PMID- 37515308
OWN - NLM
STAT- MEDLINE
DCOM- 20230911
LR  - 20230912
IS  - 1098-2825 (Electronic)
IS  - 0887-8013 (Print)
IS  - 0887-8013 (Linking)
VI  - 37
IP  - 13-14
DP  - 2023 Jul
TI  - Association between polymorphism rs2421943 of the insulin-degrading enzyme and 
      schizophrenia: Preliminary report.
PG  - e24949
LID - 10.1002/jcla.24949 [doi]
LID - e24949
AB  - BACKGROUND: Insulin-degrading enzyme (IDE) is an important gene in studies of the 
      pathophysiology of type 2 diabetes mellitus (T2DM). Recent studies have suggested 
      a possible link between type 2 diabetes mellitus (T2DM) and the pathophysiology 
      of schizophrenia (SZ). At the same time, significant changes in insulin-degrading 
      enzyme (IDE) gene expression have been found in the brains of people with 
      schizophrenia. These findings highlight the need to further investigate the role 
      of IDE in schizophrenia pathogenesis. METHODS: We enrolled 733 participants from 
      the Czech Republic, including 383 patients with schizophrenia and 350 healthy 
      controls. Our study focused on the single nucleotide polymorphism (SNP) rs2421943 
      in the IDE gene, which has previously been associated with the pathogenesis of 
      Alzheimer's disease. The SNP was analyzed using the PCR-RFLP method. RESULTS: The 
      G allele of the rs2421943 polymorphism was found to significantly increase the 
      risk of developing SZ (p < 0.01) when a gender-based analysis showed that both AG 
      and GG genotypes were associated with a more than 1.55 times increased risk of SZ 
      in females (p < 0.03) but not in males. Besides, we identified a potential 
      binding site at the G allele locus for has-miR-7110-5p, providing a potential 
      mechanism for the observed association. CONCLUSION: Our results confirm the role 
      of the IDE gene in schizophrenia pathogenesis and suggest that future research 
      should investigate the relationship between miRNA and estrogen influence on IDE 
      expression in schizophrenia pathogenesis.
CI  - (c) 2023 The Authors. Journal of Clinical Laboratory Analysis published by Wiley 
      Periodicals LLC.
FAU - Ambrozova, Laura
AU  - Ambrozova L
AD  - Laboratory of Neurobiology and Molecular Psychiatry, Department of Biochemistry, 
      Faculty of Science, Masaryk University, Brno, Czech Republic.
FAU - Zeman, Tomas
AU  - Zeman T
AD  - Laboratory of Neurobiology and Molecular Psychiatry, Department of Biochemistry, 
      Faculty of Science, Masaryk University, Brno, Czech Republic.
AD  - Laboratory of Neurobiology and Pathological Physiology, Institute of Animal 
      Physiology and Genetics, Czech Academy of Sciences, Brno, Czech Republic.
FAU - Janout, Vladimir
AU  - Janout V
AD  - Department of Public Health, Faculty of Medicine and Dentistry, Palacky 
      University, Olomouc, Czech Republic.
FAU - Janoutova, Jana
AU  - Janoutova J
AD  - Department of Public Health, Faculty of Medicine and Dentistry, Palacky 
      University, Olomouc, Czech Republic.
FAU - Lochman, Jan
AU  - Lochman J
AD  - Laboratory of Neurobiology and Molecular Psychiatry, Department of Biochemistry, 
      Faculty of Science, Masaryk University, Brno, Czech Republic.
AD  - Laboratory of Neurobiology and Pathological Physiology, Institute of Animal 
      Physiology and Genetics, Czech Academy of Sciences, Brno, Czech Republic.
FAU - Sery, Omar
AU  - Sery O
AUID- ORCID: 0000-0002-6062-8997
AD  - Laboratory of Neurobiology and Molecular Psychiatry, Department of Biochemistry, 
      Faculty of Science, Masaryk University, Brno, Czech Republic.
AD  - Laboratory of Neurobiology and Pathological Physiology, Institute of Animal 
      Physiology and Genetics, Czech Academy of Sciences, Brno, Czech Republic.
LA  - eng
GR  - NT14504/Agentura Pro Zdravotnicky Vyzkum Ceske Republiky/
GR  - NV18-04-00455/Agentura Pro Zdravotnicky Vyzkum Ceske Republiky/
GR  - GP309/09/P361/Grantova Agentura Ceske Republiky/
PT  - Journal Article
DEP - 20230728
PL  - United States
TA  - J Clin Lab Anal
JT  - Journal of clinical laboratory analysis
JID - 8801384
RN  - EC 3.4.24.56 (Insulysin)
SB  - IM
MH  - Male
MH  - Female
MH  - Humans
MH  - *Diabetes Mellitus, Type 2/epidemiology/genetics
MH  - *Schizophrenia/genetics
MH  - *Insulysin/genetics/metabolism
MH  - Genotype
MH  - *Alzheimer Disease/genetics/metabolism
MH  - Polymorphism, Single Nucleotide/genetics
PMC - PMC10492455
OTO - NOTNLM
OT  - candidate gene analyses
OT  - genetic association study
OT  - insulin-degrading enzyme (IDE)
OT  - miRNA
OT  - schizophrenic disorder
OT  - single nucleotide polymorphism (SNP)
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2023/07/29 11:42
MHDA- 2023/09/11 06:42
PMCR- 2023/07/28
CRDT- 2023/07/29 01:46
PHST- 2023/06/06 00:00 [revised]
PHST- 2023/03/22 00:00 [received]
PHST- 2023/07/17 00:00 [accepted]
PHST- 2023/09/11 06:42 [medline]
PHST- 2023/07/29 11:42 [pubmed]
PHST- 2023/07/29 01:46 [entrez]
PHST- 2023/07/28 00:00 [pmc-release]
AID - JCLA24949 [pii]
AID - 10.1002/jcla.24949 [doi]
PST - ppublish
SO  - J Clin Lab Anal. 2023 Jul;37(13-14):e24949. doi: 10.1002/jcla.24949. Epub 2023 
      Jul 28.