Parkinson's Disease Involving Glial Cell Dysfunction

Abstract

It is well known that the decline in the viability of dopamine neurons slowly leads to the appearance of various symptoms characteristic of Parkinson's disease (PD). These symptoms depend mainly on dysfunction of nigrostriatal dopaminergic denervation. The cause of neuronal death has not yet been elucidated, although there are several hypotheses suggesting different factors that may trigger it. One possible mechanism of neurodegeneration is the establishment of chronic inflammation in the central nervous system, where glial cells are key regulators of inflammatory responses. They also play a phagocytic role, engulfing synapses, apoptotic cells, cellular debris and released toxic proteins. An imbalance in the activation of these cells can lead to an overproduction of cytotoxic factors, which contribute to the death of dopamine neurons. As PD involves not only the loss of dopamine neurons, but also the dysfunction of glial cells, whose loss or excessive activation can contribute to neuronal death, there is a need to better understand the role of these cells in PD in order to develop effective therapies.