27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
When rs140926439 was absent, 0.10% of APOEε2/3 carriers had AD, while 0.43% of APOEε4 carriers or homozygotes had AD. 5 key findings →
Evidence: moderate
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CWPs consist predominantly of two novel arrangements of type I Aβ filaments, and we have designated them as type Ic and type Id Aβ filaments. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
It is associated with intracerebral hemorrhage (ICH), cognitive decline, and gait disturbance. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study compared the relationships of the development of both Alzheimer I & II cells to reactive astrogliosis and also their distributional patterns in the demyelinated and non-demyelinated lesions in 6 cases of Wilson's disease by the use of PAP immunohistochemical technique for glial fibrillary acidic protein (GFAP). 5 key findings →
Evidence: low
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Endolysosomal dysfunction has been increasingly implicated in the pathogenesis of neurodegenerative diseases. 4 key findings →
Evidence: low
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We evaluated known AD-associated loci (Bellenguez et al. 2022) and 27 loci reached nominal significance (p < 0.05) in at least one cognitive domain. 5 key findings →
Evidence: low
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The pathological activation of AD microglia significantly amplifies endogenous aging characteristics. 4 key findings →
Evidence: low
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The predALZ framework achieved 94% accuracy on an independent test set and approximately 96% accuracy in cross-validation for Alzheimer-related driver gene prediction. 5 key findings →
Evidence: low
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Alzheimer disease (AD) pathology affects the transentorhinal/entorhinal region early but whether entorhinal cortex (EC) astrocytes are causal drivers or therapeutic targets remains unresolved. 5 key findings →
Design: narrative review Evidence: low
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This study aims to comprehensively review the role of glial fibrillary acidic protein (GFAP) as a marker of astrocyte activation in Alzheimer's disease (AD). 3 key findings →
Evidence: low
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However, postmortem investigations indicate that the AD-typical progressive amnestic syndrome may also result from predominantly limbic non-AD neuropathology such as TDP-43 proteinopathy and argyrophilic grain disease. 3 key findings →
Evidence: low
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Alzheimer disease (AD) is a multi-factorial neurodegenerative disease that is characterized by accumulation of amyloid-beta (Aβ), protein aggregation and progressive neuronal dysfunction. 1 key finding →
Evidence: low
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BSA-polymer conjugates displayed enhanced resistance to proteolytic degradation. 5 key findings →
Evidence: low
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Alzheimer’s disease is the leading cause of dementia and represents a growing global health challenge. 1 key finding →
Evidence: low
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Alzheimer disease is characterized by gradual and progressive neurodegeneration caused by neuronal cell death. 5 key findings →
Evidence: low
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Alzheimer disease is one of the causes of dementia that could make the patient lose their memories until they unable to do normal activities. 2 key findings →
Evidence: low
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Eighteen years after it was published, Nature formally retracted the landmark 2006 paper that had proposed a specific amyloid protein (Aβ*56) as a cause of memory loss in mice, citing evidence of image manipulation, including splicing, duplication, and use of an image-editing 'eraser' tool. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Directed conversion of mature human cells, as from fibroblasts to neurons, is of potential clinical utility for neurological disease modeling as well as cell therapeutics. 2 key findings →
Evidence: low
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Although large numbers of microRNAs (miRNAs) expressed in Alzheimer disease (AD) have been detected, their functions and mechanisms of regulation remain to be fully clarified. 4 key findings →
Evidence: low
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Alzheimer disease (AD) is a heterogeneous disease with many genes are associated with AD risk. 4 key findings →
Participants: 360 Evidence: low
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Anti-amyloid immunotherapy is used to treat Alzheimer disease (AD) with moderate benefits and potentially serious side effects due to amyloid related imaging abnormality with effusions/edema (ARIA-E). 4 key findings →
Design: cross-sectional Evidence: low
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Therapies targeting amyloid, such as monoclonal antibodies like Lecanemab, Aducanumab, and Donanemab, have garnered FDA approval but remain controversial due to limited clinical benefits and significant side effects against Alzheimer. 4 key findings →
Evidence: low
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Mounting evidence suggests that defects in energy metabolism contribute to the pathogenesis of Alzheimer disease (AD). 4 key findings →
Evidence: low
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Genome-wide association studies (GWAS) typically represent Alzheimers disease (AD) risk loci by a single lead SNP, although the lead SNP may capture only part of the genetic variation at a locus. 3 key findings →
Participants: 493 Evidence: low
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Body mass index (BMI), type 2 diabetes (T2D) and related cardiometabolic features associate with Alzheimers disease (AD) risk, yet shared mechanisms remain poorly understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
9 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 9. The same 9 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 →