Topic: parkinsonism

Parkinson’s disease (PD) has been associated with alterations in neuronal activity in the basal ganglia-thalamocortical network. The motor cortex (M1) is a key node in this network and likely plays a significant role in the expression of impaired movement in PD. Altered neuronal activity in M1 has been reported and characterized at the single-unit level in PD, however, results are difficult to reconcile under one theoretical model (Doudet et al., 1990; Watts \& Mandir, 1992; Pasquereau et al., 2016). One promising avenue toward a mechanistic understanding of M1 pathophysiology in PD is to inve

Dysfunctional dopaminergic neurotransmission is implicated in several pathologies, including movement disorders such as parkinsonism and psychiatric diseases, suggesting overlapping pathological mechanisms. The dopamine transporter (DAT) is a key regulator of dopamine signalling and rare disease-associated DAT variants can cause psychiatric diseases and early-onset parkinsonism. However, the pathobiological processes that link DAT dysfunction to both parkinsonism and psychiatric symptoms are unknown. To investigate this, we developed a novel mouse disease model that expresses two mutations in

Dopamine (DA) is classically associated with learning and reward prediction error, though it is clear from deficits in the striatal dopaminergic system that DA plays a major, yet unclear, role in controlling motor behaviour. Several recent works have begun to uncover the complex roles DA plays in movement control. We have developed an experimental framework based on a dual fibre-photometry system, EMG recording and a freewheeling linear treadmill to explore the dynamics of dLight readouts during spontaneous locomotion and brief muscle twitches in head-fixed mice. In this work, we find high cor

Several studies have examined the genetic factors shared between Parkinson’s disease (PD) and schizophrenia (SZ), but the biological themes underlying their clinical relationship remain less explored. We employed systematic transcriptomic and network analyses (Figure 1) to examine the genes targeted by two sets of antipsychotic drugs (APDs), first-generation APDs inducing Parkinsonism and second-generation APDs typically effective against psychotic symptoms in PD. We also examined two sets of PD drugs, i.e., those that were contraindicated in SZ, or not. We found that, although global brain ex

The basal ganglia (BG) circuit, together with the motor cortex and the thalamus, plays an essential role in voluntary movement. In Parkinson’s disease (PD) patients, these structures exhibit exaggerated oscillations in the beta frequencies (10-30 Hz), a phenomenon also observed in animal models of parkinsonism, namely rats and non-human primates (NHP). Several potential generation mechanisms explaining this oscillatory activity have been hypothesized in various theoretical models, but a consensus has yet to be reached. Moreover, the extensive literature characterizing these oscillations and th