In conclusion, investigating PD-participants can reveal both underlying facts of our timing and action networks, while also shedding light on the disease itself.

As an exploratory endeavour, we investigated the cerebello-thalamo-ganglion network we, proposed in bit.ly/42Yh4NE, and found that PD-patients showed altered activity for the jittered condition.

The differences in the cerebellum correlated with PD-symptoms as measured by UPDRS.

Before the onset of the expected, but omitted stimulation, we found differences in the beta band (14-30 Hz) between groups in the cerebellum and the caudate nucleus.

We had PD-participants and controls participate in a passive paradigm. Jittered and non-jittered trains of stimulation were followed by omissions.

The differences in the cerebellum correlated with PD-symptoms as measured by UPDRS

Before the onset of the expected, but omitted stimulation, we found differences in the beta band (14-30 Hz) between groups in the cerebellum and the caudate nucleus

We had PD-participants and controls participate in a passive paradigm. Jittered and non-jittered trains of stimulation were followed by omissions.

Could you expand on what those other things are?
I am curious because, in humans, we are finding out that the cerebellum is basically involved in most cognition as well.
And I am eager to learn what might be going on in other species.

Thanks

Coming back to my job call, this is exactly what I set out to test using a combination of deep brain stimulation and magnetoencephalography. 🧠📈
international.au.dk/about/profil...

This fits with our second paper, short review where we forward the hypothesis that the cerebellum is not a time-keeper per se, but an integrator of spatial and temporal information that can inform predictions about future sensory events, and allowing for informed behaviour bit.ly/4bcQd31. 🧠📈