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.

Women living in areas with higher walkability showed slower rates of decline in immediate (estimate=0.019, SE=0.009) and delayed recall (estimate=0.018, SE=0.008) (Figure 1). 5 key findings →

Design: longitudinal study Evidence: moderate

Role of PCPs in diagnosing dementia in traditional Medicare and Medicare Advantage

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Alzheimer s & Dementia 2025-10-01

Among a matched sample of 15,410,030 beneficiaries, accounting for both provider and patient characteristics, the incident dementia diagnosis rate was 0.11 percentage points lower for MA beneficiaries compared to TM beneficiaries attributed to the same PCP. 5 key findings →

Evidence: moderate

The nationwide combined weighted PAF for the eight CMDs was 37% overall, with hypertension (9.6%), ischemic heart disease (6.7%), and chronic heart failure (5.7%) associated with the greatest attributable fractions of dementia cases. 5 key findings →

Evidence: low

Participants' age ranged from 45 to 87, 53% were women, and 26% were diagnosed with dementia (39% AD, 18% Lewy Body and 17% Frontotemporal Dementia; Table 1). 5 key findings →

Design: cross-sectional Participants: 255 Evidence: moderate

A total of 260,200 older adults were screened for delirium (median [IQR] age in years: 78.0 [74.0-84.0]; female: 143,402 [55.1%]; non-Hispanic Black: 40,737 [15.8%]; Hispanic: 30,760 [11.9%]; median [IQR] Area Deprivation Index: 4.0 [2.0-6.0]; median [IQR] Charlson Comorbidity Index: 10.0 [8.0-13.0]). 5 key findings →

Participants: 260,200 Evidence: low

Participants with impaired hearing (n = 179) were older (73.9 vs. 71.4 years, p <0.001), often male (61.5% vs. 36.5%, p <0.001), and had lower cognitive scores than normal-hearing individuals (n = 241). 5 key findings →

Design: cross-sectional Participants: 179 Evidence: low

Living in more deprived neighborhoods was associated with an accelerated disease course in bvFTD, highlighting an important socioeconomic disparity in disease prognosis. 3 key findings →

Design: longitudinal study Participants: 161 Evidence: moderate

Dream recall status was associated with blood p ‐tau217 levels, APOE ε4 carriage, and future cognitive decline among older individuals cognitively healthy at baseline. 5 key findings →

Design: longitudinal study Evidence: moderate

Role of apolipoprotein E (ApoE) ε4 in cognitive impairment after a stroke: a prospective cohort study

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Aging 2025-05-08

Although apolipoprotein E (ApoE) ε4 is a well-established risk factor for Alzheimer disease, its role in the development of post-stroke cognitive impairment (PSCI) remains uncertain. 4 key findings →

Design: cohort study Evidence: moderate

Sortilin (SORT1) is a lipoprotein receptor that shows genome-wide association with hypercholesterolaemia, explained by its ability to control hepatic output of lipoproteins. 5 key findings →

Evidence: low

Milestone Review: The History of Molecular Genetics Analysis of Alzheimer's Disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Journal of Neurochemistry 2025-07-01

Alzheimer research has been driven by genetic findings: from the 1990s until about 2005, by the identification of amyloid precursor protein (APP) and presenilin (PSEN) mutations, leading to the formulation of the amyloid hypothesis, and then from ~2007 by genome-wide studies which have led to the increasing appreciation of the importance of microglial insufficiency in the disease pathogenesis. 3 key findings →

Evidence: low

Analysis of the genotyping data revealed that the TMEM106B locus consists of four major haplotypes: HA/Ha (covering the coding region), and HB/Hb (covering the upstream regulatory region). 5 key findings →

Participants: 182 Evidence: low

Alzheimer’s disease (AD) is a heterogeneous neurodegenerative disorder in which tau neurofibrillary tangles are a pathological hallmark closely associated with cognitive dysfunction and neurodegeneration. 5 key findings →

Participants: 615 Evidence: low

No significant associations were found between retinal thickness and AD risk (RNFL: odds ratio [OR]IVW = 1.001, 95% confidence interval [CI] = 0.986-1.017, P = 0.883; GCIPL: ORIVW = 1.008, 95% CI = 0.997-1.019, P = 0.172). 5 key findings →

Design: longitudinal study Participants: 31,434 Evidence: moderate

Monoclonal antibodies for treatment Alzheimer`s disease

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Reports of Vinnytsia National Medical University 2025-12-01

Annotation. Alzheimer’s disease (AD) is the leading cause of dementia in older adults, characterized by the accumulation of pathological proteins – beta-amyloid (Aβ) and hyperphosphorylated tau protein – resulting in neurodegeneration and cognitive impairment. 3 key findings →

Design: systematic review Evidence: high

The aim of this literature review is to examine and contrast four dietary patterns to evaluate their influence on Alzheimer's prevention. 1 key finding →

Design: meta-analysis Evidence: high

Amyloid-targeting therapy has recently become widely available in the United States for the treatment of patients with symptomatic mild Alzheimer disease (AD). 1 key finding →

Design: longitudinal study Evidence: moderate

Overall PiB-PET uptake increased during the first two years (before ARIA-E) and decreased during the last two years (including ARIA-E episodes) (0.03±0.05 vs. -0.04±0.04 SUVR/year, p-value=0.01, Figure 2). 5 key findings →

Design: longitudinal study Evidence: moderate

Atherosclerosis is a progressive, multifactorial disease driven by the interplay of lipid dysregulation, chronic inflammation, oxidative stress, and maladaptive vascular remodeling. 5 key findings →

Evidence: low

Of the 477 participants (70.9% women, mean age = 63 years), 339 (71.1%) completed the survey immediately after the e-learning, and 241 (50.5%) completed the three-month follow-up survey. 5 key findings →

Participants: 477 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