Characterising neuroimmune changes in the gut-brain axis in autism: alterations in gut-associated lymphoid tissue and the enteric nervous system
Characterizing neuroimmune changes in the gut-brain axis in Autism: Alterations of the Gut-Associated Lymphoid Tissue (GALT) and the Enteric Nervous System Discussion Gastrointestinal (GI) issues have been well recognized in autistic patients since the disease was first described in the 1940s (1, 15). GI dysfunction is a hallmark symptom for individuals with autistic spectral disorders (ASDs) (1). Children with ASDs are four times more prone to GI dysfunction compared to their healthy counterparts (2, 15). As a result, most patients of ASD tend to limit their diet to certain favored food items (3). The reason for such specificity towards specific food items remain unexplored (3). It is contended that changes in gut morphology and emotive functions could attribute to such phenomenon (15). Although different studies have confirmed the presence of neuronal deficits in patients with ASD, there is inconclusive evidence regarding the involvement of gastrointestinal histopathology with such deficits (2, 17). It is contended that the genes that are implicated for the neuronal deficits in ASD patients might also be responsible for the associated GI histopathology. For example, mutations in the Shank-3 and Neuroligin-3 have been strongly associated with the neuronal deficits observed in ASD patients (4, 5). Various researchers have provided mounting evidence regarding the involvement of Shank-3 gene in the genesis of GI dysfunctions that are presented by patients with ASD (4, 5, 6). The genes that control neuronal activity are…
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