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α-Synuclein (SNCA) is an essential protein that participates in the formation of aggregates, whose presence is distinctive for all α-synucleinopathies and some addictions. Alterations in the gene that codes for SNCA and in the synthesis of this protein have been related to aggregation processes that alter its conformation and acquire self-aggregating capacity, which is related to its presence in neurons and could be a significant pathophysiological factor in the progression of diseases. One of the most common SNCA gene variants is G51D, which could be an anatomopathological indicator for neuronal diseases and long-term addictions. In the present study, the expression, purification and characterization techniques of the recombinant protein SNCA G51D are presented, as well as aggregation assays. Likewise, the circumstances for obtaining the polyclonal type antibody directed towards SNCA G51D are detailed. Optimization was also carried out for the cloning of this variant, using the pET30a vector, which gave us the greatest in silico solubility. The recombinant protein allowed the obtaining of a polyclonal anti SNCA G51D antibody, which was partially characterized and could be a significant immunological tool in confirming the existence of mutant proteins in samples of interest. [ABSTRACT FROM AUTHOR]

Recently the abnormal aggregation of protein has been implicated in diseases such as Alzheimer's and Parkinson's disease and neurodegenerative disorders. Recent studies have suggested that the transmission of these protein aggregates between neurons, are the underlying mechanism to progress and the pathology of the diseases. However, the precise mechanism which transmits these aggregates between neurons is unknown. They have suggested that the exosomes, a specific group of extracellular vesicles, can participate in the proteins, RNA and DNA transfer between neurons and play an important role in the transmission of aggregates. This manuscript describes various types of vesicles and evidence supporting the role of exosomes in the transmission of aggregates between neurons, as well as their relation to neurodegenerative processes. It also describes some mechanisms involved in transmission mediated by exosomes, how in the case of the exosomes released by nerve cells whose contents have molecular profiles that represent a time of the state of health of the brain, so it can used as biomarkers of the cerebral microenvironment and contribute to the progress of neurodegenerative diseases by facilitating the spread of proteins poorly folded to distant sites. This review also summarizes some studies in exosomes in the pathophysiology of Parkinson's disease and experimental models, and their potential use as biomarkers of diseases. [ABSTRACT FROM AUTHOR]

Parkinson's disease is a progressive neurological condition that affects millions of people in the world. Its pathophysiological feature is the loss of the dopaminergic neurons in the midbrain. The possible causes of this disease are diverse and that includes genetic mutations and environmental toxins, but the exact cause leading to the neuronal death remains unknown. Some pathogenic mechanisms that are basic to the degeneration of the dopaminergic cells has been characterized, and the evidence is presented and discussed in this work. Briefly, the deficiency in the dopamine storing into the synaptic vesicles leads to its uncontrolled metabolism, generating free radicals and reactive oxygen species in the cytoplasm. This seems to be the kick off of the processes for annihilating these neurons, and eventually progressing to a Parkinson's disease. This seems to be the common pathophysiological pathway underlining both, the genetic and the sporadic forms of the disease. [ABSTRACT FROM AUTHOR]