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
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Find studies
Showing 2,451–2,475 of 2,931 studies published 2025 · free to read(page 99 of 118)· 30,980 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; 16,452 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.
Our findings support a broader interpretation of TBK1-associated neurodegeneration and highlight the importance of multimodal diagnostic approaches that integrate molecular, genetic, imaging, and neuropathological tools. 2 key findings →
✓ Peer-reviewedalzhub usefulness score 36 out of 100.·Genomic psychiatry :·2025-12-16
Tau, mainly expressed in neurons and less expressed in glial cells (astrocytes and oligodendrocytes) and peripheral tissues, is involved in the assembly and stabilization of microtubules, and other biological processes such as axonal transport, metal ion transport, etc. Dysfunction of tau, caused by mutations, hyperphosphorylation, aggregation, or reduced expression, is closely associated with tauopathies (e.g., Alzheimer disease) and psychiatric disorders. 2 key findings →
Alzheimer's disease (AD) is a neurodegenerative disease, representing the seventh cause of death worldwide and the first cause of dementia. 3 key findings →
✓ Peer-reviewedalzhub usefulness score 36 out of 100.·Aging Cell·2025-06-20
Aging is the greatest risk factor for learning and memory disorders; dementia prevalence significantly increases with age due to numerous molecular changes in the body. 5 key findings →
✓ Peer-reviewedalzhub usefulness score 36 out of 100.·Journal of Neurology·2025-06-21
26% of the participants experienced delirium prior to diagnosis of DLB, with one participant experiencing multiple episodes in the 24 months before diagnosis. 5 key findings →
A longstanding body of public enquiries and research identifies people living with dementia experience systemic inequalities within hospital settings, concluding a focus on improving care cultures is required. 3 key findings →
Improving early detection, management, and treatment of comorbid conditions to dementia in residential care could slow down cognitive and functional decline, and increase residents' quality of life. 5 key findings →
Four GPs and eleven physicians were interviewed, and four major themes emerged: (1) knowledge of best practices of BPSD management, (2) awareness of current challenges in BPSD management, (3) non-involvement, blame shifting and rationalisation: perceived reasons for the current challenges and (4) suggested solutions. 5 key findings →
✓ Peer-reviewedalzhub usefulness score 36 out of 100.·Aging and Disease·2025-01-01
Cerebral small vessel disease (CSVD) is a common disease in older people, characterized by damage to intracranial microvessels, leading to cognitive decline, increased risk of stroke, and dementia. 1 key finding →
With elevated HbA1c, greater LA-derived diol/epoxide ratios were associated with greater WMH volume (β [95% CI] = 0.565 [0.100, 1.030], p = 0.017), lower global BPF (β [95% CI] = -0.476 [-0.903, -0.048], p = 0.029), and poorer memory performance (β [95% CI] = -0.603 [-1.070, -0.136], p = 0.012), such that detrimental associations were observed only in T2DM. 5 key findings →
Autosomal dominant Alzheimer disease (ADAD) is caused by pathogenic variants in the APP, PSEN1 and PSEN2 genes, but a substantial fraction of reported variants is of unknown clinical significance. 4 key findings →
We found that COVID patients initially experienced substantially longer hospital stays (8.3 vs 4.6 days) and higher 30-day mortality (34% vs 5%) compared to patients without COVID. 4 key findings →
Participants racialized as Black living in a county with a history of lynching, disproportionate police killings, and disproportionate jail and prison incarceration were 2.8 (95%CI [-0.003, 5.834]) times more likely to have at least one incident of cognitive impairment between 2008-2020 compared to participants racialized as Black living in a county with a history of lynching and disproportionate police killings but not disproportionate incarceration. 3 key findings →
The current study provides opportunities for safer approaches that using compounds derived from plants and links it to nanotechnology, could be used in the pharmaceutical industry to treat Alzheimer’s disease. 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.
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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC
(65.2% of the library) and OpenAlex (16.4%),
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.
1,042 records (3.4% of the
library) are not peer-reviewed — 967 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.