Naslov
Neuroprotective actions of DHEA and DHEAS in primary mouse neurons and SH-SY5Y cells exposed to toxic amyloid beta oligomers
(Neuroprotective actions of DHEA and DHEAS in primary mouse neurons and SH-SY5Y cells exposed to toxic amyloid beta oligomers)

Autori
Vuić, Barbara ; Miloš, Tina ; Nikolac Perković, Matea ; Nedić Erjavec, Gordana ; Tudor, Lucija ; Konjevod, Marcela ; Pivac, Nela ; Švob Štrac, Dubravka (Ruder Boskovic Institute, Zagreb, Croatia)

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Final programme and abstracts from the 10th Croatian Congress of Pharmacology and the 1st Croatian Congress of Clinical Pharmacology and Therapeutics with international participation , Pharmaca 2022 ; 52 (Suppl. 2) / Mršić-Pelčić, Jasenka ; Vitezić, Dinko ; Janković, Tamara - Zagreb, 2022, 168-168

Skup
10th Croatian Congress of Pharmacology and the 1st Croatian Congress of Clinical Pharmacology and Therapeutics with international participation = 10. Hrvatski kongres farmakologije i 1. Hrvatski kongres kliničke farmakologije s međunarodnim sufjelovanjem

Mjesto i datum
Opatija, Hrvatska, 22.09.2022. - 25.09.2022

Vrsta sudjelovanja
Poster

Vrsta recenzije
Domaća recenzija

Ključne riječi
DHEA ; DHEAS ; BDNF ; Alzheimer´s disease ; amyloid beta aggregation

Sažetak
Introduction: Alzheimer´s disease (AD) is neurodegenerative disease characterized by cognitive impairment and progressive synaptic damage accompanied by neuronal loss. The causes of amyloid beta aggregation that form amyloid plaques in the pathogenesis of AD has been debated for more than 25 years and it is supposed that amyloid beta oligomers may be the toxic factors acting on a very early stage of AD. Currently available therapy provides only symptomatic treatment, while many studies of new effective drugs have so far been unsuccessful. Therefore, neurosteroids dehydroepiandrosterone (DHEA) and its sulfated form dehydroepiandrosterone sulfate (DHEAS) are of a great interest due to their potential to modulate neurogenesis, neuronal growth and differentiation, as well as neuroprotection. Materials and methods: Neuroprotective effects of DHEA and DHEAS were investigated using primary mouse neurons, isolated from C57BL/6 mice embryos, and human SH-SY5Y neuroblastoma cells simultaneously exposed to toxic amyloid beta oligomers during 24 hours. Various assays (MTT, Muse, Promega) were used to determine cell viability and underlying mechanisms, while GraphPad Prism was used to interpret the obtained results. Results: Our results demonstrated that DHEA and DHEAS exert neuroprotective actions on primary mouse neurons and SH-SY5Y cells exposed to amyloid beta oligomers, probably via anti-apoptotic mechanisms. Conclusions: These findings suggest that DHEA and DHEAS may have therapeutic effects against amyloid beta toxicity. DHEA(S) could potentially represent novel preventive and/or therapeutic agents for AD in the future. This study needs to be confirmed and extended by further in vitro research and studies using animal models and human samples.

Izvorni jezik
Engleski

Znanstvena područja
Farmacija

POVEZANOST RADA