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 Helpline800-272-390024 hours a day, 365 days a yearFree, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
988 Suicide & Crisis Lifeline98824/7Call 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) Helpline866-232-84849:00 am - 9:00 pm ET, seven days a weekLicensed 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.
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Find studies
Showing 926–950 of 1,426 studies scoring ≤ 29 out of 100 (page 38 of 58)· 27,380 in the whole library·How the 0–100 score works
Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)
From OpenAlex; 12,859 studies have no institution on record and are not counted here.
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.
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·bioRxiv·2026-01-12
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have shown promise in preclinical models of neurodegeneration, with emerging evidence suggesting these effects may be driven by modulation of neuroinflammation. 1 key finding →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·Research Square·2026-10-20
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 →
⚠ Preprint — not yet peer-reviewedalzhub 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 →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·Research Square·2026-09-07
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 →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·bioRxiv·2026-07-29
Our experiments revealed that nAβ expressing animals exhibit a unique loss of positively correlated neuron connectivity, premature disruption of system wide dynamics, and reduced overall neuronal activity. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub 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 →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·Research Square·2026-07-07
H. cheirifolia phenolic extracts exhibit potent, mechanism-specific antioxidant activity and promising AChE inhibition, validating traditional use in neurological complaints. 4 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-02-12
A bstract INTRODUCTION Treatment response in Alzheimer’s disease (AD) varies substantially across patients, yet no validated frameworks exist to estimate heterogeneous treatment effects (HTE) from observational data while controlling for confounding bias. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-06-04
High placebo response is an obstacle in developing drugs to treat agitation in Alzheimer’s disease (AAD), a prevalent and burdensome symptom. 4 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·Research Square·2026-10-29
Alzheimer’s disease is increasingly linked to metabolic dysfunction, with insulin resistance emerging as a key contributor to tau pathology. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·Research Square·2026-08-26
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 →
⚠ Preprint — not yet peer-reviewedalzhub 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 →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·Research Square·2026-08-18
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 →
⚠ Preprint — not yet peer-reviewedalzhub 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 →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv·2026-08-07
Long-term metformin treatment is associated with a reduced risk of dementia and better memory performance among persons with pre-diabetes or T2D. Longer follow-up with more dementia cases is needed to confirm our findings. 5 key findings →
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 tierup to 10 pts
Journal's citation recordup to 4 pts
Study designup to 12 pts
Strength of evidenceup to 5 pts
Peer-review validationup to 10 pts
How recentup to 5 pts
Sample sizeup to 4 pts
Effect reportedup to 3 pts
Studied in peopleup to 3 pts
Randomised / blindedup to 2 pts
Times citedup to 7 pts
Citations per yearup to 5 pts
Impact for its field and yearup to 6 pts
Cited by studies hereup to 6 pts
Still being citedup to 4 pts
Senior author's track recordup to 4 pts
Institution's track recordup to 3 pts
Multi-centre collaborationup to 3 pts
Indexed in PubMedup to 2 pts
Free to readup 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.