5Pigg M, Jagell S, Sillen A, et al. The Sjgren-Larsson syndrome gene is close toD17S805 as determined by linkage analysis and allelic association [J]. Nature Genet, 1994,8(4): 361-364.
6de Laurenzi V, Rogers GR, Hamrock DJ, et al. Sjgren-Larsson syndrome is causedby mutations in the fatty aldehyde dehydrogenase gene [J]. Nature Genet, 1996, 12(1):52-57.
7Rizzo WB, Lin Z, Carney G. Fatty aldehyde dehydrogenase:genomic structure,expression and mutation analysis in Sjgren-Larsson syndrome[J]. Chem Biol Interact,2001, 130-132(1-3): 297-307.
9Rizzo WB, Carney G, Lin Z. The molecular basis of Sjgren-Larsson sydrome:mutation analysis of the fatty aldehyde dehydrogenase gene [J]. Am J Hum Genet, 1999,65(6): 1547-1560.
1Sjogren T, Larsson T. Oligophrenia in combination with congenitalichthyosis and spastic disorders; a clinical and genetic study.Acta Psychiatr Neurol Scand Suppl, 1957,113: 1-112.
2Jagell S, Liden S. Ichthyosis in the Sj 5gren - Larsson syndrome.Clin Genet, 1982,21(4): 243-252.
3Willemsen MA, Ijlst L, Steijlen PM, et al. Clinical, biochemicaland molecular genetic characteristics of 19 patients with theSjogren-Larsson syndrome. Brain, 2001, 124(Pt 7): 1426-1437.
4Hofer PA, Jagell S. Sj5gren - Larsson syndrome : a dermato -histopathological study. J Cutan Pathol, 1982, 9(6): 360-376.
5Lossos A, Khoury M,Rizzo WB, et al. Phenotypic variabilityamong adult siblings with Sjbgren-Larsson syndrome. Arch Neurol,2006,63(2): 278-280.
6Pigg M, Jagell S, Sill6n A, et al. The Sjbgren-Larsson syndromegene is close to D17S805 as determined by linkage analysis andallelic association. Nat Genet, 1994, 8(4): 361-364.
7De Laurenzi V,Rogers GR,Hamrock DJ, et al. Sjogren-Larssonsyndrome is caused by mutations in the fatty aldehyde dehydro-genase gene. Nat Genet, 1996, 12(1): 52-57.
8Losito L, Gennaro L,De Rinaldis M, et al. SjSgren-Larsson syn-drome: phenotypic variability in two brothers with a neurocuta-neous disorder. Acta Neurol Belg, 2012,112(2): 205-208.
9Rizzo WB, S,Aulis D, Jennings MA, et al. Ichthyosis in Sjogren-Larsson syndrome reflects defective barrier function due to ab-normal lamellar body structure and secretion. Arch DermatolRes, 2010,302(6):443-451.
10Willemsen MA, de Jong JG, van Domburg PH, et al. Defectiveinactivation of leukotriene B4 in patients with Sjogren-Larssonsyndrome. J Pediatr, 2000, 136(2): 258-260.