27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
A rare variant in TREM2 (p.R47H, rs75932628) was recently reported to increase the risk of Alzheimer's disease (AD) and, subsequently, other neurodegenerative diseases, i.e. frontotemporal lobar degeneration (FTLD), amyotrophic lateral sclerosis (ALS), and Parkinson's disease (PD). 4 key findings →
Design: meta-analysis Participants: 828 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis. 2 key findings →
Participants: 8,074 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma markers of inflammation and complement dysregulation support diagnosis and outcome prediction in AD and MCI. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
& aims The combination of atezolizumab and bevacizumab (atezo+bev) is the current standard of care for advanced hepatocellular carcinoma (HCC), providing a median overall survival (OS) of 19.2 months. 4 key findings →
Participants: 317 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
During the past decade, a conceptual shift occurred in the field of Alzheimer's disease (AD) considering the disease as a continuum.
Full summary, score breakdown and related studies → Original source Free full text
This study showed that plasma metabolites have the potential to match the AUC of well-established AD CSF biomarkers in a relatively small cohort. 4 key findings →
Participants: 883 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Dysfunction of immune and vascular systems has been implicated in aging and Alzheimer disease; however, their interrelatedness remains poorly understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Machine learning (ML) on structural MRI data shows high potential for classifying Alzheimer's disease (AD) progression, but the specific contribution of brain regions, demographics, and proteinopathy remains unclear. 5 key findings →
Design: cross-sectional Participants: 568 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Amyloid pathology is associated with changes in structural MRI measures in CN and MCI. 3 key findings →
Participants: 337 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The study included 25 patients with iCAA (age, 44±11 years), 31 patients with sCAA (age, 75±5 years), 28 patients with AD (age, 71±8 years) and 30 controls (age, 72±8 years) from 9 case descriptions and 1 cohort study. 5 key findings →
Design: cohort study Participants: 25 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Genome-wide association studies have led to numerous genetic loci associated with Alzheimer's disease (AD). 2 key findings →
Participants: 2,247 Evidence: low
Full summary, score breakdown and related studies → Original source
Several studies, including genome wide association studies (GWAS), have strongly suggested a central role for the ATP-binding cassette transporter subfamily A member 7 (ABCA7) in Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is associated with the accumulation of β-amyloid (Aβ) as senile plaques in the brain, thus leading to neurodegeneration and cognitive impairment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We showed that the sinergistic combination of the histone deacetilase inhibitor MS-275 with the sirtuin 1 activator resveratrol, at very low doses, restores normal RelA acetylation and elicit neuroprotection in mice subjected to transient middle cerebral artery occlusion (tMCAO) and primary cortical neurons exposed to oxygen-glucose-deprivation (OGD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundPathogenic variants in GCH1 have been associated with Parkinsons disease (PD), but the clinical phenotype and longitudinal disease course of GCH1-associated PD remain incompletely characterized. 5 key findings →
Design: longitudinal study Participants: 22,825 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
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.
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.
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.
See the full, machine-readable breakdown of this library's coverage →