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 451–475 of 2,047 studies published 2026 (page 19 of 82) · 27,380 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.

Peripheral biomarkers of neuroinflammation in Alzheimer's disease and vascular dementia

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Biochemical pharmacology 2026-05-17

Alzheimer's disease (AD) and vascular dementia (VaD) are the two commonest causes of dementia in older adults and frequently coexist as mixed neurodegenerative-cerebrovascular pathology. 1 key finding →

Evidence: moderate

Peripheral immune cell infiltration and crosstalk with brain-resident cells critically drive Alzheimer's disease (AD)-associated neuroinflammation, highlighting its therapeutic potential. 3 key findings →

Evidence: low

Average adherence was 41%. Despite this, remote measures demonstrated excellent reliability (ICCs > 0.90 after 10 sessions) and strong construct validity, with tasks loading onto memory, attention, and executive function domains. 5 key findings →

Evidence: moderate

Cognitive decline is closely associated with biological aging and with interconnected processes, including chronic low-grade inflammation, oxidative stress, mitochondrial dysfunction, and cellular senescence. 2 key findings →

Design: narrative review Evidence: high

There is a need for early, objective markers of Alzheimer's disease (AD)-related synapse dysfunction in adults with Down syndrome (DS). 1 key finding →

Design: cross-sectional Participants: 131 Evidence: moderate

BackgroundAmyloid-negative tau-related neurodegeneration represents a non-Alzheimer biomarker-defined profile; however, its clinical heterogeneity and prognostic relevance remain unclear within Alzheimer's disease-related frameworks. 4 key findings →

Design: cohort study Participants: 1,280 Evidence: moderate

Among TM enrollees, prevalence of dementia was lower by 4% points in 2014 (9.0%, 95%CI: 7.8%, 9.3%) compared to 2000 (13.0%, 95%CI: 12%, 14%). 5 key findings →

Design: cross-sectional Participants: 18,381 Evidence: low

Dementia Diagnosis Underreporting and Care Engagement and Planning Among Older Adults

✓ Peer-reviewed alzhub usefulness score 47 out of 100. JAMA Network Open 2026-08-26

Among 6158 person-waves with a claims-based dementia diagnosis from 3278 PWPD (3134 [50.9%] aged 65-84 years; 4282 [69.5%] female; 1176 [19.1%] non-Hispanic Black, 617 [10.0%] Hispanic, and 4256 [69.1%] non-Hispanic White), the adjusted proportion not reporting their diagnosis was 42% (95% CI, 40%-43%) among all respondents and 67% (95% CI, 64%-69%) among self-respondents. 5 key findings →

Design: cohort study Evidence: moderate

Mapping social health and dementia risk: A register-based study of older adults in Finland

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Social Science & Medicine 2026-03-05

This study investigates the role of individual and area-level social health factors in shaping geographic variation in dementia incidence among older adults in Finland. 1 key finding →

Participants: 185,712 Evidence: low

The Centiloid method demonstrates strong intertracer and interscanner harmonization when standardized to the 11C-Pittsburgh compound B reference, with high correlation (r2 > 0.9) across 18F-labeled tracers, including florbetapir, flutemetamol, and florbetaben. 5 key findings →

Design: longitudinal study Evidence: moderate

A total of 30 variants were overrepresented in four pathways: presenilin/Alzheimer disease, cadherin/WNT signaling, gonadotropin-releasing hormone receptor, and transforming growth factor-β (TGF-β) signaling. 5 key findings →

Participants: 204 Evidence: low

Higher AD-PRS was associated with faster CD in the full clinical cohort and in biomarker subset, independently of APOE genotype. 5 key findings →

Design: longitudinal study Participants: 7,233 Evidence: moderate

Anti-Amyloid Monoclonal Antibodies in Early Alzheimer Disease: Lecanemab and Donanemab

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Neurology International 2026-09-11

Pivotal trials demonstrated statistically significant but modest average slowing of decline: Clarity AD showed a 0.45-point between-group difference in CDR-SB worsening at 18 months, and TRAILBLAZER-ALZ 2 showed a 3.25-point iADRS difference in the low/medium-tau population at 76 weeks. 5 key findings →

Design: meta-analysis Evidence: high

Appetite disturbances were present in 9.4% of participants and were associated with greater neuropsychiatric burden and disease severity. 4 key findings →

Design: cross-sectional Participants: 7,223 Evidence: moderate

Despite comprising the largest segment of the sexual minority population and experiencing unique stressors and health disparities, bi+ dementia caregivers remain underrepresented in health and caregiving research. 3 key findings →

Design: cross-sectional Participants: 125 Evidence: low

Novel insights into Alzheimer's disease through the study of individuals with Down syndrome

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Alzheimer s & Dementia 2026-01-01

Novel insights into Alzheimer's disease through the study of individuals with Down syndromePeople with Down syndrome (DS) represent the largest genetically defined population at risk for Alzheimer's disease (AD). 1 Virtually all adults with DS develop AD neuropathology by midlife due to triplication of the amyloid precursor protein (APP) gene on chromosome 21.As medical advances and social integration have extended life expectancy into the 60s, AD has emerged as the major determinant of cognitive decline, morbidity, and mortality in this DS population. 2 What was once viewed as an inevitable consequence of aging in DS is now recognized as a unique scientific opportunity to uncover the earliest events that drive AD.The predictable and accelerated course of DS-associated AD (DSAD) provides an unparalleled window into the molecular and cellular origins of amyloid and tau pathology, neuroinflammation, cerebrovascular pathology, and neurodegeneration. 1 key finding →

Design: longitudinal study Evidence: moderate

These findings provide no evidence of a group-level Alzheimer-related p-tau217 elevation in young people with DSRD and support DSRD as a condition distinct from Alzheimer’s disease. 5 key findings →

Design: longitudinal study Participants: 132 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 27,380 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