Noradrenergic Pathway to the Cerebellum: the Study Must Go On

In 1967, Anden, Fuxe, and Ungerstedt demonstrated the presence of monoamine-containing fibers in the rat cerebellum. Over the past 50 years, this finding has provided clinical relevance of the noradrenergic system to the cerebellum. Cerebellar dysfunction and noradrenergic system may relate to tremor in Parkinson disease and essential tremor, motor learning, and the vestibulo-ocular reflex in spinocerebellar ataxias. Cognition and emotion may also be linked to the cerebellar noradrenergic system, in relation to the symptoms of Alzheimer disease, dementia with Lewy bodies, and attention-deficit/hyperactivity disorder. Despite recent technological advances in neuroimaging for evaluating the noradrenergic system, we need more evidence to understand the precise pathophysiological relationship between the cerebellum and the noradrenergic system and its clinical implications.

Automated summary

In 1967, the presence of monoamine-containing fibers in the rat cerebellum was demonstrated, providing clinical relevance of the noradrenergic system to the cerebellum. Cerebellar dysfunction and the noradrenergic system may be implicated in various diseases and symptoms, such as tremor in Parkinson's disease, motor learning in spinocerebellar ataxias, and cognitive and emotional symptoms in Alzheimer's disease and attention-deficit/hyperactivity disorder. While recent advances in neuroimaging have helped evaluate the noradrenergic system, more research is needed to fully understand the pathophysiological relationship between the cerebellum and the noradrenergic system and its clinical implications.