<?xml version="1.0"?>
<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dc="http://purl.org/dc/elements/1.1/"><rdf:Description rdf:about="https://repozitorij.uni-lj.si/IzpisGradiva.php?id=163672"><dc:title>Involvement of purinergic signaling components in selected structures of the forebrain of rats suffering from experimental autoimmune encephalomyelitis</dc:title><dc:creator>Dokmanović,	Tamara	(Avtor)
	</dc:creator><dc:creator>Kreft,	Marko	(Mentor)
	</dc:creator><dc:creator>Dragić,	Milorad	(Komentor)
	</dc:creator><dc:subject>multiple sclerosis</dc:subject><dc:subject>experimental autoimmune encephalomyelitis</dc:subject><dc:subject>eN/CD73</dc:subject><dc:subject>adenosine
receptors</dc:subject><dc:subject>adenosine deaminase</dc:subject><dc:subject>AMPase</dc:subject><dc:subject>ADPase</dc:subject><dc:description>Multiple sclerosis (MS) is a chronic autoimmune disease of the central nervous system
(CNS) accompanied by demyelination and subsequent neuronal damage that leads to
permanent disability in young adults. The most commonly used experimental model for
studying MS is experimental autoimmune encephalomyelitis (EAE), which exhibits
main pathological features of the human disease. EAE is considered an inflammatory
disease, and the neuroinflammation caused by EAE is tightly regulated by purinergic
signaling. Various pathological events lead to neuronal damage, triggering release of
large amounts of ATP, which then acts differently on purinoreceptors. Furthermore,
exogenous ATP is removed by cascade hydrolysis by the action of the ectonucleotidase
enzyme chain. The last step in ATP degradation is the dephosphorylation of AMP into
adenosine by the action of ecto-5'-nucleotidase (eN/CD73). In this paper, we compare
the expression levels of purinoreceptors A1R, A2AR, A2BR, and A3R, and the activity of
purinergic enzymes, ecto-5'-nucleotidase, adenosine deaminase (ADA), AMPase and
ADPase in selected brain regions of healthy control animals and animals in the peak of
EAE, aiming to better understand the role of purinergic signaling in the pathophysiology
of MS.</dc:description><dc:publisher>[T. Dokmanović]</dc:publisher><dc:date>2024</dc:date><dc:date>2024-10-10 08:15:44</dc:date><dc:type>Magistrsko delo/naloga</dc:type><dc:identifier>163672</dc:identifier><dc:language>sl</dc:language></rdf:Description></rdf:RDF>
