Åsa Petersén

This study shows that HTT CAA/CCA-loss variants increase toxicity in Huntington disease models independently of somatic repeat instability.

This study shows that mutant huntingtin in the hypothalamus causes ventral striatal neuropathology, including DARPP-32 neuron loss, and disrupts hypothalamus-ventral striatal circuitry in HD mice.

The paper uses microarray analysis to identify gene expression changes in Huntington's disease mouse models, finding differential expression and pathway dysregulation associated with wild-type and mutant HTT overexpression.

The paper measures CAG repeat size in the HTT gene in Lynch syndrome patients and controls, finding larger and more variable repeats in LS patients.

This study shows that hypothalamic expression of mutant HTT causes sex-specific metabolic imbalance, and IKKβ inhibition reduces obesity in female HD mice.

This study investigates whether excitotoxicity contributes to hypothalamic neuronal loss in HD mouse models, finding no evidence of excitotoxicity-induced damage in these models.