ovalbumin and Developmental-Disabilities

Asthma is the most common chronic childhood illness today. However, little attention is paid for the impacts of chronic asthma-induced hypoxia on cognitive function in children. The present study used immature mice to establish ovalbumin-induced chronic asthma model, and found that chronic asthma impaired learning and memory ability in Morris Water Maze test. Further study revealed that chronic asthma destroyed synaptic structure, impaired long-term potentiation (LTP) maintaining in the CA1 region of mouse hippocampal slices. We found that intermittent hypoxia during chronic asthma resulted in down-regulation of c-fos, Arc and neurogenesis, which was responsible for the impairment of learning and memory in immature mice. Moreover, our results showed that budesonide treatment alone was inadequate for attenuating chronic asthma-induced cognitive impairment. Therefore, our findings indicate that chronic asthma might result in cognitive dysfunction in children, and more attention should be paid for chronic asthma-induced brain damage in the clinical therapy.

Topics: Animals; Animals, Newborn; Asthma; Bronchodilator Agents; Budesonide; Chronic Disease; Cognition Disorders; Cytoskeletal Proteins; Developmental Disabilities; Disease Models, Animal; Female; Gene Expression Regulation, Developmental; Hippocampus; In Vitro Techniques; Ki-67 Antigen; Lung; Maze Learning; Mice; Mice, Inbred BALB C; Nerve Tissue Proteins; Ovalbumin; Pneumonia; Time Factors; Vascular Endothelial Growth Factor A