Wawrocka Anna, Krawczyński Maciej R
Katedry i Zakładu Genetyki Medycznej Akademii Medycznej w Poznaniu.
Klin Oczna. 2007;109(10-12):470-4.
The most common forms of optic atrophy are: autosomatic dominant optic atrophy (ADOA, Kjer type) and maternally-inherited Leber's hereditary optic neuropathy. Rare forms of hereditary optic neuropathies are: optic atrophy X-linked and autosomatic recessive form of optic atrophy. Autosomatic dominant optic atrophy (ADOA) is the most frequent hereditary optic neuropathy. Three loci have been reported for ADOA, a major locus maps to 3q28-q29 (OPA1). The majority of mutations responsible for autosomatic dominant optic atrophy are localized in OPA1 gene. Second locus is linked to 18q12.2-q12.3 (OPA4) and a third locus on 22q12.1-q13.1 (OPA5). This study presents the actual state of knowledge about molecular changes in different forms of optic atrophy and shows hypothesis indicating the significant participation of mitochondrial dysfunction in it's pathogenesis.
常染色体显性视神经萎缩(ADOA,凯尔型)和母系遗传的Leber遗传性视神经病变。遗传性视神经病变的罕见形式有:X连锁视神经萎缩和常染色体隐性视神经萎缩。常染色体显性视神经萎缩(ADOA)是最常见的遗传性视神经病变。已报道ADOA有三个基因座,一个主要基因座定位于3q28 - q29(OPA1)。导致常染色体显性视神经萎缩的大多数突变位于OPA1基因。第二个基因座与18q12.2 - q12.3(OPA4)连锁,第三个基因座位于22q12.1 - q13.1(OPA5)。本研究展示了不同形式视神经萎缩分子变化的实际知识状态,并提出了表明线粒体功能障碍在其发病机制中起重要作用的假说。