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 201–225 of 1,346 studies (page 9 of 54)· 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.
Overall, the available evidence suggests that natural compounds confer multitarget neuroprotective effects that directly engage with key pathological mechanisms underlying AD. 4 key findings →
✓ Peer-reviewedalzhub usefulness score 59 out of 100.·Nature·1995-08-01
The study reported the cloning of a novel gene (E5-1) encoded on chromosome 1 with sequence similarity to the S182 gene on chromosome 14q24.3. 5 key findings →
✓ Peer-reviewedalzhub usefulness score 58 out of 100.·Neurology·2021-08-11
These findings suggest that DPP-4i use is associated with low amyloid burden and favorable long-term cognitive outcome in diabetic patients with ADCI. 2 key findings →
Apolipoprotein E is immunochemically localized to the senile plaques, vascular amyloid, and neurofibrillary tangles of Alzheimer disease. 2 key findings →
✓ Peer-reviewedalzhub usefulness score 58 out of 100.·Archives of neurology·2002-07-01
The presence of epsilon 4 was associated with risk of developing AD on follow-up (relative risk, 1.92; 95% confidence interval, 1.27-2.89). 3 key findings →
✓ Peer-reviewedalzhub usefulness score 58 out of 100.·JAMA neurology·2013-03-01
Although there were no significant differences among the 3 groups of participants in their clinical ratings, neuropsychological test scores, hippocampal volumes (P = .60), or hippocampal glucose metabolism measurements (P = .12), there were significant group differences in their posterior cingulate glucose metabolism measurements (P = .001). 2 key findings →
✓ Peer-reviewedalzhub usefulness score 58 out of 100.·Annals of neurology·2015-07-28
Targeted sequencing of confirmed GWAS loci revealed an excess burden of deleterious coding mutations in LOAD, with the greatest burden observed in ABCA7 and BIN1. 4 key findings →
✓ Peer-reviewedalzhub usefulness score 58 out of 100.·Archives of neurology·2002-04-01
Compared with individuals with the APOEepsilon3/epsilon3, the odds of having AD were significantly increased among those with 1 or more copies of the epsilon4 allele; the odds ratio (OR) for the epsilon3/epsilon4 genotype was 2.6 (95% confidence interval [CI], 1.8-3.7), and the OR for the epsilon4/epsilon4 genotype was 10.5 (95% CI, 5.1-21.8). 3 key findings →
Phenotypic personality dimensions, primarily neuroticism and extraversion, moderate the relationship between APOE [Latin Small Letter Open E]-4 genotype and cognitive outcomes among older adults. 1 key finding →
✓ Peer-reviewedalzhub usefulness score 58 out of 100.·Neurobiology of aging·2010-07-08
We examined longitudinal associations between the apolipoprotein E ε4 allele (ApoE4(+) status) and several cognitive outcomes and tested effect modification by sex. 3 key findings →
✓ Peer-reviewedalzhub usefulness score 58 out of 100.·Nature medicine·2025-07-15
The APOE ε4 genetic variant is the strongest genetic risk factor for late-onset Alzheimer's disease (AD) and is increasingly being implicated in other neurodegenerative diseases. 3 key findings →
✓ Peer-reviewedalzhub usefulness score 58 out of 100.·Neuron·2022-03-16
The ε4 allele of the apolipoprotein E gene (APOE4) is a strong genetic risk factor for Alzheimer's disease (AD) and several other neurodegenerative conditions, including Lewy body dementia (LBD). 5 key findings →
✓ Peer-reviewedalzhub usefulness score 58 out of 100.·Nature neuroscience·2014-03-30
MATR3 is an RNA- and DNA-binding protein that interacts with TDP-43, a disease protein linked to amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. 4 key findings →
✓ Peer-reviewedalzhub usefulness score 58 out of 100.·Nature medicine·1998-01-01
Genetic causes of Alzheimer's disease (AD) include mutations in the amyloid precursor protein (APP), presenilin 1 (PS1), and presenilin 2 (PS2) genes. 4 key findings →
10 of the 1,344 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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.