Glial cells are a large class of cells of ectodermal (astroglia, oligodendroglia, and peripheral glial cells) and mesodermal (microglia) origin, which provide basic homeostatic support, protection, and defense to the nervous tissue. For these reasons, the potential for glial cells involvement in pathological events has been acknowledged since their discovery. Only during the past decade, research evidence has shown the key role of these non-neuronal cells in the progression of several neurological diseases. Neuropsychiatric disorders have always been widely ascribed to neuronal malfunction or loss, a “neurocentric view” that has dominated the neuropathology for a long time. However, because of the complexity of the physiological functions that glial cells perform, it is reasonable to state that they allow neurons to properly function; this “gliocentric view” has expanded the horizons to glial cells as new players to be studied and as potential pharmacological targets. This is a new and, for several aspects, undisclosed field of research. Indeed, despite a still growing body of evidence, the molecular mechanisms underlying glia involvement in psychiatric disorders have not yet been fully clarified. The present dissertation consists of an in-depth examination of glial cells in the onset and/or progression of three neuropsychiatric diseases: Alzheimer’s disease, autism spectrum disorders and acute stress. To this aim, different in vitro and in vivo preclinical models mimicking these pathologies have been used. All the results collected in this doctoral thesis demonstrate or contribute in demonstrating that glial cells are involved in the onset and in the progression of these neuropsychiatric disorders. The discovery of this common denominator among different brain pathologies represents an intriguing advance in the development of new therapeutic approaches to counteract these very frequent, but still incurable, diseases.
The role of glial cells in neuropsychiatric disorders
FACCHINETTI, ROBERTA
2020
Abstract
Glial cells are a large class of cells of ectodermal (astroglia, oligodendroglia, and peripheral glial cells) and mesodermal (microglia) origin, which provide basic homeostatic support, protection, and defense to the nervous tissue. For these reasons, the potential for glial cells involvement in pathological events has been acknowledged since their discovery. Only during the past decade, research evidence has shown the key role of these non-neuronal cells in the progression of several neurological diseases. Neuropsychiatric disorders have always been widely ascribed to neuronal malfunction or loss, a “neurocentric view” that has dominated the neuropathology for a long time. However, because of the complexity of the physiological functions that glial cells perform, it is reasonable to state that they allow neurons to properly function; this “gliocentric view” has expanded the horizons to glial cells as new players to be studied and as potential pharmacological targets. This is a new and, for several aspects, undisclosed field of research. Indeed, despite a still growing body of evidence, the molecular mechanisms underlying glia involvement in psychiatric disorders have not yet been fully clarified. The present dissertation consists of an in-depth examination of glial cells in the onset and/or progression of three neuropsychiatric diseases: Alzheimer’s disease, autism spectrum disorders and acute stress. To this aim, different in vitro and in vivo preclinical models mimicking these pathologies have been used. All the results collected in this doctoral thesis demonstrate or contribute in demonstrating that glial cells are involved in the onset and in the progression of these neuropsychiatric disorders. The discovery of this common denominator among different brain pathologies represents an intriguing advance in the development of new therapeutic approaches to counteract these very frequent, but still incurable, diseases.File | Dimensione | Formato | |
---|---|---|---|
Tesi_dottorato_Facchinetti.pdf
accesso aperto
Dimensione
39.41 MB
Formato
Adobe PDF
|
39.41 MB | Adobe PDF | Visualizza/Apri |
I documenti in UNITESI sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
https://hdl.handle.net/20.500.14242/175104
URN:NBN:IT:UNIROMA1-175104