Intense exercise helps delay Parkinson's disease progression.

Neuroscientists from the Faculty of Medicine of the Catholic University, Rome Campus, and the A. Gemelli IRCCS Polyclinic Foundation found that intensive exercise could slow the course of Parkinson's disease and described the biological mechanisms. The finding could pave the way for new non-drug approaches.

The main effect observed in response to daily sessions of treadmill training is a reduction in the spread of pathological alpha-synuclein aggregates, which in Parkinson's disease leads to the gradual and progressive dysfunction of neurons in specific brain areas (the substantia nigra pars compacta and the striatum – constituting the so-called nigrostriatal pathway), essential to motor control.

The neuroprotective effect of physical activity is associated with the survival of neurons releasing the neurotransmitter dopamine and with the consequent striatal neurons' ability to express a form of dopamine-dependent plasticity, aspects otherwise impaired by the disease.

As a result, motor control and visuospatial learning, which depend on nigrostriatal activity, are conserved in animals that practice intensive training.

Neuroscientists have also found that BDNF, whose levels increase with exercise, interacts with the NMDA receptor for glutamate, enabling neurons in the striatum to respond efficiently to stimuli, with effects that persist beyond the exercise practice

Reference: "Intensive exercise ameliorates motor and cognitive symptoms in experimental Parkinson's disease by restoring striatal synaptic plasticity", Science Advances