) is the most common cause of dementia worldwide, but the molecular and cellular mechanisms underlying cognitive impairment remain poorly understood. 3 key findings →

Participants: 427 Evidence: low

Mid- and late-life diabetes in relation to the risk of dementia: a population-based twin study

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Diabetes 2008-10-24

We aimed to verify the association between diabetes and the risk of dementia, Alzheimer's disease, and vascular dementia in twins and to explore whether genetic and early-life environmental factors could contribute to this association. 4 key findings →

Design: case-control study Participants: 13,693 Evidence: moderate

Insulin resistance, brain atrophy, and cognitive performance in late middle-aged adults

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Diabetes care 2012-10-15

This longitudinal study examined whether insulin resistance among late middle-aged, cognitively healthy individuals was associated with 1) less gray matter in Alzheimer disease-sensitive brain regions and 2) worse cognitive performance. 4 key findings →

Design: longitudinal study Participants: 372 Evidence: moderate

The heterogeneous patterns and severity of conditions produce distinctive cumulative effects for each individual.5 Multimorbidity is associated with many adverse consequences, including death, disability, institutionalization, greater use of healthcare resources, poorer quality of life, and higher rates of adverse effects of treatment or interventions.1 Comprehensive strategies for healthcare delivery that are not disease specific, as well as interventions that target geriatric syndromes common in older adults with multimorbidity, show promise for this population,5-9 although the best approaches to decision-making and clinical management of older adults with multimorbidity remain unclear. 5 key findings →

Design: systematic review Evidence: high

The genetic component of early-onset Alzheimer disease (EOAD), accounting for ~10% of all Alzheimer's disease (AD) cases, is largely unexplained. 3 key findings →

Design: meta-analysis Participants: 19,668 Evidence: high

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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.

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