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 476–500 of 1,426 studies scoring ≤ 29 out of 100 (page 20 of 58)· 27,380 in the whole library·How the 0–100 score works
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.·medRxiv (preprint)·2026-08-17
BackgroundAlzheimers Disease and Related Dementias (ADRD) is a growing global public health challenge, and caregivers experience high rates of burden, unmet needs, and system failures. 1 key finding →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-22
Alzheimers disease (AD) is defined by progressive neurodegeneration, yet a substantial fraction of its genetic risk maps to non-neuronal processes. 1 key finding →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-22
BackgroundThe brain age gap (BAG), the difference between neuroimaging-predicted and chronological age, captures inter-individual variation in brain aging. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-22
KEY POINTSO_LIThis paper demonstrates the feasibility of implementing Geriatric ED programs with targeted support for people living with or at risk for dementia across three distinct health systems in San Francisco. 5 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-23
Examples include subpopulations of CD4+ T cells associated with inflammatory bowel disease, characterized by enrichment for a multi-cytokine phenotype and overlap with the naive NF-kB-activated, central memory, and effector memory CD4+ T subtypes, and subpopulations of microglia associated with Alzheimers disease, characterized by depletion of homeostatic programs and localization to the midtemporal gyrus, dorsolateral prefrontal cortex, and medial entorhinal cortex. 3 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-24
AbstractO_ST_ABSBackgroundC_ST_ABSGlucagon-like peptide-1 (GLP-1) receptor agonists and sodium-glucose cotransporter-2 (SGLT2) inhibitors are increasingly used for type 2 diabetes. 5 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-25
Self-repairs - in-utterance revisions in which a speaker abandons and reformulates their speech - are a promising interpretable marker for speech-based cognitive screening. 1 key finding →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-25
INTRODUCTIONNeurodegenerative research identifies biomarkers to confirm presence of disease and inform about risk for clinical symptoms. 4 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-25
We examined whether their metabolomic profiles also differed and whether subtype-related metabolic patterns were associated with dementia, stroke, and all-cause mortality. 5 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-25
In the fully adjusted Cox model, baseline statin exposure was associated with a lower risk of incident AMI (HR, 0.805; 95% CI, 0.731-0.887). 3 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-25
Persistent racial disparities in dementia raise concerns regarding the validity and generalizability of existing prognostic models across diverse populations. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-26
IntroductionNeuropsychiatric symptoms (NPS)--including aggression, psychosis, anxiety, apathy, and depression--affect up to 85% of individuals with Alzheimers disease (AD) and are among its most disabling and costly manifestations, accelerating cognitive and functional decline, institutionalization, mortality, and healthcare costs. 1 key finding →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-26
Rapamycin, an FDA-approved inhibitor of the mammalian target of rapamycin (mTOR) pathway, has demonstrated promising anti-aging and neuroprotective effects. 4 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-27
Early identification of cognitive impairment remains challenging in settings where comprehensive cognitive and clinical assessments are not available. 1 key finding →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-27
BackgroundEpidemiological studies increasingly associate several adult vaccinations with lower risk of Alzheimers disease (AD) and dementia, but the biological mechanisms underlying these observations remain unclear. 5 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-27
Human leukocyte antigen (HLA) class II variation is implicated in Alzheimers disease (AD) and longevity, but its mechanisms within the major histocompatibility complex remain unclear. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-27
Neuropsychiatric symptoms (NPS) are increasingly recognized as critical components of the disease progression in Alzheimers disease (AD), yet their relationship with neurodegeneration remain poorly characterized. 2 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-27
Polygenic and proteomic risk scores are both proposed for pre-symptomatic stratification, yet the extent to which they provide overlapping or complementary information has not been measured across neurodegenerative disease. 3 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-28
Genome-wide genotypes were quality-controlled, imputed, functionally annotated (yielding 16,935 gene regions comprising 90,607 functional variants), and associated with latent EEG features using Bayesian reduced rank regression. 5 key findings →
⚠ Preprint — not yet peer-reviewedalzhub usefulness score 16 out of 100.·medRxiv (preprint)·2026-08-28
Impairment in the comprehension of morphosyntactic and transitivity information does not feature in current diagnostic guidelines for primary progressive aphasia (PPA) or Alzheimers Diseases (AD), despite research reporting delayed sensitivity or insensitivity of these clinical populations to these linguistic domains. 2 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.