Israeli researchers have established a significant link between Parkinson’s disease and a network of molecules surrounding the brain, opening up new avenues for research to enhance understanding of the disorder and develop precise therapies.
Parkinson’s disease is a progressive neurodegenerative condition primarily affecting movement. It progresses gradually, typically starting with minor tremors in one hand. As the disease advances, movement symptoms can worsen, including stiffness, slowed movement, and difficulties with balance and coordination. Other symptoms may involve changes in speech, writing, facial expressions, as well as cognitive decline, mood swings, and sleep disturbances.
While the exact cause of Parkinson’s remains unclear, both genetic and environmental factors are thought to contribute. As there is no cure, current treatment focuses on managing symptoms with medication, therapy, and in some cases, deep brain stimulation.
A team of researchers from the University of Haifa, led by Professor Shani Stern, delved into the complex molecular processes within the brains of Parkinson’s patients. Their findings were recently published in the peer-reviewed journal, npj Parkinson’s Disease.
The team specifically investigated the extracellular matrix (ECM), a complex network of molecules surrounding and supporting brain cells. This network is crucial for maintaining the brain’s structural integrity and regulating intercellular communication. Disruptions in the ECM composition or function have been implicated in various neurological disorders, including Alzheimer’s disease, epilepsy, and traumatic brain injury.
Parkinson’s disease, characterized by the progressive degeneration of dopamine-producing cells in the brain’s substantia nigra region, has been subject to extensive scientific investigation. However, most research efforts have focused on genetic factors, accounting for only a small portion of cases. The Haifa University researchers aimed to fill this gap by exploring the role of the extracellular matrix in both genetically linked and sporadic Parkinson’s cases.
Using innovative techniques such as cell reprogramming, the researchers obtained skin cell samples from Parkinson’s patients with known genetic mutations and those without identifiable genetic predispositions. By converting these cells into stem cells and differentiating them into dopaminergic neurons, the team created a cellular model reflective of Parkinson’s pathology.
The findings were remarkable. Across both patient groups, the study revealed significant changes in the expression of genes responsible for extracellular matrix proteins. Specifically, reduced levels of mRNA and protein components associated with the extracellular matrix were observed in cells derived from Parkinson’s patients compared to healthy controls.
Furthermore, the study uncovered a novel discovery: the aggregation of collagen 4 protein, a crucial extracellular matrix component, exclusively in Parkinson’s patients. These abnormal alterations in the extracellular matrix coincided with decreased synaptic activity and impaired neuronal communication, providing insights into the underlying mechanisms driving Parkinson’s disease progression.
The researchers anticipate that their findings will eventually pave the way for the development of targeted therapies.
