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ORAL PRESENTATION / TAM METİN SÖZLÜ SUNUM

and AOPP levels. We consider that the increased oxidative stress in the autism group
arises from mitochondrial dysfunction in the temporal cortex.

Infliximab is a monoclonal antibody belonging to the anti-TNF-α agent class,
specifically binding tumor necrosis factor-alpha (TNF-α) (Hoshiyama et al., 2018). Its

biological effects include suppression of inflammation, reduction of oxidative stress, and

inhibition of apoptosis through various cellular protective mechanisms (Zhou et al., 2021).
While infliximab is widely used to treat inflammatory diseases such as ulcerative colitis,

Crohn’s disease, and rheumatoid arthritis, recent studies have reported its
neuroprotective effects (Dehkordi et al., 2025). Specifically, it has demonstrated

therapeutic benefits in Alzheimer’s disease by targeting metabolic signaling pathways
(Clarke et al., 2025), inhibited oxidative stress and inflammation improving depressive

and anxiety-like behaviors in animal models of depression (Şahin et al., 2020), and

reduced anxiety-like behaviors, improved cognitive dysfunction, and increased brain-
derived neurotrophic factor (BDNF) expression in juvenile arthritis rat models (Poutoglidou

et al., 2021). Additionally, infliximab infusion has been shown to alleviate fatigue and
depressive symptoms, enhancing quality of life (Imabayashi et al., 2021).

However, Kalinowska et al. (2020) reported that infliximab treatment can induce
demyelination through a T cell–independent mechanism, causing oligodendrocyte

damage via toxicity. This mechanism may lead to inflammatory demyelination in the
central nervous system (CNS), potentially resulting in multiple sclerosis (MS). Yu et al.

(2021) found that lesions associated with MS demyelinating disorders related to
infliximab treatment are indistinguishable from MS lesions. According to Psarelis et al.

(2017), anti-TNF-α therapy can induce demyelination and subsequent neurological

disorders, particularly Guillain-Barré syndrome. Several studies have linked anti-TNF
agents to MS (Avasarala et al., 2021).

The underlying pathophysiological mechanism of CNS lesions developing after
infliximab therapy remains unclear (Yu et al., 2021; Avasarala et al., 2021). It has been

suggested that this may be explained through the interaction of TNF-α with its two
receptor types, TNFR1 and TNFR2. TNFR1 is a transmembrane protein, while TNFR2 is a

soluble cytokine receptor. The current literature reports TNFR1 mediates demyelination
processes, whereas TNFR2 facilitates remyelination. Moreover, inhibition of TNFR2 has

been shown to adversely affect local repair processes related to axonal damage and
myelin loss (Psarelis et al., 2017). Experimental studies by Bruce et al. (1996) showed

that mice deficient in TNFR1 and TNFR2 genes exhibited increased susceptibility to focal

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