Introduction: Addressing the formidable therapeutic hurdles posed by Alzheimer’s disease (AD), our study delves into the central role of amyloid β 1-42 (Aβ1-42) protein aggregation in its onset. Aim: Our investigation aims to assess the therapeutic potential of the isoindolinone derivative 3-(3-oxoisoindolin-1-yl)pentane-2,4-dione (ISOAC1) against the Aβ1-42- induced toxicity. Material and methods: Employing a combination of thiofl avin T fl uorescence assay and biological and cellular approaches, alongside other experimental methods, we explored ISOAC1’s ability to mitigate Aβ1-42 aggregation and toxicity. Results and conclusions: Our study unveils ISOAC1’s capacity to disrupt Aβ1-42 aggregation and impede its transition towards β-sheet structures. Furthermore, our fi ndings shed light on ISOAC1’s binding mechanisms with Aβ1-42, indicating its promise as a therapeutic agent. ISOAC1 emerges as a compelling neuroprotective compound, off ering novel avenues for AD treatment.
Biological aspects of new molecular therapies for neuropathologies / Piccialli, Ilaria; Greco, Francesca; Roviello, Giovanni N.; Josè Sisalli, Maria; Tedeschi, Valentina; di Mola, Antonia; Borbone, Nicola; de Feo, Vincenzo; Secondo, Agnese; Massa, Antonio; Pannaccione, Anna; Nolli, MARIA GRAZIA; Oliviero, Giorgia. - (2024). (Intervento presentato al convegno Modern research trends in biomedical sciences (MRTBS) 2024 tenutosi a Opole, Polonia nel 17-19 aprile 2024).
Biological aspects of new molecular therapies for neuropathologies
Ilaria Piccialli
;Valentina Tedeschi;Nicola Borbone;Agnese Secondo;Anna Pannaccione;Maria Grazia Nolli;Giorgia Oliviero
2024
Abstract
Introduction: Addressing the formidable therapeutic hurdles posed by Alzheimer’s disease (AD), our study delves into the central role of amyloid β 1-42 (Aβ1-42) protein aggregation in its onset. Aim: Our investigation aims to assess the therapeutic potential of the isoindolinone derivative 3-(3-oxoisoindolin-1-yl)pentane-2,4-dione (ISOAC1) against the Aβ1-42- induced toxicity. Material and methods: Employing a combination of thiofl avin T fl uorescence assay and biological and cellular approaches, alongside other experimental methods, we explored ISOAC1’s ability to mitigate Aβ1-42 aggregation and toxicity. Results and conclusions: Our study unveils ISOAC1’s capacity to disrupt Aβ1-42 aggregation and impede its transition towards β-sheet structures. Furthermore, our fi ndings shed light on ISOAC1’s binding mechanisms with Aβ1-42, indicating its promise as a therapeutic agent. ISOAC1 emerges as a compelling neuroprotective compound, off ering novel avenues for AD treatment.File | Dimensione | Formato | |
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