New study finds that exercise can protect brain cells in Parkinson’s disease

Neuroscientists at the Faculty of Medicine of the Catholic University, Rome Campus, and the A. Gemelli IRCCS Polyclinic Foundation have made a groundbreaking discovery related to Parkinson’s disease. They found that intensive exercise can slow the progression of the disease, potentially leading to new non-drug treatments.

The study, titled “Intensive exercise ameliorates motor and cognitive symptoms in experimental Parkinson’s disease by restoring striatal synaptic plasticity,” was published in the esteemed journal Science Advances. The research was a collaborative effort involving various institutions, including San Raffaele Telematic University Rome, CNR, TIGEM, University of Milan, and IRCCS San Raffaele, Rome. Their investigation unveiled a novel mechanism responsible for the positive effects of exercise on brain plasticity.

The corresponding author, Full Professor of Neurology at the Catholic University and director of UOC Neurology at the University Polyclinic A. Gemelli IRCCS, Paolo Calabresi, expressed excitement over their discovery. He mentioned that exercising in the early stages of Parkinson’s disease can induce lasting benefits on movement control, even after the training is stopped.

The researchers found that intensive physical activity leads to increased production of a critical growth factor called brain-derived neurotrophic factor (BDNF). They replicated this phenomenon in an animal model of early-stage Parkinson’s disease by subjecting them to a four-week treadmill training protocol. This study marked the first time that the role of BDNF in the brain’s beneficial response to physical activity was demonstrated.

The research, spearheaded by Drs. Gioia Marino and Federica Campanelli from the Faculty of Medicine, Catholic University, Rome, employed a multidisciplinary approach using various techniques to measure improvements in neuronal survival, brain plasticity, motor control, and visuospatial cognition. The most notable outcome of the daily treadmill sessions was a reduction in the spread of pathological alpha-synuclein aggregates, which cause neuron dysfunction in specific brain areas responsible for motor control (the substantia nigra pars compacta and the striatum).

The neuroprotective effect of exercise was associated with the survival of dopamine-releasing neurons and their ability to express dopamine-dependent plasticity in the striatum. This aspect, which is impaired by Parkinson’s disease, resulted in preserved motor control and visuospatial learning in animals undergoing intensive training.

One significant finding was that BDNF interacts with the NMDA receptor for glutamate, enabling efficient responses to stimuli in the striatum, even after exercise cessation.

To further validate their findings, the research team is conducting a clinical trial to investigate whether intensive exercise can identify new markers for monitoring disease progression in early-stage Parkinson’s patients.

Furthermore, as Parkinson’s disease involves neuroinflammatory and neuroimmune components, the researchers plan to explore the involvement of glial cells, specialized cells that support neurons and their environment. This deeper investigation aims to uncover the molecular and cellular mechanisms responsible for the observed beneficial effects of exercise.

The results of this study offer hope for a novel approach to managing Parkinson’s disease and pave the way for potential non-drug treatments to complement existing therapies.

Source: Universita Cattolica del Sacro Cuore

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