28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Loss-of-function mutations in progranulin (GRN) cause ubiquitin- and TAR DNA-binding protein 43 (TDP-43)-positive frontotemporal dementia (FTLD-U), a progressive neurodegenerative disease affecting approximately 10% of early-onset dementia patients. 4 key findings →
Evidence: low
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Obstructive sleep apnea (OSA) is highly prevalent but very frequently undiagnosed. 5 key findings →
Evidence: high
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Vascular risk factors for Alzheimer disease (AD) and vascular dementia (VaD) have been evaluated; however, few studies have compared risks by dementia subtypes and sex. 1 key finding →
Evidence: moderate
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Cognitive dysfunction, including mild cognitive impairment and dementia, is increasingly recognised as an important comorbidity and complication of diabetes that affects an individual's well-being and diabetes management, and is associated with diabetes treatment-related complications. 2 key findings →
Evidence: low
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Several changes of magnesium (Mg) metabolism have been reported with aging, including diminished Mg intake, impaired intestinal Mg absorption and renal Mg wasting. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Synapses are essential components of neurons and allow information to travel coordinately throughout the nervous system to adjust behavior to environmental stimuli and to control body functions, memories, and emotions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The activity of the pyruvate dehydrogenase complex (PDHC) was reduced in affected areas of brain from patients with Huntington disease (caudate, putamen) and Alzheimer disease (frontal cortex) where choline acetyltransferase (CAT) activity was low. 1 key finding →
Evidence: low
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We propose the following sequence of events in the development of neuropathologic changes of Alzheimer disease in Down syndrome: (1) intracellular accumulation of Abeta in neurons and astrocytes, (2) deposition of extracellular Abeta and formation of diffuse plaques, and (3) development of neuritic plaques and neurofibrillary tangles with activation of microglial cells. 1 key finding →
Participants: 14 Evidence: low
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Down syndrome (also known as trisomy 21) is the model human phenotype for all genomic gain dosage imbalances, including microduplications. 4 key findings →
Evidence: low
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Alzheimer disease (AD) represents an oncoming epidemic that without an effective treatment promises to exact extraordinary human and financial burdens. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In patients with Down syndrome, senile plaques and neurofibrillary tangles accumulate in the cortex at an earlier age than in persons of normal karyotype. 5 key findings →
Participants: 20 Evidence: low
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People with Down syndrome (DS) are at high risk for developing Alzheimer disease (AD) with age. 2 key findings →
Participants: 32 Evidence: low
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In DS, longitudinal characterization of all previously identified proteins revealed distinct trajectories over time and an association of baseline levels with future cognitive decline. 5 key findings →
Design: cross-sectional Participants: 59 Evidence: moderate
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Class 2 CRISPR-Cas systems endow microbes with diverse mechanisms for adaptive immunity. 1 key finding →
Evidence: low
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Insulin has functions in the brain and dysregulation of these functions may contribute to the expression of late-life neurodegenerative disease. 1 key finding →
Evidence: low
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TAR DNA-binding protein (TDP-43) is an evolutionarily conserved heterogeneous nuclear ribonucleoprotein (hnRNP) involved in RNA processing, whose abnormal cellular distribution and post-translational modification are key markers of certain neurodegenerative diseases, such as amyotrophic lateral sclerosis and frontotemporal lobar degeneration. 3 key findings →
Evidence: low
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TDP-43 (also known as TARDBP) regulates different processes of gene expression, including transcription and splicing, through RNA and DNA binding. 3 key findings →
Evidence: low
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Some cases of autosomal dominant familial amyotrophic lateral sclerosis (FALS) are associated with mutations in the gene encoding Cu/Zn superoxide dismutase (SOD1), suggesting that oxidative damage may play a role in ALS pathogenesis. 2 key findings →
Evidence: low
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Mutations in the glucocerebrosidase (GBA) gene, which encodes the lysosomal enzyme that is deficient in Gaucher's disease, are important and common risk factors for Parkinson's disease and related disorders. 1 key finding →
Evidence: low
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Aggregation of the microtubule associated protein Tau is associated with several neurodegenerative disorders, including Alzheimer disease and frontotemporal dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Transactive response DNA-binding protein 43 (TDP-43) forms abnormal ubiquitinated and phosphorylated inclusions in brain tissues from patients with amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration. 3 key findings →
Evidence: low
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The misfolding and aggregation of specific proteins is a seminal occurrence in a remarkable variety of neurodegenerative disorders. 1 key finding →
Evidence: low
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Mutations in valosin-containing protein (VCP) cause inclusion body myopathy (IBM), Paget's disease of the bone, and frontotemporal dementia (IBMPFD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 is the major component protein of ubiquitin-positive inclusions in brains of patients with frontotemporal lobar degeneration (FTLD-TDP) or amyotrophic lateral sclerosis (ALS). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To date, molecular genetic analyses have identified over 500 distinct DNA variants in five disease genes associated with familial Parkinson disease; alpha-synuclein (SNCA), parkin (PARK2), PTEN-induced putative kinase 1 (PINK1), DJ-1 (PARK7), and Leucine-rich repeat kinase 2 (LRRK2). 1 key finding →
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 →