Opallo, Nicola (2024) Neuroinflammation in CNS disorders and their comorbidities: possible pharmacological control. [Tesi di dottorato]
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| Tipologia del documento: | Tesi di dottorato |
|---|---|
| Lingua: | English |
| Titolo: | Neuroinflammation in CNS disorders and their comorbidities: possible pharmacological control. |
| Autori: | Autore Email Opallo, Nicola nicola.opallo@unina.it |
| Data: | 10 Dicembre 2024 |
| Numero di pagine: | 115 |
| Istituzione: | Università degli Studi di Napoli Federico II |
| Dipartimento: | Farmacia |
| Dottorato: | Scienza del farmaco |
| Ciclo di dottorato: | 37 |
| Coordinatore del Corso di dottorato: | nome email Meli, Rosaria meli@unina.it |
| Tutor: | nome email Mattace Raso, Giuseppina [non definito] |
| Data: | 10 Dicembre 2024 |
| Numero di pagine: | 115 |
| Parole chiave: | obesity, mood disorders, neuroinflammation |
| Settori scientifico-disciplinari del MIUR: | Area 05 - Scienze biologiche > BIO/14 - Farmacologia |
| Informazioni aggiuntive: | Il mio ciclo di dottorato è il 37esimo ma a causa di un disservizio di tale portale di ateneo i dottorati selezionabili arrivano fino al ciclo 36 di conseguenza specifico qui come i miei colleghi |
| Depositato il: | 19 Nov 2025 14:00 |
| Ultima modifica: | 02 Set 2026 08:07 |
| URI: | https://www.fedoa.unina.it/id/eprint/16390 |
Abstract
Neuroinflammation is increasingly considered as a central player in the development and progression of several CNS disorders, including both neuropsychiatric and neurodegenerative diseases. Chronic activation of microglia and astrocytes within the brain triggers the release of pro-inflammatory cytokines, chemokines, and reactive oxygen species, leading to synaptic dysfunction, imbalance in monoamine circuits, and neuronal damage. These processes are closely linked to the exacerbation of mood disorders, such as anxiety and depression, and contribute to long-term cognitive decline observed in neurodegenerative diseases, like Alzheimer’s and Parkinson’s. The modulation of neuroinflammatory pathways, as a novel pharmacological strategy, could be crucial in mitigating the harmful effects deriving from chronic inflammation, with the aim of improving neurological and psychiatric outcomes in affected patients. This thesis investigates these issues through different approaches. First, a high-fat diet (HFD)-induced obesity model in mice is used to examine how metabolic dysregulation contributes to neuroinflammation and anxiety-like behaviors. The study evaluates (1) the effect of Bisphenol A (BPA), a pro-inflammatory environmental pollutant, in worsening these outcomes, and (2) the therapeutic potential of 2-Pentadecyl-2-Oxazoline (PEA-OXA), a compound known for its anti-inflammatory properties, in alleviating both neuroinflammation and anxiety-related symptoms. Finally, a neonatal exposure of lipopolysaccharide (LPS) in rats is used to simulate early-life immune challenges, assessing the long-term neuropsychiatric consequences of early neuroinflammatory insults. This model recapitulates the development of Pediatric Acute-Onset Neuropsychiatric Syndrome (PANS) and the role of early inflammation in predisposing individuals to psychiatric disorders later in life. Together, these studies seek to provide novel insights into the mechanisms by which neuroinflammation contributes to CNS disorders.
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