| pubmed-article:18799783 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18799783 | lifeskim:mentions | umls-concept:C0027746 | lld:lifeskim |
| pubmed-article:18799783 | lifeskim:mentions | umls-concept:C0031672 | lld:lifeskim |
| pubmed-article:18799783 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:18799783 | lifeskim:mentions | umls-concept:C0314603 | lld:lifeskim |
| pubmed-article:18799783 | lifeskim:mentions | umls-concept:C0243067 | lld:lifeskim |
| pubmed-article:18799783 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:18799783 | pubmed:dateCreated | 2008-10-28 | lld:pubmed |
| pubmed-article:18799783 | pubmed:abstractText | Mutations in the gene encoding phospholipase A(2) group VI (PLA2G6) are associated with two childhood neurologic disorders: infantile neuroaxonal dystrophy (INAD) and idiopathic neurodegeneration with brain iron accumulation (NBIA). INAD is a severe progressive psychomotor disorder in which axonal spheroids are found in brain, spinal cord, and peripheral nerves. High globus pallidus iron is an inconsistent feature of INAD; however, it is a diagnostic criterion of NBIA, which describes a clinically and genetically heterogeneous group of disorders that share this hallmark feature. We sought to delineate the clinical, radiographic, pathologic, and genetic features of disease resulting from defective phospholipase A(2). | lld:pubmed |
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| pubmed-article:18799783 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18799783 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:18799783 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18799783 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:18799783 | pubmed:issn | 1526-632X | lld:pubmed |
| pubmed-article:18799783 | pubmed:author | pubmed-author:RodriguezDD | lld:pubmed |
| pubmed-article:18799783 | pubmed:author | pubmed-author:SantosMM | lld:pubmed |
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| pubmed-article:18799783 | pubmed:author | pubmed-author:CoryellJ CJC | lld:pubmed |
| pubmed-article:18799783 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18799783 | pubmed:day | 28 | lld:pubmed |
| pubmed-article:18799783 | pubmed:volume | 71 | lld:pubmed |
| pubmed-article:18799783 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18799783 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18799783 | pubmed:pagination | 1402-9 | lld:pubmed |
| pubmed-article:18799783 | pubmed:dateRevised | 2010-9-21 | lld:pubmed |
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| pubmed-article:18799783 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18799783 | pubmed:articleTitle | Neurodegeneration associated with genetic defects in phospholipase A(2). | lld:pubmed |
| pubmed-article:18799783 | pubmed:affiliation | Department of Molecular and Medical Genetics, Oregon Health & Science University, L103a, 3181 SW Sam Jackson Park Rd., Portland, OR 97239-3098, USA. | lld:pubmed |
| pubmed-article:18799783 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18799783 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:18799783 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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