27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Biological staging of individuals with Alzheimer's disease (AD) may improve diagnostic and prognostic workup of dementia in clinical practice and the design of clinical trials. 4 key findings →
Design: longitudinal study Participants: 426 Evidence: moderate
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At baseline, 2,279 dementia-free participants with available blood samples were included (median age 72 (interquartile range, 61-81) years; 62% female). 4 key findings →
Design: cohort Participants: 2,279 Evidence: moderate
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The BioFINDER-2 main cohort included 872 participants, with an additional 156 participants in the Knight ADRC cohort for independent validation. 2 key findings →
Design: cohort Participants: 1,028 Evidence: high
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Men have a shorter life expectancy compared with women but the underlying factor(s) are not clear. 4 key findings →
Design: case-control study Evidence: moderate
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Evidence regarding the clinical validity of blood biomarkers of Alzheimer's disease (AD) in the general population is limited. 3 key findings →
Evidence: moderate
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A total of 3363 adults were enrolled in SNAC-K (73.3% participation rate). 5 key findings →
Design: cohort study Participants: 3,363 Evidence: moderate
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Cerebrospinal fluid (CSF) α-synuclein (α-syn) seed amplification assays (SAAs) can detect Lewy body pathology (LBP) with high accuracy but are invasive and costly. 2 key findings →
Design: cohort Participants: 1,567 Evidence: early
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Using the Swedish BioFINDER-2 cohort [n = 1702, 50.7% male, mean (standard deviation) age 68.4 (12.2) years], we compared the associations between tau/Aβ-PET load and fluid biomarkers alone versus biomarkers in a ratio with a reference protein (Aβ40 or np-tau) in univariate linear regression models. 5 key findings →
Design: longitudinal study Participants: 1,702 Evidence: moderate
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Neurodegenerative diseases (NDs), such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and frontotemporal dementia (FTD), exhibit distinct yet overlapping pathological mechanisms. 2 key findings →
Participants: 10,527 Evidence: low
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Co-pathology is a common feature of neurodegenerative diseases that complicates diagnosis, treatment and clinical management. 4 key findings →
Design: cross-sectional Participants: 17,187 Evidence: early
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Over a mean follow-up of 8.4 years (range, Conclusions and relevance This cohort study of older adults found that adherence to a dietary pattern with lower inflammatory potential was associated with lower dementia risk among individuals with AD pathology and broader neurobiological risk. 3 key findings →
Design: cohort Participants: 1,865 Evidence: early
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The APOE locus is the strongest genetic factor for Alzheimer's disease, with ε4 increasing and ε2 decreasing risk, yet the basis of these opposing effects remains unclear. 1 key finding →
Design: cohort Evidence: moderate
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Disease staging, whereby the spatial extent and load of brain pathology are used to estimate the severity of Alzheimer disease (AD), is pivotal to the gold-standard neuropathological diagnosis of AD. 5 key findings →
Evidence: low
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Moreover, there is limited knowledge regarding associations with domain-specific cognitive decline and modifying effects of key individual characteristics. 4 key findings →
Design: cohort study Participants: 2,008 Evidence: moderate
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Population health research is increasingly focused on the genetic determinants of healthy ageing, but there is no public resource of whole genome sequences and phenotype data from healthy elderly individuals. 4 key findings →
Evidence: moderate
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Diet can impact cognitive aging, but comprehensive data from human studies is lacking and the underlying biological mechanisms are still not fully understood. 4 key findings →
Design: cross-sectional Participants: 1,907 Evidence: low
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Blood biomarkers of Alzheimer's disease (AD) are promising for dementia prediction, but their association with progression across intermediate stages of cognitive decline in the general population remains unclear. 3 key findings →
Evidence: moderate
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Our results provide a framework for precision nutrition approaches aiming to modulate the AD gut microbiota. 2 key findings →
Participants: 27 Evidence: low
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Alzheimer's disease (AD) is a debilitating neurodegenerative disorder with a global impact, yet its pathogenesis remains poorly understood. 3 key findings →
Evidence: low
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< 0.001), with the automated approach more likely to classify a scan as tau negative and lower agreement between methods in more severe cases and AD clinical variants. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
β-Site amyloid precursor protein cleaving enzyme1 (BACE1) is one of the key enzymes involved in the processing of the amyloid precursor protein (APP) and formation of amyloid β peptide (Aβ) species. 4 key findings →
Design: clinical trial Evidence: low
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Alzheimer's disease (AD) is a common and increasing societal problem due to the extending human lifespan. 5 key findings →
Evidence: low
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Our results provide further insights into the architecture and underlying mechanisms of complex rearrangements on acrocentric chromosomes. 3 key findings →
Evidence: low
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The amyloid precursor protein intracellular domain (AICD), a cleavage product of amyloid precursor protein implicated in Alzheimer disease and amyloid lateral sclerosis, is a functionally important but structurally elusive intrinsically disordered protein. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Mediterranean diet (MedDiet) is among the most extensively studied dietary patterns and has been consistently associated with reduced risk of all-cause mortality, cardiovascular disease, metabolic disorders, cognitive decline and several types of cancers. 2 key findings →
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →