Abstract
Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder worldwide. Clinically, it is characterized by severe motor complications caused by a progressive degeneration of dopaminergic neurons (DAn) and dopamine loss. Current treatment is focused on mitigating the symptoms through administration of levodopa, rather than on preventing DAn damage. Therefore, the use and development of neuroprotective/disease-modifying strategies is an absolute need, which can lead to promising gains on PD translational research. Mesenchymal stem cells (MSCs)–derived exosomes have been proposed as a promising therapeutic tool, since it has been demonstrated that they can act as biological nanoparticles with beneficial effects in different pathological conditions, including PD. Thus, considering their potential protective action in lesioned sites, MSCs-derived exosomes might also be active modulators of the neuroregeneration processes, opening a door for their future use as therapeutical strategies in human clinical trials. Therefore, in this review, we analyze the current understanding of MSCs-derived exosomes as a new possible therapeutic strategy for PD, by providing an overview about the potential role of miRNAs in the cellular and molecular basis of PD.
Highlights
Described by James Parkinson in 1817, Parkinson’s disease (PD) is the second most common chronic neurodegenerative disease in the world, affecting over 10 million people, and approximately 1%of the world population over 60 years old [1]
In the context of PD, we have recently shown that its administration in the substantia nigra pars compacta (SNpc)-STR pathway was able to partially revert the motor and histological symptoms of a 6-OHDA PD rat model [64], indicating that Mesenchymal stem cells (MSCs)-secretome can be used as a therapy for PD
Following on this work we have identified the presence of important neuroregulatory molecules in the secretome of MSCs, including BDNF, IGF-1, VEGF, Pigment epithelium-derived factor (PEDF), DJ-1, and Cystatin-C (Cys-C), that are being described as potential therapeutic mediators against PD [62,65], as well as matrix metalloproteinases (MMPs), namely MMP 2, known for being able to degrade alpha synuclein aggregates [65,66], and have correlated their presence with the impact observed in our in vitro and in vivo models
Summary
Described by James Parkinson in 1817, Parkinson’s disease (PD) is the second most common chronic neurodegenerative disease in the world, affecting over 10 million people, and approximately 1%. There are other brain areas presenting the above referred hallmarks, such as the olfactory bulb, neocortex, limbic system, and brainstem cells nuclei, suggesting a prion disease-like propagation and progression [4]. With this insight, a model was proposed, supporting LB transmission among cells as a possible route for disease onset and progression. A model was proposed, supporting LB transmission among cells as a possible route for disease onset and progression This model, called the Braak system, is divided in several stages, in which the autonomic nervous system (ANS) is the first affected by the pathology (stage 0), followed by. The development of management strategies is crucial, in which the diagnosis and the evaluation of the condition of the patient should be accurate, being followed by the development and application of personalized strategies, aiming to ameliorate the patient’s quality of life [8]
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