Neuroprotektivni učinak dehidroepiandrosteron-sulfata (DHEAS) u staničnim modelima Alzheimerove bolesti

master's thesis

• Title (english): The neuroprotective effect of dehydroepiandrosterone-sulphate (DHEAS) in in vitro models of Alzheimer's disease
• Author: Robert Pendelić
• Mentor: Gordana Nedić Erjavec (mentor)
• Mentor: Dubravka Hranilović (komentor)
• Committee member: Dubravka Hranilović (predsjednik povjerenstva)
• Committee member: Petra Korać (član povjerenstva)
• Committee member: Duje Lisičić (član povjerenstva)
• Committee member: Biljana Balen (član povjerenstva)
• Granter: University of Zagreb; Faculty of Science; (Department of Biology); Zagreb
• Defense date and country: 2023-09-21, Croatia
• Scientific / art field, discipline and subdiscipline: NATURAL SCIENCES; Biology

Abstract

Alzheimerova bolest (AB) je najučestaliji oblik demencije koji se očituje kroz gubitak raznih
kognitivnih sposobnosti. Uzrokovana je propadanjem neurona i sinaptičkih veza unutar mozga
i visoko je povezana s nakupljanjem peptida amiloid beta (Aβ) u središnjem živčanom sustavu.
Uglavnom se razvija kod ljudi starijih od 65 godina, a udio oboljelog stanovništva je u stalnom
porastu. Bolest je posljedica velikog broja čimbenika, što je čini vrlo složenom i zasad
neizlječivom. Istraživanja u biomedicini su, između ostalog, usmjerena i na pronalazak
tretmana koji bi značajno usporili proces odumiranja neurona u mozgu. Potencijalan kandidat
za to je neurosteroid dehidroepiandrosteron-sulfat (DHEAS) koji u središnjem živčanom
sustavu pomaže u očuvanju neurona, a njegove endogene razine pozitivno koreliraju s
kognitivnim sposobnostima. Cilj ovog rada bio je istražiti potencijalni učinak DHEAS-a u
promociji preživljenja stanica korištenjem dvaju in vitro modela AB-a, primarne kulture mišjih
neurona i stanične linije SH-SY5Y, tretiranih oligomerima Aβ. Rezultati istraživanja sugeriraju
neuroprotektivno djelovanje DHEAS-a u staničnom modelu AB-a temeljenom na primarnoj
kulturi mišjih neurona. S druge strane, isti učinak nije bilo moguće postići na staničnoj liniji
SH-SY5Y tretiranoj oligomerima Aβ.

Abstract (english)

Alzheimer's disease (AD) is the main cause of dementia which is characterised by the loss of
various cognitive abilities. It is caused by neural and synaptic loss within the brain and is highly
associated with the accumulation of amyloid beta (Aβ) peptide in the central nervous system.
It mostly affects people older than 65 years and the overall percentage of people affected by it
is constantly increasing. Many factors play a role in the formation of the disease, which makes
it very complex and currently incurable. Research in biomedicine is, among other things,
focused on finding treatments that would significantly reduce the neural loss in the brain. A
potential candidate for this is the neurosteroid dehydroepiandrosterone-sulphate (DHEAS)
which participates in neuronal preservation in the central nervous system, and its endogenous
levels positively correlate with cognitive abilities. The aim of this research was to investigate
the potential effect of DHEAS in promoting cell survival using two in vitro models of AD,
primary cultures of mouse neurons and the SH-SY5Y cell line, both treated with Aβ oligomers.
The obtained results suggest a neuroprotective effect of DHEAS in an in vitro model of AD
based on the primary culture of mouse neurons. On the other hand, the same effect could not
be achieved on the SH-SY5Y cell line treated with Aβ oligomers.

• Keywords: DHEAS; neurosteroid; demencija; in vitro studija; tretman; apoptoza
• Keywords (english): DHEAS; neurosteroid; dementia; in vitro study; treatment; apoptosis
• Language: croatian
• URN:NBN: urn:nbn:hr:217:787617
• Study programme: Title: Molecular Biology; Study programme type: university; Study level: graduate; Academic / professional title: magistar/magistra molekularne biologije (magistar/magistra molekularne biologije)
• Type of resource: Text
• File origin: Born digital
• Access conditions: Embargoed access; Embargo expiration date: 2024-09-21
• Created on: 2023-11-15 13:19:56