INFLAMMATION IS A KEY FACTOR IN CLINICAL MANIFESTATIONS OF AUTISM

Analyses of a variety of clinical manifestations show that inflammation, directly or indirectly, is an etiopathogenetic factor underlying the clinical picture of autism. Hearing problems, including central auditory processing disorders, are inflammatory and associated with elevated expression of proinflammatory cytokines and microglial activation[1]. The Inflammation of the vestibular nerve can be followed by demyelination and loss of function[2]. Prolonged nasal inflammation can damage the epithelial and neuronal cells lining the olfactory mucosa and olfactory sensory neurons, leading to hyposmia or anosmia[3]. Neuroinflammation can affect both the eye and the CNS visual system leading to many vision dysfunctions[4]. The motor problems and some other autistic symptoms and signs in children with ASD, can be explained by inflammation in the cerebellum, a brain region responsible for motor control and higher cognitive functions used in language, social skills, and emotional regulation[5] [6]. In depression, inflammation is likely a critical disease modifier and promotor capable of increasing susceptibility to this neuropathology[7] and inflammatory cytokines are among the causative factors in the etiology of depression[8]. Evidence suggests that the gut microbiome plays a facilitating role in inflammation, stress response, anxiety, and depression[9]. The study of inflammation in fear- and anxiety-based disorders indicates that pro-inflammatory markers can directly modulate affective behavior[10]. The inflammatory diseases and a pro-inflammatory state have been associated with ADHD, bipolar disorder, and anxiety[11]. Evidence shows an interplay between immune dysregulation, inflammation, anxiety, and an altered acute neuroendocrine stress response that may exist in these disorders[12]. The data indicate that immune system and inflammatory processes are involved in obsessive-compulsive disorder (OCD)[13].
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