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Image: Institute for Bioengineering of Catalonia (IBEC).
 28.02.2017

A new therapeutic target that could slow the progression of Parkinson’s disease

Researchers from IBEC at PCB have identified a potential way to slow down the neurodegenerative progression of Parkinson’s disease. This breakthrough –a result of a collaboration of three research groups at IBEC together with colleagues in the Tòquio Metropolitan Institute of Medical Science, the Bellvitge University Hospital (HUB), the Vall d'Hebron Institute of Research (VHIR) and the Aragón Institute for Engineering Research (I3A)– could also apply to other types of neurodegenerative diseases, including some types of dementia such as Alzheimer’s disease, or multiple system atrophy.

 

The researchers focused their study – published this week in Molecular Neurobiology (doi:10.1007/s12035-017-0451-4)– on the cellular prion protein (PrPc), a specialized molecule located in the membranes of neurons that’s involved in a number of functions such as cell cycle control and neurotransmission.

In this work they found that aside from carrying out these functions, PrPc also binds to and increases the spreading of damaged α-synuclein – the protein responsible for neuronal degeneration and death in diseases such as Parkinson’s – between neurons. This points to PrPc as a possible pharmacological target to slow neurodegeneration in these types of pathologies.

Parkinson’s is a chronic neurodegenerative disease that affects movement. It develops when a particular type of neurons degenerate and die off, affecting the central nervous system’s motor and cognitive functions. The culprits responsible for this degeneration are Lewy bodies, abnormal aggregates of a malignant version of α-synuclein, a protein found in the neuron’s cytoplasm, that develop inside neurons. 

“PrPc is a key player in the spreading of Lewy bodies,” adds José Antonio Del Río, leader of one of the IBEC groups involved – the others were those of Josep Samitier and Eduard Torrents – and coordinator of the study. “If we could prevent them from propagating and grouping to form these accumulations, we could stop the progression of neuronal death in diseases like Parkinson’s.”

 

• Image description: Left: a) Microfluidic device used in the study. Primary cortical neurons can be seen after 15 days in vitro. b)Immunolocalization of the malignant version of α-synuclein (green) growing in microfluidic devices after inoculation with recombinant α-synuclein. c) Photomicrograph showing examples of adult cortical neurons with relevant degenerated synuclein content 45 days after α-synuclein injection in the striatum.
 

More information: IBEC website [+]