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EHDN News ENGLISH ARTICLE OF THE MONTH 03/2011 January 2011 · Issue 12 Cell loss in the motor and cingulate cortex correlates with symptomatology in Huntington’s disease als, ranging from 0 to 51% in the motor cortex and from 0 to 65% in the cingulate cortex. Some brains that showed major cell loss in the motor cortex had minimal cell loss in the cingulate cortex, whereas other brains showed the opposite trend. Doris C. V. Thu et al., Brain (2010), 133: 1094-1110 Background The symptoms of Huntington’s disease (HD) vary markedly between individuals. Some patients show pronounced motor symptoms but only mild behavioural and/or cognitive disturbances. Others present severe mood problems and cognitive impairments but minimal movement abnormalities, while others are affected in all three domains to a similar extent. The cause of this variation is unknown. The pattern of cell loss clearly correlated with the symptom phenotype (see figure). Brains from individuals with predominantly motor symptoms showed major cell loss in the motor cortex with no significant cell loss in the cingulate cortex. By contrast, brains from patients in whom mood was primarily affected showed extensive cell loss in the cingulate cortex, with no significant cell loss in the motor cortex. Brains from individuals with mixed motor and mood symptoms showed considerable cell loss in both the motor and cingulate cortices. In each of the affected regions, the neurones that remained showed marked pathological changes in morphology. There was no correlation between CAG repeat number and cell loss from either region. Conclusions Tippett et al. (Brain 2007, 130: 206-21) have shown previThe heterogeneous pattern of cell loss in the motor and ously that mood dysfunction correlates with gamma-aminocingulate cortices correlates with the variability of motor and butyric acid (GABA) receptor and cell loss in the striatum. mood symptoms presented in each case. The authors conHowever, in recent years, a number of studies have shown cluded that the HD mutation produces variable topographithat atrophy of the whole brain and thinning of1102 the cerebral cal 133; patterns of cortical neurodegeneration that contribute to 1102| |Brain Brain 2010: 2010: 133; 1094–1110 1094–1110 cortex occur in premanifest and manifest HD, demonstrating specific symptoms. that HD pathology extends beyond the striatum. The present Total neuronal population (NeuN) study aimed to examine whether or not the symptom variability in HD can be related to different patterns of neurodegeneration in the cerebral cortex. 1102 | Brain 2010: 133; 1094–1110 © Thu et al. (2010) with permission from the Oxford University Press The extent of cell loss in two different regions of the cerebral cortex varies greatly between HD patients depending on whether the main symptoms they present are in the motor domain, behavioural domain, or both. D. C. V. Thu et al. Methods The study was double-blinded and used unbiased stereological cell counting methods to quantify cell loss in the primary motor cortex and anterior cingulate cortex in the post mortem brains of 12 HD patients and 15 control subjects. The primary motor cortex is involved in the control of movements, whilst the anterior cingulate cortex plays a role in the regulation of emotions and mood. Brain 2010: 133; 1094–1110 D. C. V. Thu et al. Detailed information of motor and behavioural symptoms was collected retrospectively from family members and from mining clinical records. HD patients were classified into three Total number of neurones (expressed as a percentage of the congroups depending on whether their dominant symptoms were trol) in the primary motor cortex and anterior cingulate cortex in the motor domain, behavioural domain, or both domains. of the three different HD groups (motor, mixed and mood). The total average number of neurones in both primary motor cortex and anterior cingulate cortex was significantly reduced in HD patients compared to control subjects. Surprisingly, the extent of cell loss varied greatly between individu- Imprint: © 2011 European Huntington’s Disease Network, Chairman Prof. G.B. Landwehrmeyer, Oberer Eselsberg 45/1, 89081 Ulm, Germany Summary by Diana Raffelsbauer, PharmaWrite; Design by Gabriele Stautner, Artifox. The information contained in this article is subject to the European HD Network Liability Disclaimer. – Please consult a doctor for medical advice. – Except as otherwise noted, this work is licensed under the Creative Commons Attribution-No Derivative Works 3.0 Unported License. Downloaded from http://brain.o Results Figure Figure 4 4Graph Graph showing showing (A)(A) thethe total total number number of of NeuN-positive NeuN-positive neurons neurons andand (B)(B) SMI32-positive SMI32-positive py percentage percentage of of thethe control) control) in the in the primary primary motor motor cortex cortex andand thethe anterior anterior cingulate cingulate cortex cortex of of thethe three thred Huntington’s Huntington’s disease disease cases cases (HD; (HD; motor, motor, mixed mixed andand mood). mood). Asterisks Asterisks indicate indicate statistically statistically significant significant diffd