Age-associated microglial dysfunction contributes to the accumulation of amyloid-β (Aβ) plaques in Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Age-associated microglial dysfunction contributes to the accumulation of amyloid-β (Aβ) plaques in Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Heterozygous genetic variants within the TREM2 gene show a strong association with increased Alzheimer's disease (AD) risk. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We explored the potential link between chronic inflammatory arthritis and COVID-19 pathogenic and resolving macrophage pathways and their role in COVID-19 pathogenesis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Metabolic dysfunction-associated steatohepatitis (MASH), formerly known as nonalcoholic steatohepatitis (NASH), is an advanced stage of metabolic fatty liver disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The triggering receptor expressed on myeloid cells 2 (TREM2) is an immune receptor that affects cellular phenotypes by modulating phagocytosis and metabolism, promoting cell survival, and counteracting inflammation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Sodium glucose cotransporter 2 (SGLT2) inhibitors originally developed for the treatment of type 2 diabetes are clinically very effective drugs halting chronic kidney disease progression. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is an incurable neurodegenerative disease currently affecting 1.75% of the US population, with projected growth to 3.46% by 2050. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To study the mechanisms by which the p.R47H variant of the microglia gene and Alzheimer's disease (AD) risk factor TREM2 increases dementia risk, we created Trem2 R47H KI rats. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The identification of neuroinflammation as a critical factor in Alzheimer's disease (AD) has expanded the focus of research beyond amyloid-β and tau pathology. 4 key findings →
Evidence: low
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Herein, we demonstrate that endogenous Tyrobp transcription is specifically increased in recruited microglia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is increasingly recognized as a disorder not solely of amyloid and tau accumulation but also of chronic immune dysregulation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It is clear that innate immune system status is altered in numerous neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Using spatial cell-type-enriched transcriptomics, we compare plaque-induced gene (PIG) expression in microglia-touching plaques, neighboring plaques, and far from plaques in an aged Alzheimer's mouse model with late plaque development. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The present study explores the associations of soluble TREM2, an important regulator of microglial activity linked to Alzheimer's disease (AD), with other known inflammatory proteins in cerebrospinal fluid (CSF). 4 key findings →
Participants: 303 Evidence: low
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Tauopathies are a class of neurodegenerative diseases marked by intracellular aggregates of hyperphosphorylated Tau. 4 key findings →
Evidence: low
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HIV-associated neurologic disorders (HAND) continue to develop in many patients with HIV. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is concern that AIDS dementia complex (ADC) may be complicated by Alzheimer disease (AD). 2 key findings →
Evidence: low
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Many neurodegenerative proteinopathies share a common pathogenic mechanism: the abnormal accumulation of disease-related proteins. 4 key findings →
Evidence: low
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Research progress has provided detailed understanding of the molecular pathogenesis of Alzheimer disease (AD). 4 key findings →
Evidence: low
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After 2 years, 34 subjects (16%) were lost for follow-up. 4 key findings →
Participants: 34 Evidence: low
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There is a need for an accessible biomarker that can complement current cerebrospinal fluid and imaging biomarkers in an accurate and early diagnosis of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Levels of amyloid-β (Aβ) and tau peptides in brain have been associated with Alzheimer disease (AD). 4 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is a devastating disease and a global health problem, and current treatments are only symptomatic. 4 key findings →
Participants: 242 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Study objectives To evaluate the role of orexin-A with respect to cerebrospinal fluid (CSF) Alzheimer disease (AD) biomarkers, and explore its relationship to cognition and sleep characteristics in a group of cognitively normal elderly individuals. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Previous research has shown that elevated blood C-reactive protein (CRP) is associated with increased Alzheimer disease (AD) risk only in APOE ε4 allele carriers; the objective of this study was to examine the interactive effects of plasma CRP and APOE genotype on cognition and AD biomarkers. 4 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 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 →