27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
CTS significantly attenuated atherosclerotic plaque formation and enhanced plaque stability in ApoE −/− mice by inhibiting the expression of lectin‐like ox LDL receptor‐1 ( LOX ‐1) and MMP ‐9, as well as inhibiting reactive oxygen species ( ROS ) generation and NF‐κB activation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Physiologically, the retinal pigment epithelium (RPE) expresses immunosuppressive signals such as FAS ligand (FASL), which prevents the accumulation of leukocytes in the subretinal space. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A marked reduction in atherosclerotic lesions was observed. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral amyloid angiopathy (CAA) is caused by the cerebrovascular deposition of Alzheimer amyloid beta protein (Abeta) and shows an increased incidence in carriers of the apolipoprotein E (APOE) epsilon4 genotype. 1 key finding →
Evidence: low
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Age of onset (AO) of Huntington disease (HD) is known to be correlated with the length of an expanded CAG repeat in the HD gene. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
H]UCB-J was found to be reduced in frontal cortex from patients with AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hierarchical linear regression was used to assess an incremental contribution of the set of inflammatory markers’ PRS to explaining VF variance compared to the null model. 5 key findings →
Participants: 135 Evidence: low
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Previous observational studies demonstrated that lung cancer and both Alzheimer disease (AD) and Parkinson disease (PD) may be related. 5 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
Full summary, score breakdown and related studies → Original source Free full text
APOE and PICALM are prominent risk genes for late-onset Alzheimer’s disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The knockdown of α7 nAChR in the hippocampus of adult mice rapidly induced cognitive deficits, impairments in learning and memory, and led to the increase of amyloid-β levels, Tau protein aggregation, neuronal damage, and the activation of astrocytes and microglia. 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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The IVW analysis indicated that antithrombotic agents (odds ratio [OR] = 2.12, 95% confidence interval [CI] = 1.03-4.34, p = 0.04), HMG CoA reductase inhibitors (OR = 1.36, 95% CI = 1.07-1.72, p = 0.01), and salicylic acid and derivatives (OR = 2.77, 95% CI = 1.44-5.32, p = 0.002) are a strong risk factor for dementia with Lewy bodies (DLB); diuretics (OR = 1.13, 95% CI = 1-1.27, p = 0.047) and calcium channel blockers (OR = 1.16, 95% CI = 1.04-1.29, p = 0.007) might be a risk factor for vascular dementia; thyroid preparations (OR = 1.03, 95% CI = 1.01-1.06, p = 0.01), diuretics (OR = 1.06, 95% CI = 1.02-1.11, p = 0.004), and immunosuppressants (OR = 1.07, 95% CI = 1.01-1.12, p = 0.001), are a risk factor for frontotemporal dementia; HMG CoA reductase inhibitors is a risk factor for dementia in Alzheimer disease (OR = 1.32, 95% CI = 1.05-1.65, p = 0.01). 5 key findings →
Evidence: low
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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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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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Neben ihrer Wirkung auf Gewichtskontrolle und kardiometabolische Parameter könnten GLP-1RA auch die endokrine Funktion von Adipozyten sowie die chronische Inflammation bei der Adipositas und damit die Entstehung adipositasassoziierter Tumoren modulieren. 5 key findings →
Participants: 3,021,508 Evidence: low
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The role of noise pollution as a risk factor for Alzheimer disease (AD) is unclear, with observational studies yielding conflicting results susceptible to confounding and reverse causality. 3 key findings →
Evidence: low
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The onset and sustenance of Alzheimers and Parkinsons is solely dependent on the driving power of the immune cytokine interleukin-1 beta (IL-1β), arising from neuronal distress and release of sAPPα, which activates microglia for synthesis and release of IL-1β driving synthesis of βAPP, Aβ plaques and synthesis and activation of MAPKp38 for phosphorylation of tau for neurofibrillary tangle formation in Alzheimers and for a-synuclein for formation of Lewy bodies in Parkinsons. 1 key finding →
Evidence: low
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Alzheimer disease (AD) is a neurodegenerative disorder characterized by amyloid plaque deposition, neurofibrillary tangles, and chronic neuroinflammation. 3 key findings →
Evidence: low
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Poly(ADP-ribosyl)ation (PARylation), a crucial post-translational modification, is catalyzed by ADP-ribosyltransferases (ARTs) and has significant implications in various cellular processes, including DNA damage response, cell signaling, and immune processes. 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 →