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.

Regression analysis indicated that APOE ε4 non-carriers showed significantly greater improvement in MMN amplitude (β = ‒0.449, p = 0.027). 3 key findings →

Design: randomized controlled trial Participants: 21 Evidence: high

Among 2889 patients with delirium (mean age 85 years; 54.7% female), 59.8% were triaged at SETS 1–2 (high priority) and 40.2% at SETS 3–4 (low priority). 5 key findings →

Design: cohort study Participants: 2,889 Evidence: moderate

Among 118,174 beneficiaries who received an AWV, 27.62% initiated ACP within 4 years compared with 17.46% of nonrecipients (HR, 1.86; 95% CI, 1.84-1.89). 5 key findings →

Design: cohort study Participants: 959,405 Evidence: moderate

Non-modifiable (age, apolipoprotein E (APOE) ɛ4 genotype and sex) and modifiable risk factors (co-morbidities at baseline, such as hypertension and cardiovascular disease, BMI, and sleep duration) were analyzed with mixed-effects models, adjusted for age and sex, to predict longitudinal measurements of WMH, Aβ and tau. 5 key findings →

Design: longitudinal study Participants: 494 Evidence: moderate

Traumatic brain injury (TBI), a major cause of persistent cognitive impairment (CI), increases the long-term risk of developing dementia, including Alzheimer's disease (AD). 3 key findings →

Design: longitudinal study Participants: 29 Evidence: moderate

This first evaluation of 18 F-MK6240 in DS demonstrates its suitability as a sensitive biomarker for Alzheimer's disease tau pathology. 2 key findings →

Evidence: moderate

Two components were identified. Proinflammatory Component 2 was elevated in AD/MCI and in Black/African American participants, and strongly associated with poorer cognition (independently of neurofilament light [NfL], phosphorylated tau 217 [p-tau217], and glial fibrillary acidic protein [GFAP]). 3 key findings →

Evidence: moderate

Among nursing home residents with dementia, discontinuing long-term antipsychotic medication use was associated with lower risks of hospitalization, pneumonia, and urinary tract infections, suggesting clinical benefits in this population. 4 key findings →

Design: cohort Participants: 4,222 Evidence: moderate

Increasing oily fish intake has been proposed as a strategy for Alzheimer's disease (AD) prevention, but evidence for long-term benefit remains limited. 2 key findings →

Design: cohort Participants: 2,012 Evidence: null result

Plasma Alzheimer Biomarkers and Diagnostic Decision-Making in Memory Clinics

✓ Peer-reviewed alzhub usefulness score 52 out of 100. JAMA Network Open 2026-08-03

Among 356 patients (79%) with AD as the primary suspected etiology, assessment of BBM classified 149 patients (42%) as high, 101 patients (28%) as intermediate, and 106 patients (30%) as low probability of AD. 5 key findings →

Design: cohort Participants: 450 Evidence: moderate

The results of this study indicate an AD-specific peripheral complement signature associated with disease development, highlighting complement factors as critical immune mediators that link aging and AD. 2 key findings →

Design: cohort Participants: 558 Evidence: moderate

Bacopa consumption is known to enhance cognitive performance in healthy individuals and is associated with alterations in pathways related to branched-chain and aromatic amino acid biosynthesis. 3 key findings →

Participants: 76 Evidence: high

Orexin, Sleep, and Cognition in Alzheimer Disease: Non-REM Oscillatory Activity and Neural Resilience

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neurology 2026-07-14

Sleep spindles (SPs) and slow oscillations (SOs) are linked to cognition and neurodegeneration; however, their relationship with CSF orexin concentrations in symptomatic AD has not been characterized. 4 key findings →

Design: cohort study Evidence: moderate

Plasma Phosphorylated Tau 217 in Participants at Risk for Chronic Traumatic Encephalopathy

✓ Peer-reviewed alzhub usefulness score 52 out of 100. JAMA network open 2026-07-01

In vivo biomarkers for detecting neuropathologies from repetitive head impacts (RHI), including chronic traumatic encephalopathy (CTE), are needed. 4 key findings →

Design: case-control study Participants: 231 Evidence: moderate

This study investigated whether longitudinal changes in CSF AD biomarkers were associated with 18 F-MK6240 tau PET measures in early Braak stage subregions. 4 key findings →

Design: cross-sectional Participants: 78 Evidence: moderate

Overall, both algorithms demonstrated comparable performance in MA and FFS populations, with high specificity (>97.9%) and negative predictive value [NPV] (>92.9%). 5 key findings →

Participants: 5,018 Evidence: low

Of 57 participants (mean age ± SD = 66.6 ± 7.2 years; female = 52.6%), 38.6% (n = 22) had MCI-level functional impairment and 17.5% (n = 10) had dementia-level functional impairment. 5 key findings →

Design: longitudinal study Participants: 22 Evidence: moderate

This meta-analysis included cross-sectional amyloid PET scans acquired with 5 radiotracers from 49 227 participants across 53 studies from 15 countries (mean age, 71 years; 54% female, 62% cognitively impaired). 5 key findings →

Design: meta-analysis Participants: 48 Evidence: high

With the advancement of anti-amyloid treatments for Alzheimer disease, accurate assays for amyloid-β (Aβ) pathology are essential. 1 key finding →

Design: cross-sectional Participants: 431 Evidence: moderate

Hearing aid use was associated with a modestly lower risk of probable dementia overall (Hazard Ratios, HR, 0.91), but the association was confined to participants reporting improvements in hearing (HR 0.86), with no apparent benefit among those reporting poor improvement in hearing (HR 0.98). 2 key findings →

Design: longitudinal study Participants: 61,089 Evidence: moderate

In both cohorts, CSF MTBR-tau243 was associated with tau-PET temporal meta-ROI burden (BioFINDER-2: β = 1.1, p = < 0.0001 and Knight-ADRC: β = 0.7, p = < 0.0001), and this association did not differ by sex (BioFINDER-2 β = 0.04, p = 0.6 and Knight-ADRC: β = 0.009, p = 0.9). 3 key findings →

Design: cross-sectional Participants: 446 Evidence: low

Our study included 467 caregivers. Most (92.5%) caregivers performed at least one health care interaction task. 5 key findings →

Design: cross-sectional Participants: 467 Evidence: low

One-third of adults with neurological conditions in China have low health literacy, with pronounced socioeconomic and geographic disparities. 4 key findings →

Design: cross-sectional Participants: 1,120 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