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Mitochondrial aspartate/glutamate carrier SLC25A12 and autism spectrum disorder: a meta-analysis

Mitochondrial aspartate/glutamate carrier SLC25A12 and autism spectrum disorder: a meta-analysis
Mitochondrial aspartate/glutamate carrier SLC25A12 and autism spectrum disorder: a meta-analysis
Mitochondrial dysfunction has been reported to be involved in the pathophysiology of autism spectrum disorder (ASD). Studies investigating the possible association between ASD and polymorphism in SLC25A12, which encodes the mitochondrial aspartate/glutamate carrier, have yielded inconsistent results. We conducted a systematic review and meta-analysis of such studies to elucidate if and which SLC25A12 single nucleotide polymorphisms (SNPs) are associated with ASD. We searched PubMed, Ovid, Web of Science, and ERIC databases through September 20th, 2014. Odds ratios (ORs) were aggregated using random effect models. Sensitivity analyses were conducted based on study design (family-based or case-control). Fifteen out of 79 non-duplicate records were retained for qualitative synthesis. We pooled 10 datasets from 9 studies with 2001 families, 735 individuals with ASD and 632 typically developing (TD) individuals for the meta-analysis of rs2292813, as well as 11 datasets from 10 studies with 2016 families, 852 individuals with ASD and 1058 TD individuals for the meta-analysis of rs2056202. We found a statistically significant association between ASD and variant in rs2292813 (OR?=?1.190, 95 % CI 1.052–1.346, P?=?0.006) as well as in rs2056202 (OR?=?1.206, 95 % CI 1.035–1.405, P?=?0.016). Sensitivity analyses including only studies with family-based design demonstrated significant association between ASD and polymorphism in rs2292813 (OR?=?1.216, 95 % CI 1.075–1.376, P?=?0.002) and rs2056202 (OR?=?1.267, 95 % CI 1.041–1.542, P?=?0.018). In contrast, sensitivity analyses including case-control design studies only failed to find a significant association. Further research on the role of SLC25A12 and ASD may pave the way for potential innovative therapeutic interventions.
0893-7648
Aoki, Yuta
806ea614-51b3-4018-b68b-d12b7f1487c1
Cortese, Samuele
53d4bf2c-4e0e-4c77-9385-218350560fdb
Aoki, Yuta
806ea614-51b3-4018-b68b-d12b7f1487c1
Cortese, Samuele
53d4bf2c-4e0e-4c77-9385-218350560fdb

Aoki, Yuta and Cortese, Samuele (2015) Mitochondrial aspartate/glutamate carrier SLC25A12 and autism spectrum disorder: a meta-analysis. Molecular Neurobiology.

Record type: Article

Abstract

Mitochondrial dysfunction has been reported to be involved in the pathophysiology of autism spectrum disorder (ASD). Studies investigating the possible association between ASD and polymorphism in SLC25A12, which encodes the mitochondrial aspartate/glutamate carrier, have yielded inconsistent results. We conducted a systematic review and meta-analysis of such studies to elucidate if and which SLC25A12 single nucleotide polymorphisms (SNPs) are associated with ASD. We searched PubMed, Ovid, Web of Science, and ERIC databases through September 20th, 2014. Odds ratios (ORs) were aggregated using random effect models. Sensitivity analyses were conducted based on study design (family-based or case-control). Fifteen out of 79 non-duplicate records were retained for qualitative synthesis. We pooled 10 datasets from 9 studies with 2001 families, 735 individuals with ASD and 632 typically developing (TD) individuals for the meta-analysis of rs2292813, as well as 11 datasets from 10 studies with 2016 families, 852 individuals with ASD and 1058 TD individuals for the meta-analysis of rs2056202. We found a statistically significant association between ASD and variant in rs2292813 (OR?=?1.190, 95 % CI 1.052–1.346, P?=?0.006) as well as in rs2056202 (OR?=?1.206, 95 % CI 1.035–1.405, P?=?0.016). Sensitivity analyses including only studies with family-based design demonstrated significant association between ASD and polymorphism in rs2292813 (OR?=?1.216, 95 % CI 1.075–1.376, P?=?0.002) and rs2056202 (OR?=?1.267, 95 % CI 1.041–1.542, P?=?0.018). In contrast, sensitivity analyses including case-control design studies only failed to find a significant association. Further research on the role of SLC25A12 and ASD may pave the way for potential innovative therapeutic interventions.

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More information

Published date: 10 February 2015
Organisations: Clinical Neuroscience

Identifiers

Local EPrints ID: 380132
URI: https://eprints.soton.ac.uk/id/eprint/380132
ISSN: 0893-7648
PURE UUID: 9fe049ce-8d87-4d45-ae9c-7e18062384c7
ORCID for Samuele Cortese: ORCID iD orcid.org/0000-0001-5877-8075

Catalogue record

Date deposited: 19 Aug 2015 11:17
Last modified: 06 Jun 2018 12:21

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