Alzheimer's disease (AD) is a complex genetic disorder with no effective treatments. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cross-sectional data, including CSF analytes, molecular imaging of cerebral fibrillar β-amyloid (Aβ) with PET using the [ 11 C] benzothiazole tracer Pittsburgh compound B (PiB), MRI-based brain structures, and clinical/cognitive outcomes harmonized from 8 studies, collectively involving 3,284 cognitively normal individuals 18 to 101 years of age, were analyzed. 4 key findings →
Design: cross-sectional Evidence: low
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The 21-point Brain Care Score (BCS) was developed through a modified Delphi process in partnership with practitioners and patients to promote behavior changes and lifestyle choices in order to sustainably reduce the risk of dementia and stroke. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
TabCAT tests showed good convergent validity with traditional pen-and-paper tests. 5 key findings →
Design: longitudinal study Participants: 146 Evidence: moderate
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The final model, which included age, systolic blood pressure >140, atrial fibrillation, and tobacco use, achieved an AUC of 0.83 (95% CI 0.75-0.90) in the development cohort (N=143, 62.4±12.6 years, 44% female, 36% non-white race) and 0.85 (95% CI 0.77-0.92) in the validation cohort (N=127, 65.2±16.8 years, 51% female, 34% non-white race), with similar results using WMH measurements derived from cMRI (N=120, p=0.98, AUC=0.86, 95% CI 0.77-0.93). 5 key findings →
Participants: 143 Evidence: moderate
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We conclude that PiB-positron emission tomography can detect cerebrovascular beta-amyloid and may serve as a method for identifying the extent of CAA in living subjects.
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Among nursing home residents with dementia, discontinuing long-term antipsychotic medication use was associated with lower risks of hospitalization, pneumonia, and urinary tract infections, suggesting clinical benefits in this population. 4 key findings →
Design: cohort Participants: 4,222 Evidence: moderate
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52/100
Defining a signature of cortical regions of interest preferentially affected by Alzheimer disease (AD) pathology may offer improved sensitivity to early AD compared to hippocampal volume or mesial temporal lobe alone. 3 key findings →
Participants: 588 Evidence: moderate
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52/100
The presubiculum captures unique AD-related biological variation that is not reflected in total hippocampal volume. 2 key findings →
Participants: 127 Evidence: low
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Endocytosis is critical to the function and fate of molecules important to Alzheimer's disease (AD) etiology, including the beta protein precursor (betaPP), amyloid beta (Abeta) peptide, and apolipoprotein E (ApoE). 3 key findings →
Evidence: low
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Late-onset Alzheimer's disease (AD) is 50-70% heritable with complex genetic underpinnings. 4 key findings →
Participants: 104 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although observational data cannot establish causality, our findings are consistent with the hypothesis that decreasing cardiac function, even at normal cardiac index levels, is associated with accelerated brain aging. 5 key findings →
Evidence: moderate
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The AS task is a useful measure of executive function across the AD spectrum. 1 key finding →
Participants: 182 Evidence: low
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The prevalence of dementia in Latin America and the Caribbean is growing rapidly, increasing the burden placed on caregivers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The clinical prediction model can play a beneficial role in decision-making for preventative measures for patients at risk of developing a delirium. 3 key findings →
Participants: 207 Evidence: low
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So-called idiopathic rapid eye movement (REM) sleep behaviour disorder (RBD), formerly seen as a rare parasomnia, is now recognized as the prodromal stage of an α-synucleinopathy. 5 key findings →
Evidence: low
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Gene defects play a major role in the pathogenesis of degenerative disorders of the nervous system. 3 key findings →
Evidence: low
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Research increasingly suggests that subjective cognitive decline (SCD) in older adults, in the absence of objective cognitive dysfunction or depression, may be a harbinger of non-normative cognitive decline and eventual progression to dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tests of both episodic memory and executive function are predictors of time to progression from mild impairment to a clinical diagnosis of Alzheimer disease. 1 key finding →
Participants: 235 Evidence: low
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Proteomic studies for Alzheimer's disease (AD) are instrumental in identifying AD pathways but often focus on single tissues and sporadic AD cases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral amyloid angiopathy (CAA) is driven by vascular Aβ (amyloid-beta) deposition, which can be detected as reduced Aβ species in cerebrospinal fluid (CSF). 4 key findings →
Design: cross-sectional Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Several mutations in the amyloid precursor protein (APP) gene have been found to associate with pathologic deposition of the beta-amyloid peptide (Abeta) in neuritic plaques or in the walls of cerebral vessels. 4 key findings →
Evidence: low
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Cerebral amyloid angiopathy is a common cause of spontaneous lobar hemorrhage in elderly patients. 4 key findings →
Evidence: low
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The symptoms of Alzheimer disease reflect a loss of neural circuit integrity in the brain, but neurons do not work in isolation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In Alzheimer's disease (AD), pathological tau protein shows a progressive accumulation of post-translational modifications (PTMs), reflecting disease severity, progression, and prion-like activity. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Where “Free full text” comes from
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 tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up 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.
See the full, machine-readable breakdown of this library's coverage →