27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Emerging evidence transcends the traditional central nervous system (CNS)-centric perspective, revealing that neutrophils, red blood cells (RBCs), and platelets may play critical roles in AD pathogenesis by modulating systemic inflammatory responses, disrupting blood-brain barrier integrity, and participating in the CNS-peripheral interactions. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is neuropathologically characterized by neuritic plaques and neurofibrillary tangles. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Forced overexpression of wild-type Alzheimer amyloid precursor protein (APP) causes postmitotic neurons to degenerate. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
APOE and PICALM are prominent risk genes for late-onset Alzheimer’s disease (AD). 5 key findings →
Evidence: low
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The accuracy of α-synuclein-SAA for DLB was 87% (95% confidence interval [CI]: 77% to 98%) in CSF, 85% (95% CI: 75% to 98%) in skin, 58% (95% CI: 47% to 69%) in olfactory mucosa, and 59% (95% CI: 51% to 66%) in urine. 5 key findings →
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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Most Alzheimer disease (AD) susceptibility genes have poorly understood roles in the central nervous system (CNS). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Studies were undertaken to assess the extent to which messenger RNA prepared from the postmortem Alzheimer's disease (AD) brain can be used for the successful preparation of a recombinant cDNA library. 2 key findings →
Evidence: low
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Mutations in the presenilin 1 (PS1) gene (PSEN1) are associated with familial Alzheimer disease (FAD). 4 key findings →
Evidence: low
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Among 15,346 White, 829 Latino, 637 Black/African American, and 321 Asian individuals, 51% were female, mean age was 75.7 years, 535 (3.8%) resided in ADI 91 to 100 decile, and 61.6% were amyloid PET positive. 3 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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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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BackgroundEpigenetic mechanisms, particularly histone modifications at gene promoters, are crucial for controlling gene transcription. 4 key findings →
Evidence: low
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This report highlights a case of relapsing remitting rapidly progressive dementia due to cerebral amyloid angiopathy-related inflammation (CAA-ri), focusing on the diagnostic challenges and the dramatic response to corticosteroid treatment. 1 key finding →
Evidence: low
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Cerebral amyloid angiopathy (CAA), which is prevalent among older adults, constitutes a major cause of brain hemorrhage, dementia, and cognitive decline. 4 key findings →
Evidence: low
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Alzheimer disease (AD) is a progressive neurodegenerative disorder characterized by synaptic dysfunction, neuroinflammation, and cognitive impairment. 5 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive memory loss and cognitive decline. 1 key finding →
Evidence: low
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Previous studies have shown a marked decline in neuronal and an increase in glial gene expression in Alzheimer's disease (AD) neocortex. 2 key findings →
Evidence: low
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To determine the relationship between regional brain edema caused by anti-amyloid monoclonal antibody therapy (ARIA-E) and the degree of regional β-amyloid (Aβ) positron emission tomography (PET) signal reduction. 1 key finding →
Evidence: low
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Microglia are central regulators of Alzheimer's disease pathogenesis, but their roles cannot be reduced to a simple protective-versus-harmful dichotomy. 4 key findings →
Evidence: low
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In AβO-injected mice, AR, particularly at 200 mg/kg, attenuated memory deficits, reduced hippocampal neuronal degeneration, preserved synaptic protein immunoreactivity and increased markers of hippocampal cell proliferation and immature neurons. 5 key findings →
Evidence: low
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Alzheimer's disease currently has no cure and is usually detected too late for interventions to be effective. 3 key findings →
Evidence: low
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Of note, using large-scale transcriptome and chromatin profiling, we show that T cell shape microglia-specific metabolic plasticity in both genetic and epigenetic resolution. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 1,344 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →