Autism: Metabolism, Mitochondria, and the Microbiome

摘要: New approaches are needed to examine the diverse symptoms and comorbidities of growing family neurodevelopmental disorders known as autism spectrum disorder (ASD). ASD originally was thought be a static, inheritable disorder, our understanding it is undergoing major shift. It emerging dynamic system metabolic immune anomalies involving many organ systems, including brain, environmental exposure. The initial detailed observation inquiry patients with related conditions histories their caregivers families have been invaluable. How gastrointestinal (GI) factors not yet clear. Nevertheless, history previous antibiotic exposure or hospitalization, GI symptoms, abnormal food cravings, unique intestinal bacterial populations, which proposed relate variable symptom severity. In addition traditional scientific inquiry, clinical recording exacerbations, remissions, needed. This article reviews role that enteric short-chain fatty acids, particularly propionic (also called propanoic) acid, produced from ASD-associated bacteria, may play in etiology some forms ASD. Human populations partial metabolizers acid more common than previously thought. results pre-clinical laboratory studies show acid-treated rats display ASD-like repetitive, perseverative, antisocial behaviors seizure. Neurochemical changes, consistent predictive findings patients, neuroinflammation, increased oxidative stress, mitochondrial dysfunction, glutathione depletion, altered phospholipid/acylcarnitine profiles, observed. Propionic has bioactive effects on (1) neurotransmitter (2) intracellular acidification calcium release, (3) metabolism, (4) gap junction gating, (5) function, (6) alteration gene expression warrant further exploration. Traditional experimentation verify hypothesis acids potential trigger Novel collaborative developments systems biology, examining microbiome its host expression, hold great promise