28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease is a progressive, irreversible, and fatal disease for which accumulation of amyloid beta is thought to play a key role in pathogenesis. 4 key findings →
Design: clinical trial Participants: 1,638 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The first single-stage individual patient data meta-analysis from randomized double-blind placebo-controlled clinical trials provides evidence to support benefits of antihypertensive treatment in late-mid and later life to lower the risk of dementia. 5 key findings →
Design: meta-analysis Participants: 28,008 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The mean CDR-SB score at baseline was approximately 3.2 in both groups. 2 key findings →
Design: clinical trial Participants: 1,795 Evidence: low
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
We included randomized controlled trials (RCTs) and nonrandomized controlled studies at lower risk of bias comparing ChEI treatment with placebo or usual treatment, for 6 months or longer, in patients with dementia of any type. 5 key findings →
Design: systematic review Participants: 79,153 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The non-linear function indicates that a higher dose is not necessarily better in multidomain interventions. 3 key findings →
Design: randomized controlled trial Participants: 749 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
This study found that CSF-based estimates using adjusted data-driven cutoffs were up to 10% higher than PET-based estimates in people without dementia, whereas the results were similar among people with dementia. 3 key findings →
Design: cross-sectional Participants: 97 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Overall, 2,277 individuals had at least 1 baseline blood biomarker available (n = 357 for CSF subsample, n = 649 for PET subsample), among whom 257 were diagnosed with clinical AD/mixed dementia during follow-up. 2 key findings →
Design: prospective cohort Participants: 357 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the leading cause of dementia, has an estimated heritability of approximately 70% 1 . 3 key findings →
Participants: 32,558 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this genetic association study, a novel variant associated with AD was identified: R251G always coinherited with ε4 on the APOE gene, which mitigates the ε4-associated AD risk. 5 key findings →
Design: case-control study Participants: 37 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among 580 participants (PREVENT-AD, 128; HABS, 153; AIBL, 48; Knight ADRC, 251), mean (SD) age ranged from 67 (5) to 76 (6) years across cohorts, with between 55% (137/251) and 74% (95/128) female participants. 2 key findings →
Design: cohort study Participants: 580 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In DIAD, solanezumab was not associated with ARIA. 5 key findings →
Design: cross-sectional Participants: 52 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study showed that some deficits on IC domains, as measured by simple screening tests and questions, can be associated with higher healthcare costs. 4 key findings →
Design: randomized controlled trial Participants: 442 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
A fully automated computational approach included classical statistical methods, support vector machine procedures, and machine learning techniques (random forest and sequential feature selection procedures). 4 key findings →
Design: cross-sectional Participants: 1,794 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Gonadal development is a complex process that involves sex determination followed by divergent maturation into either testes or ovaries 1 . 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study shows that Hcy levels could modify the association between red blood cell n-3 PUFA and executive function. 2 key findings →
Participants: 1,680 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Baseline plasma MCP-1 levels were associated with longitudinal declines in overall cognitive and episodic memory performance in older adults over a 4-year follow-up. 5 key findings →
Design: longitudinal study Participants: 1,097 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The proposed novel, pragmatic method to determine CSF biomarker cutoffs for AD does not require assessment of other biomarkers or assumptions concerning the clinical diagnosis of patients. 1 key finding →
Participants: 497 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Long-term use of urate-lowering therapies (ULT) may reduce inflammaging and thus prevent cognitive decline during aging. 3 key findings →
Design: randomized controlled trial Participants: 51 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Brain macrophage populations include parenchymal microglia, border-associated macrophages, and recruited monocyte-derived cells; together, they control brain development and homeostasis but are also implicated in aging pathogenesis and neurodegeneration. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The implication of gut microbiota in the control of brain functions in health and disease is a novel, currently emerging concept. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Age-related frailty and disease-related frailty may represent different degrees of frailty severity on a biological level. 5 key findings →
Design: cross-sectional Participants: 1,199 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cardiovascular risk factors and lifestyle factors are associated with an increased risk of cognitive decline and dementia in observational studies, and have been targeted by multidomain interventions. 5 key findings →
Participants: 4,162 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 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.
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 →