Evidence map›Paper›PMID 32854783›Full record

ArticleClinical epigenetics2020

The fusiform gyrus exhibits an epigenetic signature for Alzheimer's disease.

Dingailu Ma, Irfete S Fetahu, Mei Wang, Rui Fang, Jiahui Li, Hang Liu, Tobin Gramyk, Isabella Iwanicki, Sophie Gu, Winnie Xu and 3 more

Open access · goldAbstract read
In one paragraph

Article in Clinical epigenetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 42 citations in OpenAlex.

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  10. Fair CCA for Fair Representation Learning: An ADNI Study.ACM-BCB ... ... : the ... ACM Conference on Bioinformatics, Computational Biology and Biomedicine. ACM Conference on Bioinformatics, Computational Biology and Biomedicine · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 2 countries.

Dingailu MaLaboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Irfete S FetahuDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Mei WangDepartment of Geriatrics, Shanghai General Hospital, Shanghai, 200080, China.
Rui FangDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Jiahui LiLaboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Hang LiuLaboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Tobin GramykDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Isabella IwanickiDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Sophie GuDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Winnie XuLaboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Li TanLaboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Feizhen WuLaboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China. wufz@fudan.edu.cn.
Yujiang G ShiDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA. yujiang_shi@hms.harvard.edu.ORCID 0000-0001-9490-7081
Brigham and Women's Hospital · USFudan University · CNShanghai First People's Hospital · CN

Funding

National Centralized Repository for Alzheimer's Disease and Related Dementias (NCRAD)U24AG021886 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI TATIANA M. FOROUD · 2002 to 2026
$119.8M
NATIONAL ALZHEIMERS COORDINATING CENTER (NACC)U01AG016976 · NIA · UNIVERSITY OF WASHINGTON · PI KUKULL, WALTER ANTHONY · 1999 to 2020
$72.8M
Alzheimer's Disease Genetics ConsortiumU01AG032984 · NIA · UNIVERSITY OF PENNSYLVANIA · PI SCHELLENBERG, GERARD DAVID · 2009 to 2024
$60.4M
CHARGE Consortium: Omics Discovery for CVD and Aging PhenotypesR01HL105756 · NHLBI · UNIVERSITY OF WASHINGTON · PI Bruce M Psaty, NICHOLAS L SMITH · 2011 to 2026
$9.5M
Collaborative GWAS of Dementia, AD and related MRI and Cognitive EndophenotypesR01AG033193 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SESHADRI, SUDHA · 2009 to 2016
$4.4M
NHLBI NIH HHS R01 HL105756NIA NIH HHS R01 AG033193NIA NIH HHS U01 AG016976NIA NIH HHS U01 AG032984NIA NIH HHS U24 AG021886Wellcome Trust
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is the most common type of dementia, and patients with advanced AD frequently lose the ability to identify family members. The fusiform gyrus (FUS) of the brain is critical in facial recognition. However, AD etiology in the FUS of AD patients is poorly understood. New analytical strategies are needed to reveal the genetic and epigenetic basis of AD in FUS.

resultsA complex of new analytical paradigms that integrates an array of transcriptomes and methylomes of normal controls, AD patients, and "AD-in-dish" models were used to identify genetic and epigenetic signatures of AD in FUS. Here we identified changes in gene expression that are specific to the FUS in brains of AD patients. These changes are closely linked to key genes in the AD network. Profiling of the methylome (5mC/5hmC/5fC/5caC) at base resolution identified 5 signature genes (COL2A1, CAPN3, COL14A1, STAT5A, SPOCK3) that exhibit perturbed expression, specifically in the FUS and display altered DNA methylome profiles that are common across AD-associated brain regions. Moreover, we demonstrate proof-of-principle that AD-associated methylome changes in these genes effectively predict the disease prognosis with enhanced sensitivity compared to presently used clinical criteria.

conclusionsThis study identified a set of previously unexplored FUS-specific AD genes and their epigenetic characteristics, which may provide new insights into the molecular pathology of AD, attributing the genetic and epigenetic basis of FUS to AD development.

Indexed as

Alzheimer DiseaseEpigenesis, GeneticGene ExpressionHumansTemporal LobeAlzheimer’s diseaseBase-resolution DNA methylome analysisEpigeneticsFusiform gyrusGenome-wide transcriptome analysisiPSC-derived neuronPostmortem brainProtein-protein interaction networks

Identifiers

PMID32854783
PMCPMC7457273
OpenAlexW3082960444

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.