Titlebook: Neuroacanthocytosis Syndromes II; Ruth H. Walker,Shinji Saiki,Adrian Danek Book 2008 Springer-Verlag Berlin Heidelberg 2008 Neurorehabilit

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An Update on the Hardie Neuroacanthocytosis Seriesfication of several different molecular causes. We have revisited the original Queen Square series in an attempt to correlate the clinical picture and natural history of each case with the new genetic findings.

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Functional Imaging in Neuroacanthocytosistle, but if present appear to be particularly located in the frontal cortex. As with NA, an intriguing variety of devastating movement disorders may arise when specific striatal lesions occur. Due to the low prevalence of NA only a few patients have been investigated to date, and further studies are needed.

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A Mouse Model of Chorea-Acanthocytosistum. These are thought to be very similar to the features of the disease course and neuropathology seen in ChAc patients. Thus, this model mouse may be useful for pathogenic studies related to ChAc. Here, we review the ChAc-model mouse and recent findings on the upregulation of gephyrin and its related proteins in ChAcmodel mouse striatum.

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Neuropathology of Chorea-Acanthocytosission is ubiquitous. Interestingly, additional bands corresponding to proteins of approximately 160 kDa and 94 kDa comprising chorein N-terminal structures appear in brain as well as in several peripheral tissues. Furthermore, chorein is found at a high degree in testis and erythrocytes and at lower levels in muscle.

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Update on McLeod Syndromeng studies demonstrate striatal atrophy and subtle cerebral metabolic abnormalities. Neuropathological studies reveal striatal neuronal loss and gliosis without specific features. There is an ongoing search for a suitable animal model to disclose the pathogenetic mechanisms of the disorder and search for possible therapeutic targets.

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