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 Ct group and Ct+ee group performed significantly better than the control group in behavioural tasks and had improved dendrite profiles of DG and basal tree of CA1 region of hippocampus. 4 key findings →

Evidence: low

The evidence for cognitive training in preventing cognitive decline in Alzheimer's disease is varied, with some studies indicating cognitive benefits but showing limited impact on functional outcomes or disease progression. 1 key finding →

Evidence: low

Alzheimer's Disease (AD) is a progressive neurodegenerative condition that gradually impairs cognitive abilities such as memory, attention, and problem-solving, leading to significant challenges in everyday functioning and a decline in quality of life. 1 key finding →

Evidence: low

Cognitive training shows potential in preventing cognitive decline in individuals at risk for Alzheimer's disease, especially as part of multimodal interventions, though current evidence varies in quality and clarity. 1 key finding →

Evidence: low

Cognitive training appears effective in improving cognitive functions and delaying cognitive decline in people at risk of Alzheimer's disease but requires more standardized research for conclusive evidence. 1 key finding →

Evidence: low

Self-applied single-channel mastoid ExG for fully automated detection of REM sleep behaviour disorder

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-20

Isolated REM sleep behaviour disorder (RBD) is the strongest prodromal marker of Parkinsons disease (PD) and dementia with Lewy bodies, yet diagnosis requires video-polysomnography with assisted montage and expert scoring and does not scale to screening or trial enrichment. 5 key findings →

Design: longitudinal study Participants: 378 Evidence: moderate

One night of closed-loop auditory stimulation during sleep enhances memory consolidation in patients with Alzheimer's Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-17

INTRODUCTIONSleep-dependent memory consolidation is impaired early in Alzheimers disease (AD). 2 key findings →

Participants: 37 Evidence: high

INTRODUCTIONMultimodal lifestyle interventions can delay or slow Alzheimers disease (AD) in at-risk older adults, and plasma pTau217, a blood-based biomarker, now enables scalable AD risk stratification. 3 key findings →

Evidence: moderate

Alcohol use disorder accelerates age-related cognitive decline

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-23

ObjectiveTo investigate whether a lifetime history of DSM-5 AUD and correlated indices of alcohol consumption are associated with accelerated age-related cognitive decline in middle-aged and older adults. 5 key findings →

Design: cross-sectional Participants: 1,421 Evidence: moderate

Over a median follow-up of 13 years, 5,304 participants developed dementia. 4 key findings →

Participants: 151,832 Evidence: low

PCSK9 and High-Fat Diet Synergistically Induce Neurovascular Dysfunction and Neuroinflammation

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2025-10-31

Cerebral small vessel disease (CSVD) is strongly linked to metabolic risk factors and represents a major cause of vascular cognitive impairment and dementia. 2 key findings →

Evidence: low

Although endoplasmic reticulum (ER) stress and maladaptive unfolded protein response (UPR) are increasingly implicated in Alzheimer’s disease (AD), the influence of vitamin D (VitD) on these mechanisms remains unclear. 1 key finding →

Evidence: low

Social isolation, loneliness, and blood-based AD/ADRD biomarkers in a nationally-representative study of middle-aged and older adults

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

Social isolation was associated with elevated blood-based biomarkers of neuronal injury, with variation by patterns of exposure over time. 5 key findings →

Participants: 3,862 Evidence: low

Factors Influencing the Implementation of Computerized Cognitive Training in Chinese Community-Dwelling Elderly: A Qualitative Study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-28

Four main themes were extracted: (1) Positive experiences, including perceived improvement in cognitive function and mood; (2) Facilitators and barriers to training participation, with facilitators comprising dementia care experience, higher educational attainment, and availability of free time, and barriers including unfamiliarity with computer operation, low awareness of cognitive training, and lengthy training sessions; (3) Training content preferences, reflecting a desire for both relaxed, engaging content and professional guidance; and (4) Practical dilemmas and suggestions, including difficulties in understanding task instructions and complex login procedures, with recommendations for detailed task descriptions and simplified procedures. 4 key findings →

Evidence: low

Night-to-night REM sleep variability: a relevant marker of early amyloid-β deposition

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2025-12-27

Shorter sleep duration and greater REM sleep variability may index early AD-related brain changes, warranting longitudinal studies to establish their prognostic significance. 2 key findings →

Design: longitudinal study Evidence: high

Progressive neurodegeneration of the locus coeruleus drives rapid eye movement sleep fragmentation

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

Sleep disturbances are common early features of neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). 5 key findings →

Design: longitudinal study Evidence: moderate

We built a computer model that reproduces the rhythms and, crucially, lets the measured timing between slow waves and spindles control how strongly memories are written into cortex. 5 key findings →

Evidence: low

From across this tag

9 of the 2,021 studies in this tag that have a study page, 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 9. The same 9 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.

1,037 records (3.4% of the library) are not peer-reviewed — 964 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    Where this research is being discussed: events