The role of glial cells in neurodegenerative diseases. Part 2. Glial cells pathophysiology in neurodegeneration

The proper operation of the nervous system is strongly dependent on the interactions between neurons and glial cells. Thus, the disturbance of their relationship leads to various neurological complications. Pathological changes associated with glia, which appear in the initial stages of neurodegenerative diseases, have a significant impact on their progression. One of them is demyelination, a process that impairs the proper transmission of nerve signals, which occurs as a result of oligodendrocyte dysfunction and an immune response against myelin. This is caused i.a. due to inflammation, local pressure, hypoxia, or ischemia. Microgliosis is another pathological process taking place in neurodegeneration. For instance, the microglial cells activation due to the presence of protein aggregates leads to the induction of inflammation and immune system response directed against nerve cells, which is a characteristic of many neurodegenerative diseases. Microgliosis is often accompanied by astrogliosis, which results from nerve tissue damage. Reactive astrocytes within these lesions excrete not only pro-inflammatory, but also neurotoxic factors inhibiting the regeneration of nerve cells. Another phenomenon that is associated with glial cells is excitotoxicity – a type of neurotoxicity caused by the overstimulation of nerve cells. In particular, it concerns the excessive secretion or the limited reuptake of glutamate by astrocytes, which also happens in astrogliosis. The dysfunction of the blood-brain barrier co-created by astrocytes is associated with neurodegeneration either. This leads to a decrease in blood supply to the central nervous system and the accumulation of harmful substances. The aim of this paper was to outline the pathological processes connected with glial cells occurring in neurodegenerative diseases, which are: demyelination, astrogliosis, microgliosis, excitotoxicity, and dysfunction of the blood-brain barrier.