27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Currently available literature shows limited information on aging in RGNDs, with relatively many reports of young-onset dementia. 2 key findings →
Design: longitudinal study Participants: 25 Evidence: moderate
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The amyloid beta protein has been identified as an important component of both cerebrovascular amyloid and amyloid plaques of Alzheimer's disease and Down syndrome. 1 key finding →
Evidence: low
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Down syndrome (DS), or trisomy 21, is a common disorder associated with several complex clinical phenotypes. 1 key finding →
Participants: 30 Evidence: low
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Almost all individuals with Down Syndrome (DS) develop Alzheimer's disease (AD) by mid to late life. 3 key findings →
Participants: 229 Evidence: moderate
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A population of more than six million people worldwide at high risk of Alzheimer's disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caused by an extra copy of β-amyloid-(Aβ)-precursor-protein gene. 1 key finding →
Evidence: low
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Adults with DS have a significantly increased brain concentration of myo-inositol, and this is associated with reduced cognitive ability. 5 key findings →
Design: case-control study Participants: 38 Evidence: moderate
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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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The mechanisms by which trisomy 21 leads to the characteristic Down syndrome (DS) phenotype are unclear. 5 key findings →
Participants: 685 Evidence: low
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The ε4 allele of the apolipoprotein E gene (APOE ε4) is associated with an additional risk for AD. 5 key findings →
Design: cross-sectional Participants: 240 Evidence: low
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Regeneration of injured nerves is likely occurring in the peripheral nervous system, but not in the central nervous system. 4 key findings →
Design: meta-analysis Evidence: high
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Genetic variations in promoter sequences that alter gene expression play a prominent role in increasing susceptibility to complex diseases. 1 key finding →
Evidence: low
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Transactive response DNA-binding protein 43 pathology occurs in FAD and DS, similar to that observed in sporadic Alzheimer disease. 2 key findings →
Participants: 42 Evidence: low
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Novel insights into Alzheimer's disease through the study of individuals with Down syndromePeople with Down syndrome (DS) represent the largest genetically defined population at risk for Alzheimer's disease (AD). 1 Virtually all adults with DS develop AD neuropathology by midlife due to triplication of the amyloid precursor protein (APP) gene on chromosome 21.As medical advances and social integration have extended life expectancy into the 60s, AD has emerged as the major determinant of cognitive decline, morbidity, and mortality in this DS population. 2 What was once viewed as an inevitable consequence of aging in DS is now recognized as a unique scientific opportunity to uncover the earliest events that drive AD.The predictable and accelerated course of DS-associated AD (DSAD) provides an unparalleled window into the molecular and cellular origins of amyloid and tau pathology, neuroinflammation, cerebrovascular pathology, and neurodegeneration. 1 key finding →
Design: longitudinal study Evidence: moderate
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Trisomy of chromosome 21, the cause of Down syndrome (DS), is the most commonly occurring genetic cause of Alzheimer’s disease (AD). 3 key findings →
Evidence: low
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Disorders associated with early-life alterations in amyloid precursor protein production or processing are associated with a distinct pattern of early striatal fibrillary Aβ deposition before significant cognitive impairment. 2 key findings →
Evidence: low
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Mouse trisomy 16 has been proposed as an animal model of Down syndrome (DS), since this chromosome contains homologues of several loci from the q22 band of human chromosome 21. 1 key finding →
Evidence: low
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This study assesses whether C-terminal fragments (CTF) of the amyloid precursor protein (APP) are present in cerebrospinal fluid (CSF) and their potential as biomarkers for Alzheimer's disease (AD). 2 key findings →
Evidence: low
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The amyloid cascade hypothesis as the etiological underpinning of Alzheimer disease (AD) is supported by a large body of literature, the most influential of which are genetic studies of the 1980s and 1990s. Other evidence includes the neuropathology of Down syndrome, apparent toxicity of oligomeric amyloid-β (Aβ), interactions with apolipoprotein E, and the analogy of cardiac amyloidosis. 1 key finding →
Evidence: low
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Adults with Down syndrome (DS) have an exceptionally high frequency of Alzheimer disease (AD) with a wide variability in onset, from 40 to 70 years of age. 2 key findings →
Participants: 232 Evidence: low
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The patterns of FDG decline are distinct in these 2 genetically determined forms of AD. 1 key finding →
Design: cross-sectional Participants: 76 Evidence: low
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Deposits of amyloid fibers are found in large numbers in the walls of blood vessels and in neuritic plaques in the brains of patients with Alzheimer disease and adults with Down syndrome. 2 key findings →
Evidence: low
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Genetic variation in the APOE gene and variation in chromosome 21 genotypes, including the APP locus, may influence age-associated cognitive decline in adults with Down syndrome. 3 key findings →
Design: longitudinal study Evidence: moderate
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Early-onset Alzheimer disease (AD)-like pathology in Down syndrome is commonly attributed to an increased dosage of the amyloid precursor protein (APP) gene. 5 key findings →
Evidence: low
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The gene encoding the beta-amyloid precursor protein has been assigned to human chromosome 21, as has a gene responsible for at least some cases of familial Alzheimer disease. 2 key findings →
Evidence: low
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Alzheimer disease was transmitted in a pattern consistent with an autosomal dominant trait in three families. 1 key finding →
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 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 →