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.

Alzheimer's Disease as the Result of Aberrant Reactivation of Embryonic Brain Pathways Silenced Decades Earlier

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-07-22

These findings shift AD modeling from passive proteotoxicity to an active, misregulated developmental structural engine, offering a mechanical framework that explains early olfactory vulnerability and non-linear anti-tau clinical trial responses. 3 key findings →

Evidence: moderate

Alzheimer's disease (AD) and Down Syndrome (DS) are characterized by the aggregation of tau tangles. 1 key finding →

Evidence: low

Conformation-based detection of tau seeds with a novel VHH

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2025-12-08

In Alzheimer’s disease (AD) and related tauopathies, progressive pathology has been linked to prion mechanisms whereby ordered tau assemblies, or “seeds,” form in one cell and transit to neighboring or connected cells where they serve as templates for their own replication. 1 key finding →

Evidence: low

Plasma pTau-181 demonstrates flat or declining longitudinal trajectories and minimal cognitive correlation, suggesting tau is a static biomarker rather than a dynamic therapeutic target in mid-to-late adulthood. 2 key findings →

Design: cross-sectional Participants: 2,523 Evidence: moderate

mRNA vaccine platform demonstrates potent immunotherapeutic targeting of amyloid-β and tau pathologies in Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2025-09-16

Current Alzheimer’s disease (AD) immunotherapeutics face efficacy and safety limitations with antibody-based approaches. 5 key findings →

Evidence: low

Eligible studies reported MACE or dementia outcomes in adults ≥ 50 years for at least one of three intervention classes (RZV, SGLT2i, GLP-1 RA) versus placebo or active comparator, with follow-up ≥ 6 months. 5 key findings →

Design: systematic review Evidence: high

Alzheimer's disease continues to be one of the major critical neurodegenerative ailments of the modern era, with acetylcholinesterase (AChE) inhibition standing as a foundational therapeutic strategy. 2 key findings →

Evidence: low

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that is the leading cause of dementia in older people. 2 key findings →

Evidence: low

Docking-Guided Design and Biological Evaluation of a Lead Convolvine-Based Acetylcholinesterase Inhibitor for Alzheimer's Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-01

Alzheimer's disease (AD) is a progressive neurodegenerative condition marked by cognitive decline, memory loss, and cholinergic dysfunction [1]. 3 key findings →

Evidence: low

In silico design and physicochemical characterisation of a dual-action intranasal nanoparticle formulation for Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-09-28

Approved Alzheimer’s disease therapies fail to address the two drivers of cognitive decline: loss of BDNF-TrkB signalling and accumulation of hyperphosphorylated tau protein. 1 key finding →

Evidence: low

This study reports the eco-friendly green synthesis of a multifunctional silver nanocomposite (DS-MC-Ag-nanocomposite) utilizing ethanolic extract of waste date seeds ( Phoenix dactylifera ) and methyl cellulose (MC) as dual reducing and stabilizing agents. 4 key findings →

Evidence: low

Computational Screening of FDA-Approved Drugs as Potential BACE1 Inhibitors for Alzheimer's Disease Drug Repurposing

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-07-27

Alzheimer's disease is a progressive neurodegenerative disorder affecting over 55 million people worldwide, with no disease-modifying treatments currently approved. 2 key findings →

Evidence: low

H. cheirifolia phenolic extracts exhibit potent, mechanism-specific antioxidant activity and promising AChE inhibition, validating traditional use in neurological complaints. 4 key findings →

Evidence: low

These findings identify an age-dependent breakdown of the metabolic resilience network formed by NAMPT, NAD⁺, SIRT1, and AMPK as a key mechanistic driver of metabolic stress-induced early AD-like pathology. 3 key findings →

Evidence: low

Hepatic and Brain Spatial Gene Expression Changes in Intragastric Alcohol Fed APP/PS1 Alzheimer's Disease Mouse Model

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-24

These findings implicate significant liver–brain crosstalk through which chronic alcohol exposure may modulate AD-relevant pathology and reinforce the growing recognition of the liver as a critical organ in AD pathogenesis. 5 key findings →

Evidence: low

Cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) are central regulators of synaptic homeostasis, plasticity, and dysfunction during Alzheimer’s disease (AD) progression. 3 key findings →

Evidence: low

Repurposing probucol for prevention of dementia: a nationwide cohort study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-13

In this nationwide cohort, probucol use was associated with substantially lower dementia risk than statins, supporting evaluation of probucol for repurposing in dementia prevention. 2 key findings →

Participants: 52,532 Evidence: moderate

Computational Screening of 1,348 FDA-Approved Drugs as Potential BACE1 Inhibitors for Alzheimer's Disease Drug Repurposing

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-07-28

Alzheimer's disease (AD) remains one of the most devastating and economically costly neurological conditions of the modern era, affecting over 55 million individuals worldwide with no approved disease-modifying therapy. 3 key findings →

Participants: 1,348 Evidence: low

In this trial, $5 and $25 noncontingent monetary incentives included in mailed recruitment letters did not produce a detectable improvement in response among ADRD caregiving dyads. 4 key findings →

Design: randomized controlled trial Participants: 103 Evidence: high

Older adults in senior living communities (SLCs) often face barriers to maintaining emotional well-being and family ties. 4 key findings →

Design: randomized controlled trial Participants: 90 Evidence: high

↑ 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