## Abstract Huntington's disease (HD) is caused by an abnormally expanded CAG repeat in the __IT__‐__15__ gene, which encodes a widely expressed protein called huntingtin. Abnormalities of mitochondrial respiratory chain function, specifically complex II/III, have been identified in HD striatum and
Basal ganglia volume and clinical correlates in ‘preclinical’ Huntington’s disease
✍ Scribed by Caroline K. Jurgens; Lotte van de Wiel; Ad C. G. M. van Es; Yvette M. Grimbergen; Marie-Noëlle W. Witjes-Ané; Jeroen van der Grond; Huub A. M. Middelkoop; Raymund A. C. Roos
- Publisher
- Springer
- Year
- 2008
- Tongue
- English
- Weight
- 200 KB
- Volume
- 255
- Category
- Article
- ISSN
- 0340-5354
No coin nor oath required. For personal study only.
📜 SIMILAR VOLUMES
## Abstract The early stages of Huntington's disease (HD) present with motor, cognitive, and emotional symptoms. Correspondingly, current models implicate dysfunction of the motor, associative, and limbic basal ganglia‐thalamocortical circuits. Available data, however, indicate that in the early st
## Abstract Future clinical trials of neuroprotection in prodromal Huntington's (known as preHD) will require sensitive in vivo imaging biomarkers to track disease progression over the shortest period. Since basal ganglia atrophy is the most prominent structural characteristic of Huntington's patho
## Abstract The basal ganglia are thought to play an important role in regulating motor programs involved in gait and in the fluidity and sequencing of movement. We postulated that the ability to maintain a steady gait, with low stride‐to‐stride variability of gait cycle timing and its subphases, w
## Abstract Functional disability of patients with Huntington's disease (HD) is determined by impairment of voluntary motor function rather than the presence of chorea. However, only few attempts have been made to quantify this motor impairment. By using a simple reaction time paradigm, we measured