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Significance Huntington’s disease (HD) is a devastating neurodegenerative genetic disorder characterized by progressive decline of motor control. Although the genetic mutation responsible for the syndrome associated with HD has been clearly identified, a specific treatment for HD is not yet available. Therefore, there is a tremendous need for new therapeutic approaches and new molecular therapeutic targets. Using HD mouse models, we show age-dependent alterations of corticostriatal transmission paralleled by alterations of M4 muscarinic acetylcholine receptor (mAChR)-mediated control of corticostriatal glutamate signaling. Also, chronic treatment with the selective M4 mAChR positive allosteric modulator VU0467154 improves motor and synaptic deficits in 5-mo-old YAC128 mice. This suggests that M4 may represent a therapeutic target for the treatment of HD.

Allosteric activation of M 4 muscarinic receptors improve behavioral and physiological alterations in early symptomatic YAC128 mice

Allosteric activation of M ₄ muscarinic receptors improve behavioral and physiological alterations in early symptomatic YAC128 mice