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
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Find studies
Showing 11,401–11,425 of 27,146 studies marked Peer-reviewed(page 457 of 1086)· 28,180 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; 13,658 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.
✓ Peer-reviewedalzhub usefulness score 49 out of 100.·Cell·2012-03-01
cis-trans isomerization of proteins phosphorylated by proline-directed kinases is proposed to control numerous signaling molecules and is implicated in the pathogenesis of Alzheimer's and other diseases. 5 key findings →
The aim of the study is to evaluate whether depression or apathy in patients with amnestic-mild cognitive impairment (MCI) increases the risk of progressing to Alzheimer's disease (AD). 3 key findings →
There is accumulating evidence that soluble amyloid-beta (Abeta) oligomers, rather than amyloid fibrils, are the principal pathogenic species in Alzheimer disease (AD). 4 key findings →
Nerve growth factor (NGF) is critical for the regulation, differentiation, and survival of basal forebrain cholinergic neurons that degenerate in the late stage of Alzheimer disease (AD). 3 key findings →
Alzheimer's disease (AD) not only involves loss of memory functions, but also prominent deterioration of sleep physiology, which is already evident at the stage of mild cognitive impairment (MCI). 3 key findings →
✓ Peer-reviewedalzhub usefulness score 49 out of 100.·Archives of neurology·2005-11-01
These data provide evidence for clinical and functional heterogeneity among subjects with aMCI and suggest that 18FDG-PET findings combined with memory scores may be useful in predicting short-term conversion to AD. 3 key findings →
We believe this to be the first demonstration of myelin loss in MCI, Alzheimer's disease, and vascular dementia using a method that provides a quantitative magnetic resonance imaging-based measure of myelin. 2 key findings →
TP42/40 demonstrated value in the identification of individuals suffering a-MCI, in the prediction of progression to dementia, and in the detection of underlying AD pathology revealed by FDG-PET, Amyloid-PET and CSF biomarkers, being, thus, consistently associated with all the well-established indicators of AD. 3 key findings →
Alzheimer's disease (AD) is a neurodegenerative disorder accounting for over 50% of all dementia patients and representing a leading cause of death worldwide for the global ageing population. 5 key findings →
Although Alzheimer's disease (AD) is primarily a neurocognitive disorder, it also results in prominent neuropsychiatric symptoms (NPS). 2 key findings →
Recent findings suggest that Alzheimer's disease (AD) is a disconnection syndrome characterized by abnormalities in large-scale networks. 4 key findings →
✓ Peer-reviewedalzhub usefulness score 49 out of 100.·Neurobiology of aging·2005-03-24
Identifying pre-clinical Alzheimer's disease (AD) in subjects with mild cognitive impairment (MCI) is a major issue in clinical diagnosis. 5 key findings →
Our novel neuropsychological approach improved the staging of MCI by (1) capturing individuals at an early symptomatic stage, (2) minimizing false-positive cases, and (3) identifying a late MCI group further along the disease trajectory. 2 key findings →
The combination of neuropsychological tests and P300 measurements proved useful in improving reliability and increasing sensitivity to early cognitive decline or disease progression in AD patients. 3 key findings →
✓ Peer-reviewedalzhub usefulness score 49 out of 100.·Neuron·1995-11-01
Transgenic FVB/N mice overexpressing human (Hu) or mouse (Mo) Alzheimer amyloid precursor protein (APP695) die early and develop a CNS disorder that includes neophobia and impaired spatial alternation, with diminished glucose utilization and astrogliosis mainly in the cerebrum. 4 key findings →
Progressive cerebral deposition of extracellular filaments composed of the beta-amyloid protein (beta AP) is a constant feature of Alzheimer disease (AD). 4 key findings →
The Alzheimer A beta amyloid peptide (A beta) is the principal proteinaceous component of amyloid associated with Alzheimer disease (AD). 4 key findings →
✓ Peer-reviewedalzhub usefulness score 49 out of 100.·Brain research·2008-04-07
We previously reported that intraperitoneal (i.p.) injection (20 mg/kg) of (-)-epigallocatechin-3-gallate (EGCG), the main polyphenolic constituent of green tea, decreased beta-amyloid (Abeta) levels and plaques via promotion of the non-amyloidogenic alpha-secretase proteolytic pathway in "Swedish" mutant amyloid precursor protein overexpressing (APPsw, Tg) mice. 4 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC
(61.7% of the library) and OpenAlex (18.1%),
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.
1,034 records (3.7% 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.