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

Showing 1,776–1,800 of 3,858 studies published 2025 (page 72 of 155) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

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.

Rapamycin is not detectable in the CSF before or after treatment, but several Alzheimer's disease and inflammatory biomarkers increase after treatment. 4 key findings →

Design: clinical trial Evidence: low

As novel, anti-amyloid therapies have become more widely available, access to timely and accurate diagnosis has become integral to ensuring optimal treatment of patients with early-stage Alzheimer's disease (AD). 1 key finding →

Evidence: low

Alzheimer's disease (AD) is a complex and multifactorial neurodegenerative disorder, recognized as the most prevalent form of dementia. 5 key findings →

Evidence: low

Down syndrome is a condition caused by trisomy of chromosome 21 and is the most common genetic cause of intellectual disability. 4 key findings →

Participants: 118,539 Evidence: low

Cerebral amyloid angiopathy (CAA) is a heterogeneous small vessel disease that can occur independently or alongside Alzheimer disease (AD). 4 key findings →

Evidence: low

The underlying mechanisms of mild behavioral impairment (MBI), a marker for cognitive impairment and dementia, have remained unclear especially in a multiethnic Asian population. 4 key findings →

Participants: 305 Evidence: low

Alzheimer disease (AD)-modifying therapies are approved for treatment of early-symptomatic AD. 4 key findings →

Participants: 200 Evidence: low

Currently available literature on the relationships between cerebrospinal fluid (CSF) biomarkers and cognitive performance in frontotemporal dementia (FTD) is very limited and inconclusive. 4 key findings →

Design: cohort study Participants: 61 Evidence: moderate

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

↑ 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 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