International Graduate School of Neuroscience

Research Interests

My research focuses on understanding the cellular and molecular mechanisms underlying neurodegeneration and neuroinflammation, with an emphasis on the following areas:

Neuroinflammation and Degeneration in ALS:

We investigate the role of neuroinflammation in the progression of amyotrophic lateral sclerosis (ALS), focusing on spinal cord pathology. Our recent study (Cihankaya et al., 2024) identified the activation of the NLRP3 inflammasome as a key driver of motor neuron degeneration in ALS. This activation leads to Caspase-1 autoactivation, resulting in the release of pro-inflammatory cytokines and pyroptotic cell death in spinal motor neurons. These findings highlight the critical role of inflammation in ALS progression and open avenues for therapeutic strategies targeting inflammasome modulation to mitigate neuroinflammatory cell death.

Gut-Brain Axis in Neurodegenerative Diseases:

Our research explores the impact of gut-brain interactions on neurodegeneration, focusing on neuroimmune crosstalk. We investigate how alterations in gut microbiota and intestinal permeability influence neuroinflammatory processes in the central nervous system. Emerging evidence suggests that microbial metabolites and immune signaling from the gut can modulate neurodegenerative disease progression. Understanding these mechanisms may help identify new therapeutic approaches targeting gut-derived factors to mitigate neurodegeneration.

Oxidative Stress and Metabolic Dysfunctions in Neurodegeneration:

We examine the role of oxidative stress and metabolic dysfunction in ALS and other neurodegenerative disorders. Studies such as Röderer et al. (2018) have demonstrated that downregulation of Nmnat2 leads to increased oxidative stress and neuroinflammatory processes in the spinal cord. Further investigations into dysfunctions in the glutathione (GSH) system (Junghans, Johan et al., 2022; Wunsch et al., 2023) and NAD imbalance (Zwilling et al., 2020) suggest that these factors exacerbate neuronal damage and contribute to disease progression. Our findings provide potential therapeutic targets aimed at modulating oxidative stress, which is increasingly recognized as a key driver of neuroinflammation.