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Role of adenosine in the pathophysiology and treatment of attention deficit hyperactivity disorder. | LitMetric

Role of adenosine in the pathophysiology and treatment of attention deficit hyperactivity disorder.

Purinergic Signal

Department of Rehabilitation Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Child Neurodevelopment and Cognitive Disorders, Chongqing, 400014, China.

Published: October 2024

AI Article Synopsis

  • ADHD is a complex condition marked by ongoing issues with inattention, hyperactivity, and impulsivity, and its exact causes are still being studied.
  • The adenosine system, which affects neurotransmitter release and cognitive functions, plays a significant role in ADHD and is linked to its symptoms.
  • This review discusses how targeting the adenosine system could lead to new treatment options for managing ADHD.

Article Abstract

Attention deficit hyperactivity disorder (ADHD) is a complex neurodevelopmental condition characterized by persistent inattention, hyperactivity, and impulsivity. Although its precise etiology remains unclear, current evidence suggests that dysregulation within the neurotransmitter system plays a key role in the pathogenesis of ADHD. Adenosine, an endogenous nucleoside widely distributed throughout the body, modulates various physiological processes, including neurotransmitter release, sleep regulation, and cognitive functions through its receptors. This review critically examines the role of the adenosine system in ADHD, focusing on the links between adenosine receptor function and ADHD-related symptoms. Additionally, it explores how adenosine interacts with dopamine and other neurotransmitter pathways, shedding light on its involvement in ADHD pathophysiology. This review aims to provide insights into the potential therapeutic implications of targeting the adenosine system for ADHD management.

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Source
http://dx.doi.org/10.1007/s11302-024-10059-2DOI Listing

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