Editing Huntington's disease (section)

===Differential diagnosis===

About 99% of HD diagnoses based on the typical symptoms and a [[family history (medicine)|family history]] of the disease are confirmed by genetic testing to have the expanded trinucleotide repeat that causes HD. Most of the remaining are called [[Huntington's disease-like syndrome|HD-like (HDL) syndromes]].<ref name="lancet07" /><ref name="HD-LIKE"/> The cause of most HDL diseases is unknown, but those with known causes are due to mutations in the [[PRNP|prion protein gene]] (HDL1), the [[JPH3|junctophilin 3 gene]] (HDL2), a recessively inherited unknown gene (HDL3—only found in two families and poorly understood), and the gene encoding the [[TATA binding protein|TATA box-binding protein]] ([[Spinocerebellar ataxia|SCA17, sometimes called HDL4]]). Other autosomal dominant diseases that can be misdiagnosed as HD are [[dentatorubral-pallidoluysian atrophy]] and [[Adult-onset basal ganglia disease|neuroferritinopathy]]. Also, some [[autosomal recessive]] disorders resemble sporadic cases of HD. These include [[chorea acanthocytosis]] and [[pantothenate kinase-associated neurodegeneration]]. One [[Sex linkage|X-linked]] disorder of this type is [[McLeod syndrome]].<ref name="HD-LIKE">{{cite journal | vauthors = Schneider SA, Walker RH, Bhatia KP | title = The Huntington's disease-like syndromes: what to consider in patients with a negative Huntington's disease gene test | journal = Nature Clinical Practice. Neurology | volume = 3 | issue = 9 | pages = 517–525 | date = September 2007 | pmid = 17805246 | doi = 10.1038/ncpneuro0606 | s2cid = 9052603 }}</ref>