Mechanisms of neurodegeneration in Huntington’s disease
Article first published online: 12 NOV 2008
© The Authors (2008). Journal Compilation © Federation of European Neuroscience Societies and Blackwell Publishing Ltd
European Journal of Neuroscience
Volume 28, Issue 10, page 2156, November 2008
How to Cite
Gil, J. M. and Rego, A. C. (2008), Mechanisms of neurodegeneration in Huntington’s disease. European Journal of Neuroscience, 28: 2156. doi: 10.1111/j.1460-9568.2008.06522.x
- Issue published online: 12 NOV 2008
- Article first published online: 12 NOV 2008
Vol. 27, Issue 11, 2803–2820, Article first published online: 28 JUN 2008
In the published paper of Gil & Rego (2008), there were three textual errors. We reproduce the corrected sentences here. The authors apologise for any inconvenience caused.
In the second paragraph of section 1. Huntington’s disease, ‘(4p16.3)’ was misspelled as ‘(4p63)’. The corrected sentence is as follows.
‘This is an unstable expansion of CAG repeats within the coding region of the HD gene, which is located on the short arm of chromosome 4 (4p16.3) and encodes the protein huntingtin, whose proposed functions will be discussed on Section 2.1 of this review.’
In the second and third paragraphs of section 1.3. Genetics, ‘paternal’ was misspelled as ‘parental’. The corrected sentences are as follows.
‘The mutant allele is unstable during meiosis, changing in length in the majority of intergenerational transmissions, with either slight increases of 1–4 units or decreases of 1–2 units. In rare occasions, larger-sized increases occur in paternal transmissions, reflecting a particularly high mutation rate during spermatogenesis (The Huntington’s Disease Collaborative Research Group, 1993).’
‘Alleles of 40–50 units give rise to the most common adult-onset form of the disease, whereas the longest repeats (normally associated with high allele instability during paternal transmission) are responsible for the severe juvenile and infantile cases (The Huntington’s Disease Collaborative Research Group, 1993).’