Beth J. Synek

TL;DR: It is concluded that mRNA changes are not attributable to cell loss alone, and data from bona fide HD brains comprise an important reference for hypotheses related to HD and other neurodegenerative diseases.

TL;DR: The findings suggest that the heterogeneity in clinical symptom atology that characterizes Huntington's disease is associated with variation in the extent of cell loss in the corresponding functional regions of the cerebral cortex whereby motor dysfunction correlates with primary motor cortex cell loss and mood symptomatology is associatedwith cell lossIn the cingulate cortex.

TL;DR: These patients differ from those with the more common paraneoplastic cerebellar degeneration by the predominance of truncal over limb ataxia, the presence of myoclonus, the absence of severe dysarthria, a tendency for remission, and the preservation of Purkinje cells.

TL;DR: It is suggested that variation in clinical symptomatology in Huntington's disease is associated with variation in the relative abnormality of GABA(A) receptor expression in the striosomes and matrix compartments of the striatum, and that striosome-related circuits may modulate mood functioning.

TL;DR: Binding to A1 adenosine receptors and NMDA receptors was reduced in epileptic temporal cortex, while the other neurochemical parameters were unchanged, indicating loss of anticonvulsant A1 receptors may contribute to the human epileptic condition.