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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Genetics

Topic: Amyloid, tau and blood-test diagnosis

Importance Late-onset Alzheimer disease (AD), the most common form of dementia, places a large burden on families and society. Although epidemiological and clinical evidence suggests a relationship between inflammation and AD, their relationship is not well understood and could have implications for treatment and prevention strategies. Objective To determine whether a subset of genes involved with increased risk of inflammation are also associated with increased risk for AD. Design, setting, and participants In a genetic epidemiology study conducted in July 2015, we systematically investigated genetic overlap between AD (International Genomics of Alzheimer's Project stage 1) and Crohn disease, ulcerative colitis, rheumatoid arthritis, type 1 diabetes, celiac disease, and psoriasis using summary data from genome-wide association studies at multiple academic clinical research centers. P values and odds ratios from genome-wide association studies of more than 100 000 individuals were from previous comparisons of patients vs respective control cohorts. Diagnosis for each disorder was previously established for the parent study using consensus criteria. Main outcomes and measures The primary outcome was the pleiotropic (conjunction) false discovery rate P value. Follow-up for candidate variants included neuritic plaque and neurofibrillary tangle pathology; longitudinal Alzheimer's Disease Assessment Scale cognitive subscale scores as a measure of cognitive dysfunction (Alzheimer's Disease Neuroimaging Initiative); and gene expression in AD vs control brains (Gene Expression Omnibus data). Results Eight single-nucleotide polymorphisms (false discovery rate P Conclusions and relevance Our findings demonstrate genetic overlap between AD and immune-mediated diseases and suggest that immune system processes influence AD pathogenesis and progression.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Yokoyama, J. S., Wang, Y., Schork, A. J., Thompson, W. K., Karch, C. M., Cruchaga, C., et al. (2016). Association Between Genetic Traits for Immune-Mediated Diseases and Alzheimer Disease. JAMA neurology. https://doi.org/10.1001/jamaneurol.2016.0150

Vancouver

Yokoyama JS, Wang Y, Schork AJ, Thompson WK, Karch CM, Cruchaga C, et al. Association Between Genetic Traits for Immune-Mediated Diseases and Alzheimer Disease. JAMA neurology. 2016. doi:10.1001/jamaneurol.2016.0150. PMID: 27088644.

BibTeX

@article{yokoyama2016-27088644,
  author  = {Yokoyama, J. S. and Wang, Y. and Schork, A. J. and Thompson, W. K. and Karch, C. M. and Cruchaga, C. and McEvoy, L. K. and Witoelar, A. and others},
  title   = {{Association Between Genetic Traits for Immune-Mediated Diseases and Alzheimer Disease}},
  journal = {JAMA neurology},
  year    = {2016},
  doi     = {10.1001/jamaneurol.2016.0150},
  pmid    = {27088644},
  url     = {https://doi.org/10.1001/jamaneurol.2016.0150}
}

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.

Key findings

Why it matters

This genetic epidemiology study found overlap between genes associated with Alzheimer's disease and genes associated with several immune-mediated diseases, suggesting that immune system processes influence Alzheimer's disease pathogenesis and progression. It does not show that treating inflammation treats, cures, or prevents Alzheimer's disease.

Study details

How this study scored 57/100
How this study's score is builtJournal tier 9 of 10; Journal's citation record 2 of 4; Study design 7 of 12; Strength of evidence 3 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 5 of 7; Citations per year 3 of 5; Impact for its field and year 4 of 6; Cited by studies here 3 of 6; Still being cited 2 of 4; Senior author's track record left out, no data; Institution's track record 2 of 3; Multi-centre collaboration 2 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. 55 of the 96 points it could be judged on, which is 57 of 100. Total 57 of 100.55 of the 96 points we could judge = 57 of 100

Published in a leading specialty journal, and it is a longitudinal study following the same people over time. Scored zero for sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on senior author's track record, so that was left out: it earned 55 of the 96 points we could judge it on, which is 57 out of 100.

ComponentPointsWhy
Journal tier 9 / 10 Tier 2 — leading specialty journal (JAMA neurology)
Journal's citation record 2 / 4 JAMA Neurology: journal h-index 235 (OpenAlex, 2026-10-29)
Study design 7 / 12 A longitudinal study following the same people over time
Strength of evidence 3 / 5 Rated “moderate” in our summary
Peer-review validation 10 / 10 Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent 1 / 5 2016 — within 20 year(s) of the newest study here
Sample size 0 / 4 Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported 0 / 3 No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people 0 / 3 Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 5 / 7 Cited 177 times (OpenAlex, 2026-10-10)
Citations per year 3 / 5 14.8 citations a year over 12 year(s) since 2016
Impact for its field and year 4 / 6 Cited 14.0× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 3 / 6 Cited by 11 other studies in this library
Still being cited 2 / 4 Cited 38 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record — / 4 Senior author's record not available — left out of this score
Institution's track record 2 / 3 Massachusetts General Hospital: institution h-index 2,057 (OpenAlex)
Multi-centre collaboration 2 / 3 OpenAlex lists 9 institution(s) in 3 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 27088644)
Free to read 0 / 2 Behind a paywall — scores zero
Points 55 / 96 Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 55 of the 96 points we could judge it on is 57 out of 100.
Total 57 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

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