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
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Find studies
Showing 176–200 of 209 studies scoring ≥ 67 out of 100 published 2025(page 8 of 9)· 31,380 in the whole library·How the 0–100 score works
From OpenAlex; 16,851 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.
In a Chinese cohort of 1,275 people spanning normal cognition to dementia, this study compared three blood markers: p-tau217 rose steadily as amyloid and tau pathology worsened and was very good at both ruling out early disease and flagging advanced tau pathology. 4 key findings →
✓ Peer-reviewedalzhub usefulness score 68 out of 100.·Neurology·2025-12-03
At baseline, 2,279 dementia-free participants with available blood samples were included (median age 72 (interquartile range, 61-81) years; 62% female). 4 key findings →
Between April 30, 2020, and May 9, 2022, we randomly allocated 204 participants (109 [53%] women and 95 [47%] men) to the intervention group and 98 (60 [61%] women and 38 [39%] men) to the control group. 218 (72%) participants at 6 months and 178 (59%) at 12 months provided cost data. 2 key findings →
In Alzheimer's disease (AD), amyloid-β (Aβ) triggers the aggregation and spreading of tau pathology, which drives neurodegeneration and cognitive decline. 3 key findings →
✓ Peer-reviewedalzhub usefulness score 68 out of 100.·Neurology·2025-05-29
Higher tau levels are associated with the fastest decline in everyday functioning in the presence of elevated amyloid, and those accumulating more tau show a faster decline in everyday functioning. 3 key findings →
✓ Peer-reviewedalzhub usefulness score 68 out of 100.·Neurology·2025-12-09
A total of 716 individuals were included in the analysis: 413 cognitively unimpaired (CU) participants (58.6% female; mean age = 70.6 years, SD = 7.9) and 303 cognitively impaired (CI) participants (54.7% female; mean age = 73.2 years, SD = 7.4). 5 key findings →
Two regions achieved genome-wide significance with TDP-43: apolipoprotein E (APOE) and TMEM106B. Three loci reached genome-wide significance with HS: APOE, TMEM106B, and granulin precursor (GRN). 5 key findings →
A total of 5 071 935 participants were included from 27 studies; approximately 49.2% of participants were female, and 14 studies were conducted in Asia, 7 in North America, 3 in Europe, and 3 in Oceania, represented by Australia. 5 key findings →
The global mortality of ADRD among adults aged ≥65 years increased by 115%, from 6.5 (95% UI 1.5-18) per 100,000 population in 1991 to 14 (95% UI 3.5-37) per 100,000 population in 2021, with an Average Annual Percentage Change (AAPC) of 1.10% (95%CI 0.45%-1.76%). 5 key findings →
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is characterized by amyloid-beta (Aβ) accumulation and neuroinflammation. 4 key findings →
Trajectories of systolic BP were separated markedly around 25 to 45 years of age, with the group below the median of cognition score having higher levels of systolic BP than the group above the median. 5 key findings →
Limbic predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) is highly prevalent in late life and a common co-pathology with Alzheimer's disease neuropathologic change (ADNC). 1 key finding →
APPLE-Tree is an accessible intervention associated with small improvements in cognition, although these results were not statistically significant. 1 key finding →
✓ Peer-reviewedalzhub usefulness score 67 out of 100.·JAMA Neurology·2025-11-01
In this systematic review and meta-analysis, estimates indicate that FTD is comparable in frequency to dementia with Lewy bodies and occurs at higher rates than progressive supranuclear palsy, corticobasal syndrome, and amyotrophic lateral sclerosis. 5 key findings →
✓ Peer-reviewedalzhub usefulness score 67 out of 100.·JAMA psychiatry·2025-01-01
Of 486 older adults who provided consent, 375 (with rMDD, MCI, or both) received at least 1 intervention session (mean [SD] age, 72.2 [6.4] years; 232 women [62%] and 143 men [38%]). 3 key findings →
✓ Peer-reviewedalzhub usefulness score 67 out of 100.·The Lancet. Neurology·2025-11-01
Understanding the neuropathological effects of amyloid β (Aβ)-targeting therapies and amyloid-related imaging abnormalities (ARIA) in Alzheimer's disease is critical for optimising treatment efficacy and patient outcomes. 4 key findings →
Review of the evidence and recommendations are provided for the diagnosis of osteoporosis, fracture-risk assessment and intervention thresholds, management of vertebral fractures, non-pharmacological and pharmacological treatments, including duration and monitoring of anti-resorptive therapy, glucocorticoid-induced osteoporosis, as well as models of care for fracture prevention. 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC
(65.6% of the library) and OpenAlex (16.2%),
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.
1,048 records (3.3% of the
library) are not peer-reviewed — 973 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.