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November 2004

Tales From the Neural GenomeThe Lessons of Homozygous Porphyria

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Copyright 2004 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.2004

Arch Neurol. 2004;61(11):1650-1651. doi:10.1001/archneur.61.11.1650

A genomic approach to the human central nervous system and its crowning intellect is now possible through the analysis of relevant genes (neural genome), RNA (neural transcriptome), proteins (neural proteome), and protein interactions (systems biology).1 Orienting this exploration are structural relationships, exemplified by 82 (56%) of 146 genes causing human neurologic disease that are similar (homologous) to genes in nematode worms and fruit flies.2 Human neural genes can further be grouped by function (eg, myelin synthesis) or sequence similarity (paralogs such as the hexaminidase genes for Tay-Sachs and Sandhoff diseases), showing remarkable expansion and redundancy that can provide alternative pathways for therapy.3 Not to be forgotten in this sea change of technology are human neurogenetic diseases with their parables linking mind and molecule, a link used elegantly by Solis et al4 to suggest a novel mechanism for mental illness and neurodegeneration.

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