Amber Southwell

Atypical expansion in mice of the sensory neuron-specific Mrg G protein-coupled receptor family.

GABA transporter deficiency causes tremor, ataxia, nervousness, and increased GABA-induced tonic conductance in cerebellum.

Intrabodies binding the proline-rich domains of mutant huntingtin increase its turnover and reduce neurotoxicity.

Intrabody gene therapy ameliorates motor, cognitive, and neuropathological symptoms in multiple mouse models of Huntington's disease.

Antibody therapy in neurodegenerative disease.

Perturbation with intrabodies reveals that calpain cleavage is required for degradation of huntingtin exon 1.

Gene therapy in mouse models of huntington disease.

Mice lacking caspase-2 are protected from behavioral changes, but not pathology, in the YAC128 model of Huntington disease.

Potent and selective antisense oligonucleotides targeting single-nucleotide polymorphisms in the Huntington disease gene / allele-specific silencing of mutant huntingtin.

Marked differences in neurochemistry and aggregates despite similar behavioural and neuropathological features of Huntington disease in the full-length BACHD and YAC128 mice.