Intellectual Disability and Ataxia: Genetic Collisions

Somayeh Kazeminasab; Hossein Najmabadi; Kimia Kahrizi

Arch Iran Med. 2018;21(1): 29-40.

PMID: 29664668
Scopus ID: 85044339219

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Review

Intellectual Disability and Ataxia: Genetic Collisions

Somayeh Kazeminasab ¹, Hossein Najmabadi ¹, Kimia Kahrizi ¹^*

¹ Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran

*Corresponding Author: Corresponding Author: Kimia Kahrizi, Genetics Research Center, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran, Email: kahrizi@yahoo.com

Abstract

Intellectual disability (ID) is a common and highly heterogeneous neurodevelopmental disorder. The prevalence of ID is around 1%–3% in the general population. ID is associated with a wide range of additional neurological disabilities and the results of various studies have disclosed the co-morbidity of ID and ataxia. The aim of this review is elucidation of the common molecular and cellular pathways in the etiology of ID and ataxia. Categorization of these genes with various cellular functions indicates several genetic collisions in the co-occurrence of ID and ataxia.

Keywords: Ataxia, Ciliogenesis, Ion channels, Intellectual disability, Mitochondria

Cite this article as: Kazeminasab S, Najmabadi H, Kahrizi K. Intellectual disability and ataxia: genetic collisions. Arch Iran Med. 2018;21(1):29–40.

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