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.

Introducción: La enfermedad de Alzheimer se considera una de las patologías neurodegenerativas de mayor impacto en la salud pública, con una prevalencia y tasa de mortalidad en incremento. 5 key findings →

Evidence: low

Introducción. La enfermedad de Alzheimer (EA) es una condición neurodegenerativa progresiva caracterizada por el deterioro cognitivo, la acumulación de beta-amiloide y la neuroinflamación. La tecnología CRISPR/Cas9 ha emergido como una herramienta prometedora para investigar y, potencialmente, tratar la EA, permitiendo ediciones precisas del genoma y la modulación de la expresión génica. 5 key findings →

Evidence: low

Chronic psychological stress is a well-known risk factor for neurodegenerative diseases including Alzheimer disease (AD), yet the underlying mechanisms remain unclear. 4 key findings →

Evidence: low

The repeated inability of Aβ therapies to pass clinical tests in sporadic AD points to the complexity of the disease and indicates that earlier or more interventions could be necessary. 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

Mechanistic studies demonstrate that pharmacological modulation of microglial phenotypes inhibition of pro inflammatory mediators TNF alpha IL 1 IL 6 and targeting pathways such as NF kappa B NLRP3 inflammasome p38 MAPK JAK STAT and TREM2 can attenuate neuroinflammatory cascades and reduce amyloid beta and tau associated neurotoxicity. 5 key findings →

Evidence: low

The human brain is one of the most metabolically active tissues in the body, due in large part to the activity of trillions of synaptic connections. 1 key finding →

Evidence: low

A doença de Alzheimer (DA) representa a principal causa de demência no mundo, caracterizando-se por um processo neurodegenerativo progressivo associado ao comprometimento cognitivo e funcional. 5 key findings →

Evidence: low

Our findings reveal various concerns about Aduhelm involving efficacy, safety, and affordability. 4 key findings →

Evidence: low

This study aims to comprehensively review the role of glial fibrillary acidic protein (GFAP) as a marker of astrocyte activation in Alzheimer's disease (AD). 3 key findings →

Evidence: low

Previous studies have shown that preeclampsia increases the risk of cerebrovascular and cardiovascular diseases, as well as cognitive impairments, up to evolving dementia in the future. 3 key findings →

Evidence: low

Alzheimer’s disease is the leading cause of dementia globally and is marked by amyloid-β plaque accumulation, decreased brain pH, disrupted metabolism, and increased permeability of the blood-brain barrier. 1 key finding →

Evidence: low

Advanced Glycation End Products (AGEs) are reactive compounds formed through the non-enzymatic glycation of proteins, lipids, or nucleic acids due to exposure to reducing sugars. 2 key findings →

Evidence: low

The Ct group and Ct+ee group performed significantly better than the control group in behavioural tasks and had improved dendrite profiles of DG and basal tree of CA1 region of hippocampus. 4 key findings →

Evidence: low

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

Alzheimer's Disease (AD) is a progressive neurodegenerative condition that gradually impairs cognitive abilities such as memory, attention, and problem-solving, leading to significant challenges in everyday functioning and a decline in quality of life. 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

There is very little documented evidence on the experiences of healthcare professionals caring for their own family outside of their role. 1 key finding →

Evidence: low

Neuropalliative Care in Dementia

✓ Peer-reviewed alzhub usefulness score 28 out of 100. CONTINUUM Lifelong Learning in Neurology 2025-12-01

Patients and their caregivers and families confronting dementia often face heavy burdens from difficult-to-control symptoms, uncertainty about the future, and a high risk of care partner burnout. 5 key findings →

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