The role of lysosomal vesicles in transporting α-synuclein aggregates, was demonstrated by scientists from the Institut Pasteur. It is responsible for Parkinson's and other neurodegenerative diseases, between neurons.
These proteins move from one neuron to the next in lysosomal vesicles which travel along the "tunneling nanotubes" between cells. These findings were published in The EMBO Journal. Synucleinopathies, a group of neurodegenerative diseases including Parkinson's disease, are characterized by the pathological deposition of aggregates of the misfolded α-synuclein protein into inclusions throughout the central and peripheral nervous system. Intercellular propagation (from one neuron to the next) of α-synuclein aggregates contributes to the progression of the neuropathology, but little was known about the mechanism by which spread occurs.
These proteins move from one neuron to the next in lysosomal vesicles which travel along the "tunneling nanotubes" between cells. These findings were published in The EMBO Journal. Synucleinopathies, a group of neurodegenerative diseases including Parkinson's disease, are characterized by the pathological deposition of aggregates of the misfolded α-synuclein protein into inclusions throughout the central and peripheral nervous system. Intercellular propagation (from one neuron to the next) of α-synuclein aggregates contributes to the progression of the neuropathology, but little was known about the mechanism by which spread occurs.
In this study, scientists from the Membrane Traffic and Pathogenesis Unit, directed by Chiara Zurzolo at the Institut Pasteur, used fluorescence microscopy to demonstrate that pathogenic α-synuclein fibrils travel between neurons in culture, inside lysosomal vesicles through tunneling nanotubes (TNTs), a new mechanism of intercellular communication.
‘Tunneling nanotubes (TNTs) play a significant part in the intercellular transfer of α-synuclein fibrils and reveals the specific role of lysosomes in this process.’
This study demonstrates that TNTs play a significant part in the intercellular transfer of α-synuclein fibrils and reveals the specific role of lysosomes in this process. This represents a major breakthrough in understanding the mechanisms underlying the progression of synucleinopathies.
These compelling findings, together with previous reports from the same team, point to the general role of TNTs in the propagation of prion-like proteins in neurodegenerative diseases and identify TNTs as a new therapeutic target to combat the progression of these incurable diseases.
Source: Eurekalert
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