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Understanding Neuron Degeneration in Parkinson's Disease

New Delhi, Aug 28: Recent research has revealed that prolonged overactivation of brain cells can lead to their degeneration and eventual death, shedding light on potential mechanisms behind Parkinson's disease. Scientists have long been aware that certain neurons deteriorate as Parkinson's progresses, but the underlying reasons remained unclear.

A study published in the journal eLife indicates that chronic stimulation of these neurons in mice can directly result in their death. The researchers propose that factors such as genetics, environmental toxins, and the compensatory demands placed on neurons could trigger this overactivation in Parkinson's patients.

"A key question in Parkinson's research has been why the most vulnerable cells succumb to the disease," stated Ken Nakamura, a researcher at the Gladstone Institutes in the US. He emphasized that understanding this could lead to new treatment strategies.

Currently, over 8 million individuals globally are affected by Parkinson's disease, which is characterized by tremors, slowed movements, muscle stiffness, and difficulties with balance and walking.

In their study, Nakamura and his team introduced a receptor into dopamine neurons of mice, enabling them to enhance neuronal activity through a drug administered via the animals' drinking water. This resulted in chronic neuron activation.

After just a few days of this overactivation, the mice exhibited disruptions in their normal day-night activity patterns. Within a week, signs of degeneration in the long projections (axons) of some dopamine neurons were observed, and by the end of the month, neuron death was evident.

Additionally, the researchers examined the molecular alterations in dopamine neurons before and after the activation. They discovered that overactivation led to changes in calcium levels and the expression of genes associated with dopamine metabolism.

When analyzing brain samples from early-stage Parkinson's patients, the researchers noted similar gene expression changes, indicating downregulation of genes linked to dopamine metabolism, calcium regulation, and healthy stress responses.