This study investigated the effect of NLRP3 inflammasome function on tau pathology and Alzheimer's disease progression. 5 key findings →
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
This study investigated the effect of NLRP3 inflammasome function on tau pathology and Alzheimer's disease progression. 5 key findings →
Full summary, score breakdown and related studies → Original source Free full text
Periodontitis is an oral inflammatory disease and may contribute to low-grade systemic inflammation. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Neuronal and glial cell interaction is essential for synaptic homeostasis and may be affected in Alzheimer's disease (AD). 4 key findings →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is the most prevalent type of dementia and is caused by the deposition of extracellular amyloid-beta and abnormal tau phosphorylation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apoptosis is crucial for the normal development of the nervous system, whereas neurons in the adult CNS are relatively resistant to this form of cell death. 3 key findings →
Evidence: low
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The symptoms of Alzheimer disease reflect a loss of neural circuit integrity in the brain, but neurons do not work in isolation. 2 key findings →
Evidence: low
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Disturbances along the brain-gut-microbiota axis may significantly contribute to the pathogenesis of neurodegenerative disorders. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most common dementia in the elderly. 4 key findings →
Evidence: low
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Here we elucidate the effect of Alzheimer disease (AD)-predisposing genetic backgrounds, APOE4, PSEN1ΔE9, and APPswe, on functionality of human microglia-like cells (iMGLs). 4 key findings →
Evidence: low
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Cumulative data suggest that neuroinflammation plays a prominent role in Alzheimer's disease (AD) pathogenesis. 4 key findings →
Evidence: low
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Microglia are resident macrophages of the CNS that are involved in its development, homeostasis and response to infection and damage. 4 key findings →
Evidence: low
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Diabetes mellitus is one of the major risk factors for cognitive dysfunction. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This neurodegenerative disorder is associated with neuronal death and gliosis heavily impacting the cerebral cortex. 4 key findings →
Evidence: low
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Alzheimer's disease (AD), a primary cause of dementia in the aging population, is characterized by extracellular amyloid-beta peptides aggregation, intracellular deposits of hyperphosphorylated tau, neurodegeneration and glial activation in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Postoperative cognitive dysfunction (POCD) is a common disorder following surgery, which seriously threatens the quality of patients' life, especially the older people. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Traumatic brain injury (TBI) refers to any insult to the brain resulting in primary (direct) and secondary (indirect) damage to the brain parenchyma. 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.
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 →