Parkinson’s, so exercise could slow the disease
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Physical activity appears to actually slow down Parkinson’s disease. And it seems to do so through a hitherto unknown mechanism, which acts on the neuronal plasticity of the striatum nucleus, an area of the brain that underlies voluntary motor control and is the “seat” of motor learning. The discovery is Italian, conducted by the Catholic University of Rome and by the IRCCS Gemelli Polyclinic Foundation, and has just been published in Science Advances. The research only involved animal models, but another study involving patients with early-stage disease is underway.
I study
Already in the past some studies had shown that intensive physical exercise is associated with an increase in the production of a growth factor essential for the survival of neurons, the brain-derived neurotrophic factor (BDNF). The association also emerged in this new study.
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The animal model of Parkinson’s was obtained with the intracerebral administration of human alpha-synuclein. When this protein aggregates abnormally, there is a gradual and progressive degeneration of the nerve cells of some brain areas – the black substance and the striatum – responsible for movement control. Well: in animals subjected to a daily workout on a treadmill for 4 weeks, the researchers observed a reduction in the spread of pathological alpha-synuclein aggregates. “The neuroprotective effect of motor activity – they report – is associated with the survival of the neurons that release the neurotransmitter dopamine, and with the ability of the neurons of the striatum to continue to perform their function. Motor control and visuo-spatial learning, functions dependent on the activity of these areas, are also intact in animals subjected to intense training”. The neuroscientists then observed that BDNF, which increases with physical exercise, interacts with the NMDA receptor for glutamate, allowing the neurons of the striatum to respond to stimuli effectively, with effects that last over time, beyond the interruption of exercise.
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The results
Therefore, for the first time, the mechanism by which BDNF produces beneficial effects on the control of voluntary movement has been demonstrated. “Our results suggest that intensive physical activity, carried out on a regular basis in the initial phase of the disease, is able to induce functional and structural changes in neurons and allows to counteract the effects of events that cause neuronal toxicity – explains Paolo Calabresi , Professor of Neurology at the Catholic University, director of the UOC Neurology at the Gemelli University Hospital and one of the main authors of the study – This new mechanism can allow the identification of new therapeutic targets and functional markers to be taken into consideration to develop non-pharmacological treatments to be adopted in combination with currently used drugs.
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The next steps
His research group is also currently involved in a clinical study to verify the effect of physical exercise in early stage patients and to identify new markers capable of following the course of the disease. In parallel, however, basic research is also continuing, with the aim of investigating the involvement of glial cells, which support the activity of neurons and are implicated in the immune response. The study is funded by the Marlene and Paolo Fresco Institute for Parkinson’s and Movement Disorders, of the Ministry of Health and MIUR, and also involves other Italian institutes: the San Raffaele Telematic University and the IRCCS San Raffaele of Rome, the Cnr, the Tigem and the University of Milan.
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