Page 40 - congress

ORAL PRESENTATION / TAM METİN SÖZLÜ SUNUM

fully understood; however, oxidative stress, neuroinflammation, mitochondrial
dysfunction, and disruptions in GABA, glutamate, dopamine, and oxytocin levels have

been reported as influential factors (Mehan et al., 2025). The temporal cortex plays a
critical role in ASD pathophysiology because it is responsible for cognitive functions

directly related to core symptoms of ASD, such as auditory processing, language

development, and social perception (Tang et al., 2013). Brodmann Area 21 (BA21) in the
lateral temporal lobe is associated with auditory perception, language production, and

neural bases of social cognitive processes, and this area has been shown to correlate with
behaviors associated with ASD (Bigler et al., 2007; Jou et al., 2010). Postmortem brain

studies indicate significant mitochondrial dysfunction in the temporal cortex of individuals
with ASD, particularly reductions in the enzymatic activities of Complex I and IV of the

electron transport chain (Chauhan et al., 2011). Furthermore, decreased levels of the

mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2) and increased
mitochondrial DNA (mtDNA) damage have been reported in the temporal cortex of

children with ASD (Giulivi et al., 2010). Significant increases in lipid hydroperoxide levels,
a marker of oxidative stress, were observed in the temporal cortex and cerebellum regions

of individuals with ASD. Chauhan and colleagues (2011) suggested that this increase
leads to decreased expression of electron transport chain complexes and results in

abnormal energy metabolism and elevated oxidative stress levels.
Propionic acid (PPA), found in cheese, dairy products, and refined wheat, is also

used as a preservative in various foods (El-Ansary et al., 2016). PPA is a weak organic
acid capable of easily crossing the blood-brain barrier (gut → blood → brain) (Bhandari

and Kuhad, 2015; Mirza and Sharma, 2018). Increased PPA levels in organs cause

intracellular acidification and trigger systemic inflammation through increased pro-
inflammatory cytokine concentrations (Shultz et al., 2015; El-Ansary et al., 2016).

Elevated PPA in neuronal cells can cause propionic acidemia and disrupt neuronal
development (Xu et al., 2012; Khalil et al., 2015). PPA administration induces various

pathophysiological processes seen in ASD, such as behavioral impairments, oxidative
stress, and neuroinflammation, making it a widely used effective preclinical model to

investigate underlying mechanisms and potential treatment options for ASD (Tiwari,
2021; Alabdali et al., 2025). Currently, there are no validated biomarkers for ASD

diagnosis, nor is there a specific pharmacological treatment available for the disorder
(Alacabey et al., 2025). Existing therapeutic interventions only provide limited relief of

38