28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Mutations in the Integral membrane protein 2B (ITM2B) gene are linked to the development of familial British and Danish dementias, two relatively early-onset dementia disorders known also to be associated with Tau neurofibrillary tangles (NFTs). 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
For the association analysis of whole-genome sequencing (WGS) studies, we propose an efficient and fast spatial-clustering algorithm. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Early-onset cataract and Alzheimer's disease occur with high frequency in Down syndrome (trisomy 21), the most common chromosome duplication in human live births. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The human ETS2 gene, a member of the ETS gene family, with sequence homology with the retroviral ets sequence of the avian erythroblastosis retrovirus E26 is located on chromosome 21. 5 key findings →
Evidence: low
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The BACE1 gene encodes the beta-site APP-cleaving enzyme 1 and has been associated with Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study aimed to investigate the bidirectional causal relationship between celiac disease (CD) and the risk of Alzheimer disease (AD) or frontotemporal dementia (FTD) using Mendelian randomization (MR), in order to clarify prior inconsistent findings. 3 key findings →
Evidence: low
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APOE and PICALM are prominent risk genes for late-onset Alzheimer’s disease (AD). 5 key findings →
Evidence: low
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Eight proteins were differently expressed in carriers with larger WMH volumes (Figure 1). 5 key findings →
Evidence: low
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Frontotemporal lobar degeneration (FTLD) represents a heterogeneous group of neurodegenerative disorders with overlapping clinical, pathological, and genetic characteristics. 1 key finding →
Evidence: low
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We found a moderate yet significant reduction in Aβ plaque size in male 5×FAD × mAPPA673T compared with 5×FAD mice. 3 key findings →
Evidence: low
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Neuroinflammation plays a key role in Alzheimer's disease (AD), but the actions of microglial mediators may vary across stages of Aβ pathology. 1 key finding →
Evidence: low
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Most Alzheimer disease (AD) susceptibility genes have poorly understood roles in the central nervous system (CNS). 4 key findings →
Evidence: low
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The PS19 mouse model expressing the P301S tau mutation exhibits tau pathology associated with frontotemporal dementia. 5 key findings →
Evidence: low
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HTT IAs carriers patients exhibited decreased survival after disease onset compared to non-carriers. 5 key findings →
Evidence: moderate
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The apolipoprotein E4 (APOE4) variant is the strongest genetic risk factor for Alzheimer disease (AD), while the APOE2 allele is protective. 1 key finding →
Evidence: low
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Reduced telomere length has recently been reported in T lymphocytes of individuals with trisomy 21 Down syndrome (DS) and dementia. 2 key findings →
Evidence: low
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Down syndrome (DS) is an aneuploidy syndrome that is caused by trisomy for human chromosome 21 resulting in a characteristic cognitive and behavioral phenotype, which includes executive functioning and adaptive behavior difficulties possibly due to prefrontal cortex (PFC) deficits. 1 key finding →
Evidence: low
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Human trisomy 21 is the most frequent live-born human aneuploidy and causes a constellation of disease phenotypes classified as Down syndrome, which include heart defects, myeloproliferative disorder, cognitive disabilities and Alzheimer-type neurodegeneration. 2 key findings →
Evidence: low
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The APOE (apolipoprotein E) ε4 allele is the strongest known genetic risk factor for sporadic Alzheimer disease (AD) and for brain amyloidosis, an early marker of disease pathophysiology. 4 key findings →
Evidence: low
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These findings suggest that sexual differentiation in early life has modest effects on adult development of AD in females, a relationship that appeared stronger in the context of APOE4 . 4 key findings →
Evidence: low
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Our findings highlight the potential of diverse genomic backgrounds to uncover protective genetic factors, such as the African-specific protective PSG2 locus, found to confer a protective effect among APOE4 carriers. 1 key finding →
Evidence: low
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In the colocalization of cis-eQTL and GWAS signals for Hispanics, we observed a high posterior probability (posterior prob = 0.9947) for the upstream gene variant rs755980338 on chromosome 11, which locally regulates EHD1 gene (GWAS p-value = 0.009, cis-eQTL p-value = 0.0041). 5 key findings →
Evidence: low
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Fifty-four participants (~8% response rate) from the MindCrowd web-based cohort (mean age of 62.39 years; 39 females; and 23 APOE ε4 carriers) completed 75 trials of Super G. Results show that Super G performance was significantly associated with each of the targeted risk factors. 5 key findings →
Evidence: moderate
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Spatial transcriptomics (ST) data provide spatially informed gene expression profiles. 5 key findings →
Evidence: low
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MTX46943-mediated TREM2 activation leads to TREM2/DAP12 receptor complex formation and stabilizes surface location required for downstream signaling and microglia activation. 5 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.
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 →