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.

Appendix B. Coding tree of main categories and specific sub categories describing factors influencing readiness for advance care planning among people with dementia, family caregivers, and healthcare professionals. 2 key findings →

Evidence: low

Appendix A. Interview guides on experiences with advance care planning, factors influencing readiness for advance care planning, and the use of conversation aids among people with dementia, family caregivers, and healthcare professionals. 2 key findings →

Evidence: low

The recent approval of disease-modifying therapies (DMTs) for early Alzheimer's disease (AD) marks a major shift in clinical practice. 5 key findings →

Evidence: low

This multisite initiative demonstrated that structured PPI is feasible in LMICs when supported by cultural adaptation, PPI coordinator roles, and tailored training for contributors and researchers. 1 key finding →

Evidence: low

In this update, we discuss the use of real-world data in the Haute Autorité de Santé assessment of economic evaluations, review how real-world evidence is supporting regulatory approvals in multiple myeloma, and consider lessons from the failed EVOKE trials of semaglutide in Alzheimer's disease for the broader application of target trial emulation. 1 key finding →

Evidence: low

BACH1/HO-1 axis dysregulation links Down syndrome to Alzheimer-like neurodegeneration

✓ Peer-reviewed alzhub usefulness score 31 out of 100. Neurochemistry international 2026-07-30

Down syndrome (DS), caused by trisomy of chromosome 21, is characterized by early-onset oxidative stress, impaired neuronal development, and an increased risk of Alzheimer's disease (AD)-like neuropathology. 2 key findings →

Evidence: low

Biomarcadores para diagnóstico e prognóstico de Alzheimer

✓ Peer-reviewed alzhub usefulness score 31 out of 100. Revista Brasileira Militar de Ciências 2026-02-06

A Doença de Alzheimer (DA) é a principal causa de demência no mundo, caracterizada por processos neurodegenerativos progressivos que comprometem cognição, comportamento e funcionalidade. 5 key findings →

Evidence: low

Theranostics—the use of diagnostic and therapeutic drugs that target the same molecular marker of disease—extends beyond the paradigm of radiopharmaceutical drug pairs used in oncologic settings (e.g., somatostatin receptor subtype 2 and prostate-specific membrane antigen theranostics) to other 1 key finding →

Evidence: low

Alzheimer’s disease (AD) is characterized by progressive accumulation of amyloid-β (Aβ) peptides, initiating a pathological cascade from soluble monomers to toxic oligomers, protofibrils, fibrils, and ultimately extracellular amyloid plaques that contribute to synaptic dysfunction and neuronal degeneration. 1 key finding →

Evidence: low

Neurodegenerative diseases are progressive disorders that damage and eventually kill neurons in the central nervous system (CNS). 1 key finding →

Evidence: low

5/15 Patient:innen zeigten initial einen visuell negativen Tau-PET Scan zur Baseline, davon konvertierten vier im Follow-up zu einem Tau-positiven Befund. 5 key findings →

Participants: 15 Evidence: low

Obstructive sleep apnea (OSA), a prevalent sleep-disordered breathing condition, is increasingly recognized as a modifiable risk factor for cognitive decline and dementia, including Alzheimer’s disease and vascular dementia. 1 key finding →

Evidence: low

Our study is the first one showing that dietary supplements improve cognition and sleep in a mouse model of DS. 1 key finding →

Evidence: low

Neurodegenerative disorders (NDDs), primarily alzheimer, dementia, parkinson, and rare NDD disease, present an escalating global health crisis, currently affecting over 55 million older adults worldwide. 1 key finding →

Evidence: low

Implications of virus-induced stress granules in tauopathies

✓ Peer-reviewed alzhub usefulness score 31 out of 100. Translational Neurodegeneration 2026-02-12

Tauopathies are characterized by aberrant tau structure and function, which is associated with neurodegenerative dementias, such as Alzheimer's disease, Pick's disease, and frontotemporal dementia, as well as the motor neuron disease amyotrophic lateral sclerosis. 1 key finding →

Evidence: low

In addition, we found sex-associated changes in the abundances of several proteins previously reported to be involved in tau pathology, such as Reelin, DARPP-32, Zyxin, Tbce, and Gng5, in JNPL3 mice. 4 key findings →

Evidence: low

The Mediterranean diet (MedDiet) is among the most extensively studied dietary patterns and has been consistently associated with reduced risk of all-cause mortality, cardiovascular disease, metabolic disorders, cognitive decline and several types of cancers. 2 key findings →

Evidence: low

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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