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 826–850 of 2,047 studies published 2026(page 34 of 82)· 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.
These findings suggest probable amyloid association with early microglial activation, while tau pathology is closely tied to wider distribution of neuroinflammation. 3 key findings →
Autologous hematopoietic stem/progenitor cell (HSC)–gene therapy (GT) represents a promising therapeutic option for progranulin (PGRN)–related neurodegenerative diseases due to mutations in the PGRN encoding gene ( GRN ), such as frontotemporal dementia (FTD) and neuronal ceroid lipofuscinosis 11 (CLN11). 1 key finding →
Across diverse viral infections, strong convergence was observed in innate immune activation pathways, including microglial priming and NLRP3 inflammasome signaling, accompanied by chronic production of proinflammatory cytokines (IL-1β, TNF-α, IFN-γ). 5 key findings →
Vascular dementia (VaD) is a leading cause of cognitive decline and arises from heterogeneous cerebrovascular pathologies, most commonly cerebral small vessel disease and chronic cerebral hypoperfusion. 1 key finding →
✓ Peer-reviewedalzhub usefulness score 39 out of 100.·Brain Pathology·2026-02-09
Synaptic loss in the (para)hippocampus is a major contributor to cognitive decline in Alzheimer's disease (AD), yet its regional specificity and pathological correlates remain poorly understood. 5 key findings →
Cognitive interventions, including cognitive stimulation therapy, cognitive rehabilitation and cognitive training, are increasingly recommended as key components of non-pharmacological post-diagnostic support for people with dementia. 5 key findings →
✓ Peer-reviewedalzhub usefulness score 39 out of 100.·Palliative Medicine·2026-02-14
End-of-life topics were discussed in 36% of consultations (in regional hospitals, 53%; in academic settings, 27%), and predominantly during diagnostic consultations (54%). 5 key findings →
In part 1 of the study, the patients with CSVD showed significant differences in Montreal Cognitive Assessment (MoCA), Auditory Verbal Learning Test (AVLT)-study, AVLT-immediate, AVLT-delay, AVLT-recognition, Trail Making Test (TMT)-A, TMT-B, and Verbal Fluency Test -fruits/vegetables compared with HCs. 5 key findings →
Despite advances in disease-modifying treatments, significant barriers in the evaluation and clinical management of people with early Alzheimer's disease (AD) remain. 1 key finding →
Counties had a mean prevalence of 65.3 per 1,000 (SD 15.5) for highly likely ADRD and 123.5 per 1,000 (SD 27.0) for all determinations. 5 key findings →
Participants’ motivations for testing and long-term adaptation to the results were strongly shaped by cognitive concerns and personal experiences of dementia in relatives. 5 key findings →
✓ Peer-reviewedalzhub usefulness score 38 out of 100.·Medicine·2026-01-30
To evaluate the possible causality between Alzheimer disease (AD) and delirium, a two-sample Mendelian randomization (MR) method and gene colocalization strategy were employed. 4 key findings →
The blood-brain barrier (BBB) displays a highly organized and complex structure, which is important for maintaining brain homeostasis and protecting the brain from foreign molecules or pathogens. 5 key findings →
Alzheimer's disease (AD) and related dementias (ADRD) are neurodegenerative conditions that cause gradual deterioration of cognition, memory and language in the elderly. 1 key finding →
✓ Peer-reviewedalzhub usefulness score 38 out of 100.·Biomedicines·2026-02-16
Across AD, ALS, and FTD, a convergent multimorbidity architecture centered on a shared metabolic and immune core was identified, accompanied by prominent neurobehavioral processes and intermediate systems including gastrointestinal, endocrine, hematological, hepatic, and sensory pathways. 5 key findings →
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia worldwide and is associated with substantial morbidity and mortality, including stroke, systemic embolism, heart failure, and dementia. 1 key finding →
The model incorporating age, brain volume, functional, and radiomics features demonstrated the highest predictive performance for SCD progression in training (C-index: 0.962; 95 % CI: 0.95-0.98) and testing (C-index: 0.911; 95 % CI: 0.861-0.968) sets. 5 key findings →
Median serum levels of tau variants were increased in patients with multiple traumatic injuries at day 0 compared with controls (t-tau: 43 [IQR, 21-95] vs 3 [IQR, 3-5] pg/mL; BD-tau: 78 [IQR, 30-343] vs 2 [IQR, 2-3] pg/mL; p-tau231: 61 [IQR, 21-79] vs 2 [IQR, 1-3] pg/mL; all, P < .001). 2 key findings →
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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.