TY - JOUR
T1 - Clinical and genetic spectrum of 104 Indian families with central nervous system white matter abnormalities
AU - Kaur, Parneet
AU - do Rosario, Michelle C.
AU - Hebbar, Malavika
AU - Sharma, Suvasini
AU - Kausthubham, Neethukrishna
AU - Nair, Karthik
AU - Shrikiran, A.
AU - Bhat Y, Ramesh
AU - Lewis, Leslie Edward S.
AU - Nampoothiri, Sheela
AU - Patil, Siddaramappa J.
AU - Suresh, Narayanaswami
AU - Bijarnia Mahay, Sunita
AU - Dua Puri, Ratna
AU - Pai, Shivanand
AU - Kaur, Anupriya
AU - Rakshith, K. C.
AU - Kamath, Nutan
AU - Bajaj, Shruti
AU - Kumble, Ali
AU - Shetty, Rajesh
AU - Shenoy, Rathika
AU - Kamate, Mahesh
AU - Shah, Hitesh
AU - Muranjan, Mamta N.
AU - Yatheesha, B. L.
AU - Avabratha, K. Shreedhara
AU - Subramaniam, Girish
AU - Kadavigere, Rajagopal
AU - Bielas, Stephanie
AU - Girisha, Katta Mohan
AU - Shukla, Anju
N1 - Funding Information:
We thank all the patients and families for participating in this study. This work was supported by Department of Health Research funded the project titled ‘Clinical and molecular characterization of leukodystrophies in Indian children’ (V.25011/379/2015‐GIA/HR) and National Institutes of Health funded projects, ‘Genetic Diagnosis of Heritable Neurodevelopmental Disorders in India: Investigating the Use of Whole Exome Sequencing and Genetic Counselling to Address the High Burden of Neurodevelopmental Disorders’(1R21NS094047–01) and ‘Genetic Diagnosis of Neurodevelopmental Disorders in India’ (Grant ID ‐ 1R01HD093570‐01A1).
Publisher Copyright:
© 2021 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd
PY - 2021/11
Y1 - 2021/11
N2 - Genetic disorders with predominant central nervous system white matter abnormalities (CNS WMAs), also called leukodystrophies, are heterogeneous entities. We ascertained 117 individuals with CNS WMAs from 104 unrelated families. Targeted genetic testing was carried out in 16 families and 13 of them received a diagnosis. Chromosomal microarray (CMA) was performed for three families and one received a diagnosis. Mendeliome sequencing was used for testing 11 families and all received a diagnosis. Whole exome sequencing (WES) was performed in 80 families and was diagnostic in 52 (65%). Singleton WES was diagnostic for 50/75 (66.67%) families. Overall, genetic diagnoses were obtained in 77 families (74.03%). Twenty-two of 47 distinct disorders observed in this cohort have not been reported in Indian individuals previously. Notably, disorders of nuclear mitochondrial pathology were most frequent (9 disorders in 20 families). Thirty-seven of 75 (49.33%) disease-causing variants are novel. To sum up, the present cohort describes the phenotypic and genotypic spectrum of genetic disorders with CNS WMAs in our population. It demonstrates WES, especially singleton WES, as an efficient tool in the diagnosis of these heterogeneous entities. It also highlights possible founder events and recurrent disease-causing variants in our population and their implications on the testing strategy.
AB - Genetic disorders with predominant central nervous system white matter abnormalities (CNS WMAs), also called leukodystrophies, are heterogeneous entities. We ascertained 117 individuals with CNS WMAs from 104 unrelated families. Targeted genetic testing was carried out in 16 families and 13 of them received a diagnosis. Chromosomal microarray (CMA) was performed for three families and one received a diagnosis. Mendeliome sequencing was used for testing 11 families and all received a diagnosis. Whole exome sequencing (WES) was performed in 80 families and was diagnostic in 52 (65%). Singleton WES was diagnostic for 50/75 (66.67%) families. Overall, genetic diagnoses were obtained in 77 families (74.03%). Twenty-two of 47 distinct disorders observed in this cohort have not been reported in Indian individuals previously. Notably, disorders of nuclear mitochondrial pathology were most frequent (9 disorders in 20 families). Thirty-seven of 75 (49.33%) disease-causing variants are novel. To sum up, the present cohort describes the phenotypic and genotypic spectrum of genetic disorders with CNS WMAs in our population. It demonstrates WES, especially singleton WES, as an efficient tool in the diagnosis of these heterogeneous entities. It also highlights possible founder events and recurrent disease-causing variants in our population and their implications on the testing strategy.
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U2 - 10.1111/cge.14037
DO - 10.1111/cge.14037
M3 - Article
AN - SCOPUS:85111598423
SN - 0009-9163
VL - 100
SP - 542
EP - 550
JO - Clinical Genetics
JF - Clinical Genetics
IS - 5
ER -