Nöroinflamasyonun Dikkat Eksikliği Hiperaktivite Bozukluğu Patofizyolojisindeki Rolünün İncelenmesi

Abstract

In the etiology of attention deficit/hyperactivity disorder (ADHD), high genetic heritability, structural/functional brain abnormalities, and dopamine/noradrenaline imbalances are prominent, emphasizing the role of gene-environment interactions. This study investigated neuroinflammatory signaling and ADHD-like behavioral changes in the prefrontal cortex (PFC) of perinatal nicotine-exposed (PNE) mice. PNE mice were exposed to a solution of 300 μg/ml nicotine and 2% sucrose in their drinking water from two weeks before mating until weaning, while the control group received only 2% sucrose. Behavioral tests were conducted in the 5th postnatal week, and cortical thickness (CT), microglial activation, and NF-κB signaling were assessed using immunohistochemistry in the anterior cingulate cortex (ACC), prelimbic cortex (PL), and infralimbic cortex (IL) of the PFC. Increased CT, microglial cell number and activation, and NF-κB expression were observed in the ACC of PNE mice, correlating with attentional impairment. These findings suggest that PNE may contribute to ADHD development through neuroinflammation.