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.

Artificial intelligence and neuroimaging enable accurate dementia prediction but often involve 'black box' models that can be difficult to trust. 5 key findings →

Evidence: low

The role of mitochondria in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Zenodo (CERN European Organization for Nuclear Research) 2026-03-25

This diploma thesis presents the work carried out during 6 months within the Laboratory directed by Professor Millet, written under the supervision and with the support of Dr. Benjamin Tournier and Silvia Braconi Quintaje. 5 key findings →

Evidence: low

Alzheimer's disease (AD) affects over 55 million people worldwide and lacks effective disease-modifying therapies targeting neuroinflammation. 5 key findings →

Evidence: low

Frontotemporal dementia (FTD) is a group of early onset and progressive disorders, characterized by degeneration in the frontal and temporal lobes, and subsequent deterioration in cognition, personality, social behavior, and language, with aggregates of the RNA-binding protein TDP-43 being present in ~45% of the cases. 1 key finding →

Evidence: low

TDP-43 and FUS are RNA-binding proteins involved in the regulation of diverse RNA-processing events and have been strongly implicated in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 3 key findings →

Evidence: low

Vascular cognitive impairment and dementia (VCID) encompasses a heterogeneous group of disorders in which cerebrovascular pathology contributes to cognitive decline. 2 key findings →

Evidence: low

The purpose of this narrative review is to examine women's cognitive health and to highlight its association with four major pillars: (1) aging, (2) estrogen decline and loss, (3) diet, and (4) neuroinflammation, and their contribution to cognitive decline, with a focus on this combination to increase awareness and address the progression and potential amelioration of Alzheimer's disease (AD). 2 key findings →

Design: narrative review Evidence: low

Hippocampal pan-histone H3 crotonylation (H3Kcr) and H3K18cr were significantly upregulated in both 5xFAD and Aβ42-injected mice compared to controls. 5 key findings →

Evidence: low

Obesity and its associated metabolic disturbances increase the risk of cognitive decline, dementia, and anxiety-related disorders. 2 key findings →

Evidence: low

Aggregation of the microtubule-binding protein tau is the histopathological hallmark of Alzheimer's disease (AD) and other neurodegenerative diseases, which are collectively known as tauopathies. 5 key findings →

Evidence: low

The Mediterranean diet, rich in plant-based foods, olive oil, and fish, has been consistently associated with slower cognitive decline and reduced risk of neurodegeneration in observational studies and some clinical trials. 4 key findings →

Evidence: high

The evidence for cognitive training in preventing cognitive decline in Alzheimer's disease is varied, with some studies indicating cognitive benefits but showing limited impact on functional outcomes or disease progression. 1 key finding →

Evidence: low

Cognitive training shows potential in preventing cognitive decline in individuals at risk for Alzheimer's disease, especially as part of multimodal interventions, though current evidence varies in quality and clarity. 1 key finding →

Evidence: low

Cognitive training appears effective in improving cognitive functions and delaying cognitive decline in people at risk of Alzheimer's disease but requires more standardized research for conclusive evidence. 1 key finding →

Evidence: low

AWVs were associated with reduced risks for falls (HR: 0.976 for 2 AWVs; 0.936 for ≥3 AWVs) and fractures (HR: 0.978 for 1 AWV; 0.960 for 2 AWVs; 0.927 for ≥3 AWVs), with greater reductions observed with more AVWs. 5 key findings →

Evidence: moderate

Misconceptions were common: 38% of participants equated ACP exclusively with decisions to forgo active treatment, and many conflated ACP with current rather than future-oriented care planning. 5 key findings →

Design: cross-sectional Evidence: low

Among 2,435,099 weighted hospitalizations, palliative care documentation was present in 65,675 (2.70%), increasing from 2.13% in 2016 to 3.43% in 2022. 5 key findings →

Design: cross-sectional Evidence: low

ACP is linked to lower EOL spending and a shift from inpatient to outpatient ADRD care; structured ACP delivery should be considered. 1 key finding →

Design: cohort study Evidence: moderate

Providing end-of-life care for patients with COPD, dementia, and cancer involves a focus on symptom management, integration of palliative care, and respecting patient preferences, while engaging families in the care process. 1 key finding →

Evidence: low

↑ 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