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.

The impact of air pollution to central nervous system in children and adults

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neuro endocrinology letters 2017-12-01

The aim of this paper was to review studies analyzing the associations between air pollution and neurodevelopment in children as well as the effect on adult population. 4 key findings →

Evidence: low

Traumatic brain injury (TBI) is one of the leading causes of death and disability worldwide, and has emerged as a critical risk factor for multiple neurodegenerative diseases, particularly Alzheimer's disease (AD). 4 key findings →

Evidence: low

Impaired insulin signaling pathway in the brain in type 2 diabetes (T2D) is a risk factor for Alzheimer disease (AD). 4 key findings →

Evidence: low

Preliminary analysis indicates significant differences in location, ethnoracial background, ADI, and TRAP exposure amongst UCD ADRC participants. 5 key findings →

Participants: 985 Evidence: moderate

Using a 2-sample Mendelian randomization (MR) approach, we evaluated MR evidence for genetically proxied effects of 10 pre-specified gut bacterial classes on type 2 diabetes mellitus (T2DM) and Alzheimer disease (AD), and assessed MR evidence for a direct genetically proxied effect of T2DM on AD. 5 key findings →

Evidence: low

According to FINDRISC score, 38.1% of adults were at mild risk, 21.9% were at moderate risk, and 20.9% were at high risk. 5 key findings →

Evidence: low

We found significant associations between ADRD risk and particulate matter <2.5 µm in diameter and nitrogen dioxide in women. 5 key findings →

Evidence: low

Diabetic-related cognitive dysfunction, especially mild cognitive impairment (MCI), is a serious complication of type 2 diabetes mellitus (T2DM). 1 key finding →

Evidence: low

BACE1 as an early biomarker and its relevance to risk factors for Alzheimer’s disease

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Brain Research Bulletin 2025-07-22

While the β-secretase BACE1 is responsible for the rate-limiting initial step to generate amyloid-β (Aβ) peptides, BACE1 inhibitor clinical trials have been halted due to a lack of efficacy and/or safety concerns at symptomatic/prodromal stages of Alzheimer's disease (AD). 3 key findings →

Evidence: low

Gene-proxy for Graves' disease was associated with an increased risk of major depressive disorder (P-value = 0.02), whereas gene-proxy for autoimmune thyroiditis was linked to a greater risk of bipolar disorder (P-value = 0.043). 4 key findings →

Evidence: low

T2D was associated with a higher risk and earlier onset of dementia, especially in cases with T2D diagnosed at ages 30-54 years. 5 key findings →

Evidence: moderate

The observation group had significantly higher blood uric acid levels than the control group (P<0.05). 5 key findings →

Participants: 84 Evidence: low

OSA components are positively associated with the risk of ADRD. 5 key findings →

Participants: 14 Evidence: low

Obesity is associated with numerous adverse neural effects, including reduced neurogenesis, cognitive impairment, and increased risks for developing Alzheimer's disease (AD) and vascular dementia. 5 key findings →

Evidence: low

Incidental covert cerebral small vessel disease: Detection and management

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Advanced Neurology 2025-01-16

Cerebral small vessel disease (CSVD) is one of the most common vascular diseases of the brain, primarily diagnosed using magnetic resonance imaging biomarkers. 5 key findings →

Design: longitudinal study Evidence: moderate

During a median follow-up period of 4.6 years, stroke, MACEs, and AD dementia occurred in 24, 36, and 21 patients, respectively. 5 key findings →

Design: post-hoc analysis Participants: 1,011 Evidence: low

Our findings suggest that metformin exerts therapeutic effects beyond glycemic control in the context of T2D. By mitigating neuroinflammation and modulating microglial autophagy, metformin emerges as a promising therapeutic agent for cognitive decline associated with diabetes and potentially other neurological disorders. 4 key findings →

Evidence: low

Compared to controls, all three clinical groups showed a pattern of mainly increased referenced standard uptake values (SUVR) for the amyloid tracer [18F]-AV45 PET, with rank order PTSD > TBI_PTSD > TBI > Control, and same rank order was seen in the deficits of cognitive functions. 5 key findings →

Evidence: low

From across this tag

10 of the 3,281 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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