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.

Traumatic Brain Injury, Chronic Traumatic Encephalopathy, and Alzheimer's Disease: Overlapping Phenotypes and Associations

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-09-14

Traumatic brain injury (TBI), chronic traumatic encephalopathy (CTE), and Alzheimer's disease (AD) share several neuropathophysiological mechanisms, including axonal injury, neuroinflammation, and abnormal protein aggregation, which may contribute to overlapping clinical manifestations. 1 key finding →

Evidence: low

Carbonaceous Components Underlying Wildfire Smoke PM 2.5 -Associated Alzheimer’s Disease and Related Dementias in Older US Adults

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-11

Wildfire smoke exposure is increasing across the U.S., but the long-term neurological effects of smoke-specific fine particulate matter (PM 2.5 ) and its carbonaceous components remain uncertain. 4 key findings →

Evidence: moderate

Higher UGS coverage was associated with a lower risk of incident AD among older adults in urban South Korea. 4 key findings →

Design: cohort study Participants: 95,822 Evidence: moderate

Diesel exhaust particles disrupt mouse and human iPSC-derived microglial function and Amyloid-β clearance in Alzheimer’s disease models

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-23

Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders, yet the environmental drivers that accelerate its progression remain poorly defined. 2 key findings →

Evidence: low

Association of Long-Term Air Pollution Exposure with Dementia-Related Neuropathologies at Autopsy in a Community-Based Cohort

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-02-05

Higher exposure to PM 2.5 was associated with cerebral arteriolosclerosis and atherosclerosis at death, consistent with the known vascular toxicity of this pollutant. 5 key findings →

Design: cohort study Participants: 909 Evidence: moderate

Mediation of the relationship between air pollution and dementia: A UK Biobank study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-02-22

Exposure to the highest quintile of PM 2·5 (Rte:1·14, 95% CI:1·06-1·23), NO x (Rte:1·11, 95% CI:1·03-1·20) or NO 2 (Rte:1·08, 95% CI:0·99-1·16), compared to the lowest quintile, was associated with higher dementia risk. 2 key findings →

Evidence: high

Direct medical and productivity-related costs associated with incident cases were estimated using a cost-of-illness (COI) framework. 4 key findings →

Evidence: low

Biopsychosocial risk factors for Alzheimer’s disease and related dementias in UK immigrants from the Middle East and North Africa (MENA)

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-05-13

The Middle East and North Africa (MENA) region represents the area of greatest projected growth in instances of Alzheimer’s disease and related dementias (ADRDs) globally, yet, it remains virtually uncharacterized in health studies of aging and ADRDs. 4 key findings →

Participants: 3,552 Evidence: low

The 2,885 participants had a mean age of 69.5 years. 4 key findings →

Design: longitudinal study Participants: 2,885 Evidence: moderate

Neuroticism, a personality trait characterized by the predisposition to experience intense and frequent negative emotions, has been associated with an increased risk of Alzheimer’s disease (AD). 5 key findings →

Participants: 1,277 Evidence: low

Associations of lifestyle factors and genetic risk with risk and rate advancement periods of dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. PsyArXiv 2026-07-23

INTRODUCTIONLittle is understood about the extent to which lifestyle factors can advance or delay the risk of developing dementia, and whether that is dependent on non-modifiable factors, e.g. sex and genetic susceptibility.METHODSAmong 224,516 UK Biobank participants aged ≥50 years at baseline, Cox regression examined the relations of apolipoprotein E gene (APOE) genotypes, and lifestyle with incident dementia. 3 key findings →

Evidence: low

Contribution of cerebrovascular lesions to neurodegeneration and cognitive decline

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-06

Vascular risk factors were associated with CSVD burden and progression, and WMH and PVS progression were further associated with cortical atrophy and cognitive decline, underscoring the interconnected contributions of vascular risk, CSVD, and neurodegeneration to cognitive aging and dementia risk. 5 key findings →

Design: cross-sectional Participants: 289 Evidence: moderate

This study reports the prevalence of CF among elderly hypertensive residents of a community in Inner Mongolia. 5 key findings →

Design: cross-sectional Evidence: low

Functional assessment improves discrimination of clinical and biomarker-defined Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-07-31

In a contemporary, diverse cohort, most established dementia risk algorithms had limited power in discriminating amyloid positivity, pTau-217 positivity, and current cognitive status despite acceptable calibration. 3 key findings →

Participants: 603 Evidence: moderate

Effect of Intensive vs Standard Blood Pressure Control According to APOE ε4 Genotype: A Secondary Analysis of SPRINT

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-07-06

In SPRINT, intensive vs standard SBP control yielded a significantly larger 4-year absolute risk reduction in dementia among APOE ε4 carriers (−1.7%) than non-carriers (0.2%; P-interaction = .045); the relative-scale interactions were directionally consistent but not significant. 3 key findings →

Design: randomized controlled trial Evidence: high

Traumatic Brain Injury Increases Risk of Psychiatric Disorders Following Neurological Disease: Evidence from the UK Biobank Cohort

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-07-06

Lifetime TBI exposure is associated with increased likelihood and long-term risk of psychiatric disorders in individuals with dementia, stroke, and Parkinson’s disease, with mood disorders being the most consistent outcome across conditions. 4 key findings →

Participants: 502,154 Evidence: moderate

Concurrent Gabapentin and Dihydropyridine Calcium Channel Blocker Use and Risk of Incident Dementia: An Active-Comparator Cohort Study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-02-09

Both classes act on neuronal calcium signaling, raising the question of whether their combined use is associated with greater cognitive risk than gabapentin alone. 5 key findings →

Design: cohort study Participants: 33,791 Evidence: moderate

Patients with peripheral artery disease (PAD), chronic limb-threatening ischemia (CLTI), and/or diabetic foot ulcer (DFU) are at increased risk for limb loss and death. 3 key findings →

Participants: 178,995 Evidence: moderate

Individual Angiotensin Receptor Blockers and Risk of Dementia: A Target Trial Emulation Study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-14

Of 22,025,599 individuals screened, 2,051,275 were eligible; matched cohorts ranged from 10,113 to 857,773, with median follow-up of 4.7 to 7.2 years. 5 key findings →

Design: cohort study Evidence: high

Systematic Review of Population-Based Studies of Prevalence and Incidence of Aging-Associated Neurodegenerative Diseases in Russia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-04-06

The prevalence of dementia and Parkinson’s disease in Russia varies widely depending on diagnostic method, age group, and study design. 2 key findings →

Design: meta-analysis Participants: 20 Evidence: high

From across this tag

10 of the 3,247 studies in this tag, 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 10. The same 10 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 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