Manganese in autism spectrum disorder and attention deficit hyperactivity disorder: The state of the art

Current Research in Toxicology, Journal Year: 2024, Volume and Issue: 6, P. 100170 - 100170

Published: Jan. 1, 2024

The objective of the present narrative review was to synthesize existing clinical and epidemiological findings linking manganese (Mn) exposure biomarkers autism spectrum disorder (ASD) attention deficit hyperactivity (ADHD), discuss key pathophysiological mechanisms neurodevelopmental disorders that may be affected by this metal. Existing data demonstrated both direct inverse association between Mn body burden ASD, or lack any relationship. In contrast, majority studies revealed significantly higher levels in subjects with ADHD, as well relationship inattention scores children, although several reported contradictory results. laboratory impaired animals following associated dopaminergic dysfunction neuroinflammation. Despite evidence on Mn-induced neurobiological alterations patients ASD a plethora neurotoxic effects overexposure interfere pathogenesis inherent these disorders. Specifically, overload shown impair not only neurotransmission, but also affect metabolism glutamine/glutamate, GABA, serotonin, noradrenaline, thus affecting neuronal signaling. turn, its ability induce oxidative stress, apoptosis, neuroinflammation, and/or neurogenesis. Nonetheless, additional detailed are required evaluate environmental at wide range concentrations estimate potential dose-dependent effects, genetic factors association.

Language: Английский

Maternal choline supplementation lessens the behavioral dysfunction produced by developmental manganese exposure in a rodent model of ADHD

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2023, Volume and Issue: unknown

Published: June 26, 2023

Abstract Studies in children have reported associations between elevated manganese (Mn) exposure and ADHD-related symptoms of inattention, impulsivity/hyperactivity, psychomotor impairment. Maternal choline supplementation (MCS) during pregnancy/lactation may hold promise as a protective strategy because it has been shown to lessen cognitive dysfunction caused by numerous early insults. Our objectives were determine whether (1) developmental Mn alters behavioral reactivity/emotion regulation, addition impairing learning, attention, impulse control, sensorimotor function, (2) MCS protects against these Mn-induced impairments. Pregnant Long-Evans rats given standard diet, or diet supplemented with additional throughout gestation lactation (G3 - PND 21). Male offspring exposed orally 0 50 mg Mn/kg/day over 1–21. In adulthood, animals tested series tasks. lasting reactivity errors reward omission, recapitulating the constellation seen ADHD children. lessened attentional partially normalized committing an error not receiving expected but provided no protection learning dysfunction. absence exposure, produces benefits errors. To conclude, deficits consistent symptomology, offered some adverse effects, adding evidence that maternal is neuroprotective for improves functioning. Highlights Developmental causes symptomology. attention reactivity. control These data support efforts increase intake pregnancy, particularly individuals at risk neurotoxicant exposure.

Language: Английский