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.

Through systematic instruction and retraining visual and sustained attention, the patient was able to engage meaningfully with a high-tech device to increase functional personal choice when supported by a partner. 2 key findings →

Design: case report Evidence: low

Precision nutrition is a tailored dietary approach that considers an individual’s genetic and metabolic profile, lifestyle factors, and specific nutritional needs to improve health and potentially modify disease progression. 5 key findings →

Design: narrative review Evidence: low

Alzheimer disease (AD) pathology affects the transentorhinal/entorhinal region early but whether entorhinal cortex (EC) astrocytes are causal drivers or therapeutic targets remains unresolved. 5 key findings →

Design: narrative review Evidence: low

Triggered by LPS and AGEs in food, inflammatory cytokines can enter the brain and stimulate microglial activation, inflammation, and oxidative damage. 5 key findings →

Design: narrative review Evidence: low

However, knowledge alone does not consistently predict screening behavior. 4 key findings →

Design: narrative review Evidence: low

Alzheimer disease involves interacting mechanisms that include amyloid-beta accumulation, abnormal tau phosphorylation and aggregation, cholinergic dysfunction, synaptic degeneration, neuronal loss, neuroinflammation, vascular pathology, and genetic susceptibility. 5 key findings →

Design: narrative review Evidence: low

Amyloid immunotherapy with lecanemab and donanemab has been approved on the basis of statistically significant slowing of cognitive and functional decline in early Alzheimer's disease (1,2). 2 key findings →

Design: post-hoc analysis Evidence: low

On June 7, 2021, the FDA granted accelerated approval to aducanumab (Aduhelm), the first new Alzheimer's drug approved since 2003 and the first ever approved for a mechanism thought to modify disease course. 3 key findings →

Design: regulatory decision Evidence: preliminary

Predicting Subjective Cognitive Decline on Future BRFSS Survey Years: An Open Multi-Language Machine Learning Benchmark

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-21

Respondents who reported no difficulty deciding (DECIDE = 2) had substantially lower odds of SCD than those who reported difficulty (DECIDE = 1; aOR approximately 0.13; FDR < 0.05). 1 key finding →

Design: post-hoc analysis Participants: 298,944 Evidence: low

ADNI identified task-dependent performance boundaries, particularly attenuated conditional T discrimination within A+. 2 key findings →

Design: post-hoc analysis Participants: 1,097 Evidence: moderate

Cannabidiol for chronic neuroinflammation: clinical pharmacology and what an interpretable trial will require

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Authorea Preprints 2026-10-05

Public interest in cannabinoid medicines has outpaced the clinical pharmacology needed to judge product, dose and route. 5 key findings →

Design: narrative review Evidence: low

NeuroMark dFNC: Transferable Dynamic-State Templates for Subject-Specific and Frequency-Resolved Chronnectomics

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-17

Dynamic functional network connectivity (dFNC) commonly identifies recurring connectivity states from resting-state fMRI, but states derived independently in each dataset lack guaranteed correspondence across studies and cannot be directly estimated in new participants. 5 key findings →

Design: post-hoc analysis Evidence: moderate

Beyond Glycemic Control: The Pleiotropic Role of GLP-1RAs and Melatonin in Combating Neuroinflammation and Mitochondrial Dysfunction

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-28

Mitochondrial dysfunction, oxidative stress, neuroinflammation, and impaired protein homeostasis form interconnected pathological networks in acute central nervous system injury and chronic neurodegenerative disease. 5 key findings →

Design: narrative review Evidence: low

Multi-site MRI analysis of morphometric differences in brain regions in the presence of hearing loss and tinnitus across the adult lifespan

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-03-10

The impact of age and hearing loss on the brain has garnered significant attention, as both factors have been implicated in the development of cognitive impairment or dementia. 5 key findings →

Design: post-hoc analysis Evidence: low

Pantethine and Neurodegeneration: A Coenzyme A-Centered Framework Linking Metabolism, Neuroinflammation, and Mitochondrial Dysfunction

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-23

Neurodegenerative diseases are a growing global health burden associated with aging and characterized by progressive neuronal dysfunction, metabolic failure, mitochondrial impairment, oxidative stress, and chronic neuroinflammation. 1 key finding →

Design: narrative review Evidence: low

Neuroprotective potential of Acetylcholinesterase Inhibitors from Natural Sources in Combating Neurodegenerative Diseases

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. ScienceOpen Preprints 2026-09-08

Neurodegenerative diseases comprise a diverse group of progressive disorders characterized by the selective and irreversible loss of neuronal structure and function within the specific regions of the central and/or peripheral nervous systems. 5 key findings →

Design: narrative review Evidence: low

Beyond “Denial”: Understanding and Responding to Help-Refusal in Dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-26

Evidence for interventions that reduce refusal is strongest for music during personal care and modified bathing methods, with some support for positive communication and person-centred approaches, though quality is generally low and few studies involve family caregivers in community settings. 5 key findings →

Design: narrative review Evidence: low

The FDA gave lecanemab (Leqembi) accelerated approval based on Phase 2 data showing it reduced amyloid plaque in the brain, ahead of full Phase 3 results. 3 key findings →

Design: regulatory decision Evidence: early

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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