28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The apolipoprotein E4 (APOE4) allele is associated with an increased risk of Alzheimer disease and a decreased risk of glaucoma, but the underlying mechanisms remain poorly understood. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Disrupted iron homeostasis is associated with several neurodegenerative diseases, including Alzheimer's disease (AD), and may be partially modulated by genetic risk factors. 4 key findings →
Participants: 27,535 Evidence: low
Full summary, score breakdown and related studies → Original source
Mutation screening revealed a novel probably pathogenic mutation (PSEN1 p.Leu232Phe). 3 key findings →
Participants: 450 Evidence: low
Full summary, score breakdown and related studies → Original source
We investigated which factors might explain the differences between the frequencies of brain β-amyloid (Aβ) deposition in Korean and European cognitively normal individuals (CNs). 1 key finding →
Participants: 434 Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 37 SuperAgers (73% female, mean [standard deviation] 82.7 [2.8] years old) and 35 controls (54% female, 83.7 [4.3] years old) were included. 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
Hippocampal subfield atrophy is a prime structural change in the brain, associated with cognitive aging and neurodegenerative diseases such as Alzheimer's disease. 3 key findings →
Participants: 1,086 Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical genetic diagnosis was achieved in 7 of 50 (14%) of the patients, with a further 8 patients (16%) found to have established risk factors which may have contributed to their EOD. 5 key findings →
Participants: 50 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We performed a genome-wide association study (GWAS) of human extreme longevity (EL), defined as surviving past the 99th survival percentile, by aggregating data from four centenarian studies. 4 key findings →
Participants: 2,304 Evidence: low
Full summary, score breakdown and related studies → Original source
Using the data from the Alzheimer's Disease Neuroimaging Initiative (ADNI), we performed a genome-wide association study (GWAS) between 565,373 single nucleotide polymorphisms (SNPs) and 16 key AD biomarkers from 1,576 subjects at four visits. 5 key findings →
Participants: 1,576 Evidence: low
Full summary, score breakdown and related studies → Original source
Dysregulation of sphingomyelin and ceramide metabolism have been implicated in Alzheimer's disease. 1 key finding →
Participants: 1,576 Evidence: low
Full summary, score breakdown and related studies → Original source
Robust and accessible biomarkers that can capture the heterogeneity of Alzheimer's disease and its diverse pathological processes are urgently needed. 2 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (APOE) plays a pivotal role in lipid including cholesterol metabolism. 2 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia and cognitive disorders are major aging-associated pathologies. 4 key findings →
Participants: 68 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia with advancing age as its strongest risk factor. 3 key findings →
Participants: 47 Evidence: low
Full summary, score breakdown and related studies → Original source
The biological processes that are disrupted in the Alzheimer's disease (AD) brain remain incompletely understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Activation of microglia is a prominent pathological feature in tauopathies, including Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical outcomes of severe acute respiratory syndrome 2 (SARS-CoV-2) infection are highly heterogeneous, ranging from asymptomatic infection to lethal coronavirus disease 2019 (COVID-19). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
APOE4 is the strongest genetic risk factor for Alzheimer's disease 1-3 . 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The human brain vasculature is of great medical importance: its dysfunction causes disability and death 1 , and the specialized structure it forms-the blood-brain barrier-impedes the treatment of nearly all brain disorders 2,3 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia in Alzheimer's disease progresses alongside neurodegeneration 1-4 , but the specific events that cause neuronal dysfunction and death remain poorly understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Macrophages are important players in the maintenance of tissue homeostasis 1 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Immature dentate granule cells (imGCs) arising from adult hippocampal neurogenesis contribute to plasticity and unique brain functions in rodents 1,2 and are dysregulated in multiple human neurological disorders 3-5 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Liver-generated plasma apolipoprotein E (apoE) does not enter the brain but nonetheless correlates with Alzheimer's disease (AD) risk and AD biomarker levels. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As the size of genome-wide association studies increase, the number of associated trait loci identified inevitably increase. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These results indicate that the compromised function of microglia in AD could be improved by controlled activation of PIEZO1 channels resulting in alleviated Aβ burden. 5 key findings →
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 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 →