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Using this model, we now demonstrate that Trkb deletion-induced iSPN dysfunction leads to a hyperdopaminergic state in the pre-symptomatic phase, before motor dysfunction onset, reminiscent of the dopaminergic dysfunction observed in the brains of patients with HD 3,4,5

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Preclinical studies indicate potential roles in: Supporting healthy fat metabolism and reduction of adipogenesis Improving insulin sensitivity in metabolic research models Enhancing NAD+ salvage pathway efficiency Exploring effects on energy homeostasis and longevity pathways These findings remain preliminary and confined to laboratory and animal models

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Gut 45, 592594 (1998)

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