Propagation of Parkinson's disease by extracellular vesicle production and secretion.
Laura E ShippeySusan Gerarda CampbellAndrew F HillDavid P SmithPublished in: Biochemical Society transactions (2022)
Parkinson's disease (PD) is a common neurodegenerative condition affecting a significant number of individuals globally, resulting in the presentation of debilitating motor and non-motor symptoms, including bradykinesia, resting tremor, as well as mood and sleep disorders. The pathology of PD has been observed to spread through the central nervous system resulting in progressive brain degeneration and a poor prognosis. Aggregated forms of the protein α-synuclein, particularly intermediary aggregates, referred to as oligomers, or preformed fibrils, have been implicated as the causative agent in the degeneration of neuronal processes, including the dysfunction of axonal transport, mitochondrial activity, and ultimately cellular death. Extracellular vesicles (EVs) have been strongly implicated in the propagation of PD pathology. Current observations suggest that aggregated α-synuclein is transported between neurons via small EVs in a series of exocytosis and endocytosis cellular processes leading to the observed spread of neurotoxicity and cellular death. Despite some understanding of the role of EVs in neurodegeneration, the exact mechanism by which these lipidic particles participate in the progression of Parkinson's pathology is not entirely understood. Here we review the current understanding of the role of EVs in the propagation of PD and explore their potential as a therapeutic target.
Keyphrases
- poor prognosis
- long non coding rna
- oxidative stress
- sleep quality
- multiple sclerosis
- spinal cord injury
- spinal cord
- heart rate
- heart rate variability
- deep brain stimulation
- white matter
- depressive symptoms
- density functional theory
- cerebrospinal fluid
- blood pressure
- case report
- amino acid
- climate change
- risk assessment
- blood brain barrier
- binding protein
- human health