27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Mass spectrometry-based proteomics empowers deep profiling of proteome and protein posttranslational modifications (PTMs) in Alzheimer's disease (AD). 5 key findings →
Design: meta-analysis Participants: 12,017 Evidence: high
Full summary, score breakdown and related studies → Original source
Hearing loss is one of the top contributors to years lived with disability and is a risk factor for dementia. 3 key findings →
Design: meta-analysis Participants: 723,266 Evidence: high
Full summary, score breakdown and related studies → Original source
Identifying ancestry-specific molecular profiles of late-onset Alzheimer's Disease (LOAD) in brain tissue is crucial to understand novel mechanisms and develop effective interventions in non-European, high-risk populations. 3 key findings →
Design: meta-analysis Participants: 731 Evidence: high
Full summary, score breakdown and related studies → Original source
Three AD subtypes were identified. Subtype 1, enriched in RNA metabolism pathways, showed the mildest atrophy and slowest cognitive decline. 5 key findings →
Design: longitudinal study Participants: 550 Evidence: moderate
Full summary, score breakdown and related studies → Original source
To date, DNA methylation is the best characterized epigenetic modification in Alzheimer's disease. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
We initiated the systematic profiling of the dorsolateral prefrontal cortex obtained from a subset of autopsied individuals enrolled in the Religious Orders Study (ROS) or the Rush Memory and Aging Project (MAP), which are jointly designed prospective studies of aging and dementia with detailed, longitudinal cognitive phenotyping during life and a quantitative, structured neuropathologic examination after death. 5 key findings →
Design: longitudinal study Participants: 2,090 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Overall, our analysis revealed a robustly defined age-related co-methylation module that is present in multiple human tissues, including blood and brain. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Oligodendrocyte dysfunction has been implicated in the pathogenesis of neurodegenerative diseases, so understanding oligodendrocyte activation states would shed light on disease processes. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
One hundred and fifty probe-sets form an accurate classifier of young versus older muscle tissue and this healthy ageing RNA classifier performed consistently in independent cohorts of human muscle, skin and brain tissue (n = 594, AUC = 0.83-0.96) and thus represents a biomarker for biological age. 5 key findings →
Design: case-control study Participants: 594 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive cognitive impairment and neurodegeneration. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nine female-specific associations were identified and replicated, involving ADGRV1, OR3A3, IFI27L1, LYRM1, STAP2, TSTD2, PDYN, and TMEM50B. We observed the preponderance of protective female-specific associations in neurons. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Chronological age offers an imperfect estimate of the molecular changes that occur with aging. 4 key findings →
Participants: 4,000 Evidence: low
Full summary, score breakdown and related studies → Original source
DNA methylation is a vital component of the epigenetic machinery that orchestrates changes in multiple genes and helps regulate gene expression in all known vertebrates. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sporadic Alzheimer's disease (AD) exclusively affects elderly people. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Six miRNAs (hsa-miR-128-3p, hsa-miR-144-5p, hsa-miR-146a-5p, hsa-miR-26a-5p, hsa-miR-29c-3p and hsa-miR-363-3p) were downregulated in the blood of individuals with low cognitive performance on the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). 4 key findings →
Design: cross-sectional Participants: 830 Evidence: low
Full summary, score breakdown and related studies → Original source
Gaining insight into the downstream consequences of non-coding variants is an essential step towards the identification of therapeutic targets from genome-wide association study (GWAS) findings. 4 key findings →
Participants: 31,684 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) affects half the US population over the age of 85 and is universally fatal following an average course of 10 years of progressive cognitive disability. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Subjective cognitive decline (SCD) is widely regarded as a potential preclinical stage of Alzheimer's disease (AD), yet its genetic basis remains poorly understood. 5 key findings →
Participants: 9,284 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Microglia, the tissue-resident macrophages of the central nervous system (CNS), play critical roles in immune defense, development and homeostasis. 1 key finding →
Participants: 141 Evidence: low
Full summary, score breakdown and related studies → Original source
Translating human genetic findings (genome-wide association studies [GWAS]) to pathobiology and therapeutic discovery remains a major challenge for Alzheimer's disease (AD). 2 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cortical neuron loss is a pathological hallmark of late-onset Alzheimer's disease (AD). 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Fusion of all five data modalities (n = 111) yielded two subtypes (n S1 = 53, n S2 = 58), which were nominally associated with diffuse amyloid plaques; however, this effect was not significant after correction for multiple testing. 5 key findings →
Participants: 111 Evidence: low
Full summary, score breakdown and related studies → Original source
There is currently little information available about how individual cell types contribute to Alzheimer's disease. 4 key findings →
Participants: 13,214 Evidence: low
Full summary, score breakdown and related studies → Original source
Previous genome-wide association studies (GWAS), conducted by our group and others, have identified loci that harbor risk variants for neurodegenerative diseases, including Alzheimer's disease (AD). 5 key findings →
Participants: 2,099 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The relationship between genetic variation and gene expression in brain cell types and subtypes remains understudied. 2 key findings →
Participants: 424 Evidence: low
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 →