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Lipidomics and Transcriptomics in Neurological Diseases
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Lipid transport and human brain development.

Christer Betsholtz1

  • 1Vascular Biology Program, Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden, and the Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden.

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|June 27, 2015
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Mutations in MFSD2A, a blood-brain barrier protein, cause microcephaly by disrupting brain lipid content during development. This finding solves a long-standing mystery of brain lipid regulation.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • The mechanisms of brain lipid accumulation during development and maintenance in adulthood are not fully understood.
  • MFSD2A is a protein primarily expressed in the blood-brain barrier.

Purpose of the Study:

  • To investigate the role of MFSD2A in brain lipid metabolism and development.
  • To elucidate the cause of microcephaly linked to MFSD2A dysfunction.

Main Methods:

  • Analysis of inactivating mutations in the MFSD2A gene.
  • Phenotypic characterization of individuals with MFSD2A mutations, focusing on brain size and lipid content.

Main Results:

  • Inactivating mutations in MFSD2A were identified as a cause of microcephaly.
  • These mutations impair the brain's ability to build up and maintain lipid content.

Conclusions:

  • MFSD2A plays a critical role in regulating brain lipid homeostasis.
  • Dysfunction of MFSD2A at the blood-brain barrier explains microcephaly and provides insight into brain lipid development.