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.

Explainability methods applied to deep learning models for Alzheimer’s disease neuroimaging produce attribution maps that vary substantially across methods and architectures, yet no validated quantitative framework exists for determining which method most faithfully localises attribution signal within established AD neuroimaging biomarker anatomy at the individual subject level. 5 key findings →

Evidence: moderate

Understanding how a stable structural connectome supports flexible cognition, especially in aging, is a fundamental question in neuroscience. 5 key findings →

Evidence: low

The phenotypic measures “Slope” and “dMMSE/dt” consistently showed strong performance across a range of data distributions, while “Time-to-MMSE10” was particularly effective in cohorts with a higher proportion of individuals experiencing severe cognitive decline. 2 key findings →

Design: longitudinal study Participants: 500 Evidence: moderate

rTMS renews long-tract myelination to improve AD cognitive function predicted by baseline myelin and E-field

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-09-25

This study reveals a myelin-mediated mechanism of rTMS action in AD, demonstrating the potential of promoting myelination as a novel therapeutic strategy for alleviating AD-related cognitive impairment. 3 key findings →

Evidence: low

How Reliable and Explainable Are Machine Learning Models for Dementia Detection? A Leakage-Aware Evaluation

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-09-09

Reported dementia-classification performance depends on how the label is defined, which clinical information the model sees, and whether participants are separated between training and test data. 5 key findings →

Participants: 150 Evidence: moderate

MTHFR C677T homozygosity was independently associated with vascular dementia (OR 3.2; 95% CI 1.1–8.9; p=0.027) and showed clustering with cognitive impairment. 5 key findings →

Evidence: low

Cognitive Performance in Spouses of Individuals with Alzheimer’s Disease: A Controlled Cross-Sectional Study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-25

We compared global and domain-level cognitive performance in older adults without a prior dementia diagnosis based on whether their cohabiting spouse had Alzheimer’s disease. 1 key finding →

Design: cross-sectional Participants: 350 Evidence: low

Association of age with clinical progression across plasma p-tau217 levels

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-08-10

STRUCTURED ABSTRACT BACKGROUND Chronological age and plasma p⍰tau217 each predicts cognitive decline, but whether their prognostic associations interact is unclear. 4 key findings →

Design: longitudinal study Participants: 3,741 Evidence: moderate

HbA1c levels had warning value for cognitive impairment in non diabetes patients with WMH, and a nonlinear correlation exists between HbA1c and WMH-related cognitive impairment. 3 key findings →

Participants: 497 Evidence: low

A Biologically Constrained Continuous-Time Framework for Long-Horizon Cognition Forecasting in Alzheimer’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-08-10

Accurate long-term forecasting of cognitive trajectories across the Alzheimer’s disease continuum is essential for early intervention, personalized prognosis, patient stratification, and clinical trial enrichment. 1 key finding →

Design: longitudinal study Participants: 300 Evidence: moderate

Differential associations of insulin resistance with anterior hippocampal volume in mild cognitive impairment and Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-08-10

Insulin resistance is increasingly recognized as a metabolic factor associated with Alzheimer’s disease (AD); however, its relevance to hippocampal structural changes—a key pathological feature of AD—across disease stages is not fully understood. 4 key findings →

Evidence: low

Sex-divergent trajectories of hippocampal and cortical NMDA receptor density across the Alzheimer’s disease continuum

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-08-07

While loss of NMDA receptors (NMDARs) is associated with Alzheimer’s disease (AD) severity, the effect of sex or the relationship between regional NMDAR density and antemortem cognitive status across the AD spectrum has not been examined. 3 key findings →

Evidence: low

A study on the Mini-cog scale in the general screening of cognitive status among the elderly in Putian city

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-03

In dialect-dominant, educationally diverse elderly, Mini-cog provides superior diagnostic accuracy for MCI versus HKBC and MoCA, and comparable accuracy for dementia. 4 key findings →

Design: cross-sectional Participants: 450 Evidence: low

Irrespective of ERG modality, ADRD was consistently associated with retinal dysfunction marked by impaired synaptic transmission and delayed neural processing across retinal circuits. 3 key findings →

Design: meta-analysis Participants: 18 Evidence: high

News headlines from many nations, including the United States, Germany, Australia, and the United Kingdom, suggest that we are facing a loneliness epidemic (http://www.campaigntoendloneliness.org/loneliness-research, http://www.spiegel.de/international/germany/germany-faces-epidemic-of-lonely-and-isolated-seniors-a-876635.html, https://startsat60.com/health/new-survey-reveals-australias-loneliness-epidemic, http://www.huffingtonpost.com.au/tania-de-jong/loneliness-is-the-global-epidemic-of-our-times), leading to the important question of whether there is evidence to support such a claim and, if so, whether we are facing a public health crisis. 5 key findings →

Design: meta-analysis Participants: 300,000 Evidence: high

Randomisation: Allocated 1 : 1 : 1 through Trials Unit, independently of trial team. 5 key findings →

Design: randomized controlled trial Participants: 326 Evidence: high

For mild to moderately severe AD, the results of the study suggested that all three treatments were beneficial when assessed using cognitive outcome measures. 5 key findings →

Design: systematic review Evidence: high

Two hundred and sixty participants were randomised (173 intervention, 87 TAU). 5 key findings →

Evidence: high

The intention-to-treat analysis identified no differences in outcome between the intervention and control conditions on primary or secondary outcomes [self-reported quality of life in Alzheimer's disease: mean difference 0.07, standard error (SE) 0.65; F = 0.48; p = 0.53]. 5 key findings →

Design: randomized controlled trial Participants: 488 Evidence: high

The current study was undertaken to unveil the protective effects of Luteolin, a natural flavonoid, against amyloid-beta (Aβ 1 - 42 )-induced neuroinflammation, amyloidogenesis, and synaptic dysfunction in mice. 5 key findings →

Evidence: low

The FDA gave lecanemab (Leqembi) accelerated approval based on Phase 2 data showing it reduced amyloid plaque in the brain, ahead of full Phase 3 results. 3 key findings →

Design: regulatory decision Evidence: early

FDA Approves Treatment for Adults with Alzheimer's Disease (Kisunla / donanemab-azbt)

⚠ Regulatory decision — not a study alzhub usefulness score 15 out of 100. U.S. Food and Drug Administration 2024-07-02

The FDA approved donanemab (Kisunla) as a monthly IV infusion for people with early symptomatic Alzheimer's disease (mild cognitive impairment or mild dementia) with confirmed amyloid plaques. 3 key findings →

Design: regulatory decision Evidence: moderate

Leqembi Recommended for Treatment of Early Alzheimer's Disease (CHMP re-examination, reversing July 2024 refusal)

⚠ Regulatory decision — not a study alzhub usefulness score 15 out of 100. European Medicines Agency 2024-11-14

The EMA's human medicines committee (CHMP) initially refused to approve lecanemab in the EU in July 2024, judging that its modest effect on cognitive decline did not outweigh ARIA risk in the broad early-Alzheimer's population studied. 3 key findings →

Design: regulatory decision Evidence: moderate

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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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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