Hexanucleotide repeat expansion in C9ORF72 is the most common genetic cause of frontotemporal dementia and motor neuron disease. 4 key findings →
Evidence: moderate
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.
Hexanucleotide repeat expansion in C9ORF72 is the most common genetic cause of frontotemporal dementia and motor neuron disease. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
About hundred years ago, Oskar Fischer proposed that the senile plaques are the consequence of the deposition of a foreign substance that could induce an inflammatory response leading to an abnormal neuritic response of the surrounding neurons. 4 key findings →
Design: cohort study Evidence: moderate
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We increased the findability, accessibility, interoperability and reusability (FAIR) status of the cohorts through harmonization of data across cohorts, implementation of medical imaging repositories for scan management, implementation of the Personal Health Train infrastructure and provision of meta-data in existing cohort catalogues. 5 key findings →
Design: meta-analysis Evidence: high
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Glial fibrillary acidic protein (GFAP) is the main astrocytic intermediate filament (IF). 1 key finding →
Evidence: low
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Vascular contributions to cognitive impairment and dementia (VCID) are characterized by the aging neurovascular unit being confronted with and failing to cope with biological insults due to systemic and cerebral vascular disease, proteinopathy including Alzheimer's biology, metabolic disease, or immune response, resulting in cognitive decline. 4 key findings →
Evidence: low
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Between 1997 and 2016, we repeatedly assessed cognitive function with 5 tests in 9514 participants aged 45-90 years from the population-based Rotterdam Study. 4 key findings →
Participants: 9,514 Evidence: low
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Building infrastructures for international collaborations is necessary for managing the worldwide public health problem of AD and dementia. 1 key finding →
Evidence: low
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The clinical prediction model can play a beneficial role in decision-making for preventative measures for patients at risk of developing a delirium. 3 key findings →
Participants: 207 Evidence: low
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Cytosolic aggregation of the RNA binding protein TDP-43 (transactive response DNA-binding protein 43) is a hallmark of amyotrophic lateral sclerosis and frontotemporal dementia. 1 key finding →
Evidence: low
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Motor neuron hyperexcitability is a broadly observed yet poorly understood feature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hexanucleotide repeat expansion in C9ORF72 is the most common genetic cause of frontotemporal dementia and motor neuron disease. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Macrophages play a major role in the pathogenesis of atherosclerosis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Oxidized phospholipids play a key role in the atherogenic potential of lipoprotein(a) (Lp[a]); however, Lp(a) is a complex particle that warrants research into additional proinflammatory mediators. 4 key findings →
Participants: 13 Evidence: low
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Female caregivers perceived a greater care burden than male caregivers. 5 key findings →
Participants: 3,067 Evidence: low
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Dementia is a clinical diagnosis without curative treatment. 3 key findings →
Design: cohort study Participants: 13,312 Evidence: moderate
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Doublecortin (DCX) is a microtubule-associated protein expressed by migrating neuroblasts and is considered to be a reliable marker of neurogenesis. 2 key findings →
Participants: 60 Evidence: low
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Alzheimer's disease (AD) is strongly associated with microglia-induced neuroinflammation. 4 key findings →
Evidence: low
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Symptomatic GRN carriers showed elevated WMHs, primarily in the frontal lobe, while no significant increase was observed in symptomatic C9orf72 or MAPT carriers. 5 key findings →
Participants: 763 Evidence: low
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To determine whether the medial temporal lobe is atrophic in subjects with mild cognitive impairment, and whether atrophy of this structure is a better predictor of dementia than memory dysfunction. 1 key finding →
Evidence: low
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We observed no mediation of individual risk factors in the effect of the interventions on dementia incidence. 5 key findings →
Participants: 1,679 Evidence: high
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Dementia is a leading health policy challenge, with cases expected to triple by 2050, particularly in low- and middle-income countries. 2 key findings →
Evidence: low
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Adult proliferation and hippocampal neurogenesis are stimulated by injury. 1 key finding →
Evidence: moderate
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Mucopolysaccharidosis type III (MPS III, Sanfilippo syndrome) is an autosomal recessive disorder, caused by a deficiency in one of the four enzymes involved in the lysosomal degradation of the glycosaminoglycan heparan sulfate. 5 key findings →
Evidence: low
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Four hundred eighty-six participants developed dementia during 37,782 person-years of follow-up. 5 key findings →
Participants: 5,205 Evidence: low
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The mammalian target of rapamycin (mTOR) signaling pathway is a key developmental pathway involved in mechanisms underlying cellular aging and neurodegeneration. 2 key findings →
Evidence: low
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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 →