Journals / Turkish Journal of Pediatrics / 2018 / Cilt: 60 - Sayı: 4

Apolipoprotein E allelic variants and cerebral palsy

Pages
361–371
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Our data show that the ApoE alleles maybe effective in the development of cerebral palsy and may be associated withsome clinical manifestations in those patients.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Cerebral palsy (CP) is the most frequent cause of mobility restriction andposture disturbance in childhood.
📊
Key Findings & Data:ApoE is a lipoprotein ofcentral nervous system encoded by ApoE gene with its 3 main co-dominantalleles, 2, 3 and 4.
💡
Conclusion & Impact:Our data show that the ApoE alleles maybe effective in the development of cerebral palsy and may be associated withsome clinical manifestations in those patients.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Domain Parameters

Özet

Cerebral palsy (CP) is the most frequent cause of mobility restriction andposture disturbance in childhood. Against the complexity in disease etiology,genetic factors, including Apolipoprotein E allelic distribution in this patientpopulation, are worthy targets for investigation. ApoE is a lipoprotein ofcentral nervous system encoded by ApoE gene with its 3 main co-dominantalleles, 2, 3 and 4. We aimed to evaluate the allelic frequencies of ApoE geneand its association with coexisting clinical entities such as vision and hearingimpairment, cognitive problems, seizures and MRI findings in a pediatricpatient population native to middle Anatolian region. Seventy-eight childrenwith CP and 60 healthy controls were genotyped. Genotypic variations alongwith coexisting clinical conditions and CP-related medical findings werecompared between the patient and control groups. The Denver DevelopmentalScreening Test for all, the Wechsler Intelligence Scale for Children-IV (shortform WISC-IV; Turkish version) for the patients >6y and the Stanford–BinetIntelligence Scale (SB-5) for those who aged 2-6 years old were employed toevaluate cognitive and mental abilities of the patients. ApoE 2 and 4 alleleswere more frequent in the patient group (p<0.05), whereas ApoE 3 allelewas more frequent in the healthy controls. ApoE 2/4 genotype has beendetermined 29% in the case group, but none in healthy control group. Inthe patient group with apolipoprotein 4 or 2 alleles, the rate of emergencycesarean section was found being significantly higher than the group with 3allele. Brain MRI findings were not significantly different among ApoE allelicvariants within the patient group. Our data show that the ApoE alleles maybe effective in the development of cerebral palsy and may be associated withsome clinical manifestations in those patients.

🔖

Cite This Article

GÜMÜŞ, E., ARAS, B. D., ÇİLİNGİR, O., YARAR, C., ÇARMAN, K. B., GÜRLEVİK, S. L., KOÇAK, O., ARTAN, S. (2018). Apolipoprotein E allelic variants and cerebral palsy. Turkish Journal of Pediatrics, Cilt: 60 - Sayı: 4, 361–371. https://ajindex.com/articles/412147

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (16)

  1. Rosenbaum P, Paneth N, Leviton A, et al. A report: The definition and classification of cerebral palsy April 2006. Dev Med Child Neurol Suppl 2007; 109: 8-14
  2. Van Naarden Braun K, Doernberg N, Schieve L, Christensen D, Goodman A, Yeargin-Allsopp M. Birth Prevalence of Cerebral Palsy: A Population-Based Study. Pediatrics 2016; 137. doi: 10.1542/peds.2015-2872
  3. Himmelmann K, Uvebrant P. The panorama of cerebral palsy in Sweden. XI. Changing patterns in the birth-year period 2003-2006. Acta Paediatr 2014; 103: 618-624
  4. Aydin R. Serebral palsi epidemiyolojisi. Türkiye Klinikleri Fiziksel Tıp ve Rehabilitasyon Dergisi Özel Sayısı 2009; 2: 1-7
  5. Erkin G, Delialioglu SU, Ozel S, Culha C, Sirzai H. Risk factors and clinical profiles in Turkish children with cerebral palsy: Analysis of 625 cases. Int J Rehabil Res 2008; 31: 89-91
  6. Badawi N, Keogh JM. Causal pathways in cerebral palsy. J Paediatr Child Health 2013; 49: 5-8
  7. Numata Y, Onuma A, Kobayashi Y, et al. Brain magnetic resonance imaging and motor and intellectual functioning in 86 patients born at term with spastic diplegia. Dev Med Child Neurol 2013; 55: 167-172
  8. Himmelmann K, Hagberg G, Uvebrant P. The changing panorama of cerebral palsy in Sweden. X. Prevalence and origin in the birth-year period 1999-2002. Acta Paediatr 2010; 99: 1337-1343
  9. MacLennan AH, Thompson SC, Gecz J. Cerebral palsy: Causes, pathways, and the role of genetic variants. Am J Obstet Gynecol 2015; 213: 779-788
  10. Costeff H. Estimated frequency of genetic and nongenetic causes of congenital idiopathic cerebral palsy in west Sweden. Ann Hum Genet 2004; 68(Pt 5): 515-520
  11. Fahey MC, Maclennan AH, Kretzschmar D, Gecz C, Kruer MC. The genetic basis of cerebral palsy. Dev Med Child Neurol 2017; 59: 462-469
  12. Oskoui M, Gazzellone MJ, Thiruvahindrapuram B, et al. Clinically relevant copy number variations detected in cerebral palsy. Nat Commun 2015; 6: 7949
  13. Wu D, Zou YF, Xu XY, et al. The association of genetic polymorphisms with cerebral palsy: A meta-analysis. Dev Med Child Neurol 2011; 53: 217-225
  14. Cedazo-Mínguez A. Apolipoprotein E and Alzheimer’s disease: Molecular mechanisms and therapeutic opportunities. J Cell Mol Med 2007; 11: 1227-1238
  15. Mahley RW, Weisgraber KH, Huang Y. Apolipoprotein E4: A causative factor and therapeutic target in neuropathology, including Alzheimer’s disease. Proc Natl Acad Sci U.S.A 2006; 103: 5644-5651
  16. Ponsford J, McLaren A, Schönberger M, et al. The associat