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.

Progressive cerebrovascular atherosclerosis and consecutive stroke are among the most common causes of dementia. 1 key finding →

Participants: 186 Evidence: low

A diffusion prepared 3D GRASE pCASL sequence with TGV regularized SPA modeling was proposed to measure BBB water permeability noninvasively with good reproducibility. k w may serve as an imaging marker of cerebral SVD and associated cognitive impairment. 2 key findings →

Evidence: moderate

GFAP positivity in neurons following traumatic brain injuries

✓ Peer-reviewed alzhub usefulness score 44 out of 100. International journal of legal medicine 2021-06-11

Glial fibrillary acidic protein (GFAP) is a well-established astrocytic biomarker for the diagnosis, monitoring and outcome prediction of traumatic brain injury (TBI). 4 key findings →

Evidence: low

Diabetic insulin resistance and pro-diabetic diet are reported to increase dementia risk through unknown mechanisms. 5 key findings →

Evidence: low

Our results indicate that SHR share behavioral and neuropathological characteristics with human cSVD patients and further undergird the relevance of immune responses for the initiation and progression of cSVD. 4 key findings →

Evidence: low

We retrospectively analyzed the charts of 58 long-term survivors of small-cell lung cancer (SCLC) (greater than 2 years) for neurological complications and their impact on the well-being of these patients. 4 key findings →

Participants: 14 Evidence: high

With the publication in 2015 of the consensus statement by the perfusion study group of the International Society for Magnetic Resonance in Medicine (ISMRM) and the EU-COST action 'ASL in dementia' on the implementation of arterial spin labelling MRI (ASL) in a clinical setting, the development of ASL can be considered to have become mature and ready for clinical prime-time. 5 key findings →

Evidence: low

In sub-populations such as diabetes mellitus type 2, proliferative diabetic retinopathy is an independent predictor of ischemic stroke. 5 key findings →

Evidence: low

Abnormalities of functional connectivity in the default mode network (DMN) recently have been reported in patients with amnestic mild cognitive impairment (aMCI), Alzheimer's disease (AD) or other psychiatric diseases. 4 key findings →

Evidence: low

In resting state condition, aMCI small-world architecture presents midway topological properties between AD subjects and healthy controls, confirming the hypothesis that aMCI is an intermediate step along the disease progression. 1 key finding →

Evidence: low

Differently from other myeloid cells, microglia derive exclusively from precursors originating within the yolk sac and migrate to the CNS under development, without any contribution from fetal liver or postnatal hematopoiesis. 4 key findings →

Evidence: low

The present study examines functional contributions of microglia in host defense, demyelination, and remyelination following infection of susceptible mice with a neurotropic coronavirus. 4 key findings →

Evidence: low

Cerebral blood flow (CBF) alterations and amyloid-β (Aβ) accumulation have been independently linked to cognitive deficits in older adults at risk for dementia. 4 key findings →

Evidence: low

Neuroinflammation has an established link with AIDS-related dementia but has not been investigated in the post-highly active anti-retroviral therapy (HAART) era. 4 key findings →

Evidence: low

Vascular dementia (VD) is defined as a progressive neurodegenerative disease of cognitive decline, attributable to cerebrovascular factors. 4 key findings →

Evidence: low

The results of gene set enrichment and gene set variation analyses indicated that immune-related pathways were upregulated in patients with VaD. 4 key findings →

Participants: 1,620 Evidence: low

From across this tag

10 of the 902 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