Abstract
Extracellular vesicles (EVs) can be classified into apoptotic bodies, microvesicles (MVs), and exosomes, based on their origin or size. Exosomes are the smallest and best characterized vesicles which derived from the endosomal system. These vesicles are released from many different cell types including neuronal cells and their functions in the nervous system are investigated. They have been proposed as novel means for intercellular communication, which takes part not only to the normal neuronal physiology but also to the transmission of pathogenic proteins. Indeed, exosomes are fundamental to assemble and transport proteins during development, but they can also transfer neurotoxic misfolded proteins in pathogenesis. The present review will focus on their roles in neurological diseases, specifically brain tumors, such as glioblastoma (GBM), neuroblastoma (NB), medulloblastoma (MB), and metastatic brain tumors and chronic neurodegenerative diseases, such as Alzheimer, Parkinson, multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Huntington, and Prion diseseases highlighting their involvement in spreading neurotoxicity, in therapeutics, and in pathogenesis.
Highlights
Extracellular vesicles (EVs) comprise a wide variety of membrane-limited vesicles released from cells
Vesicles have been proposed as promising biomarkers as well as suitable therapeutic agents
In GB the immune-modulating properties of exosome have emerged related to their cargo in HSPs capable of driving antitumor immunity, and the presence of canonical HSPs was confirmed in MB
Summary
Extracellular vesicles (EVs) comprise a wide variety of membrane-limited vesicles released from cells. Some authors proposed a neuro-toxic role for exosomes in Alzheimer’s disease with a study on primary cultured astrocytes, Wang et al reported a new mechanism of apoptosis induction by PAR-4/ceramide-enriched exosomes, which can contribute to Alzheimer’s disease (Wang et al, 2012) In their experiments, apoptosis was thwarted by shRNA-mediated downregulation of PAR-4, a protein which sensitize cells to the sphingolipid ceramide. By ELISA quantification of cargo proteins they examined the Ab42-generating system and found that γ-secretase, ADE levels of β-site amyloid precursor protein-cleaving enzyme 1, soluble amyloid precursor protein (sAPP)β, soluble Aβ42, sAPPα, glial-derived neurotrophic factor (GDNF), P-S396-tau, and P-T181-tau were significantly higher for patients, suggesting a role for activated astrocyte-neuron axis in proteinopathic dementias (Goetzl et al, 2016b) Their effort of isolating immunochemically human plasma NDEs and ADEs, containing neuron-specific cargo, permits to characterize CNS-derived exosomes in living humans. By a deep sequencing of small RNA, the authors found a characteristic signature of miRNAs (increased let-7i, let-7b, miR-21, miR-128a, miR-29b, miR-222, miR-424, and miR-3423p levels with decreased miR-146a levels) in exosomes emitted by prion infected neuronal cells respect to exosomes from
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