Serotonin dysfunction in ADHD

Journal of Neurodevelopmental Disorders, Journal Year: 2025, Volume and Issue: 17(1)

Published: April 22, 2025

Abstract It is well accepted that attention deficit hyperactivity disorder (ADHD) in part driven by dysfunction the monoaminergic neurotransmitter system, but both extent of and possible therapeutic avenues presented serotonergic neurotransmission frequently overlooked. As such, we present key evidence for transmission, as seen from biochemical, genetic pharmacological perspectives. An overall serotonin availability a common theme throughout literature, thus this review aims to explore dysfunctions synthesis pathway which result reduced bioavailability, investigate whether such could be loci change ADHD. We have identified several steps namely conversion tryptophan 5-hydroxytryptophan its use cofactor tetrahydrobiopterin, promising development novel clinical interventions

Language: Английский

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Lifelong Exposure to Polystyrene-Nanoplastics Induces an Attention-Deficit Hyperactivity Disorder-like Phenotype and Impairs Brain Aging in Mice

Journal of Hazardous Materials, Journal Year: 2025, Volume and Issue: unknown, P. 138640 - 138640

Published: May 1, 2025

Language: Английский

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Catapol: a promising natural neuroprotective agent for neurologic disorders

Acta Materia Medica, Journal Year: 2025, Volume and Issue: 4(3)

Published: Jan. 1, 2025

Neurologic disorders are the leading cause of illness and disability as a result increased life expectancy global population aging, highlighting urgent need great challenge for discovering neuroprotective agents with better efficacy minimal side-effects. Catalpol, an iridoid glycoside derived from Rehmanniae Radix, has therapeutic potential in neurologic diseases due to its diverse biological activities. This review summarizes research advances catalpol wide range disorders, including depression, cognitive impairment, stroke, Parkinson’s disease, multiple sclerosis. A comprehensive discussion experimental models used, dosages, duration treatment, mechanisms involved is provided. The common underlying effects on these closely related antioxidant, anti-neuroinflammatory, anti-apoptotic properties, well capacity promote neuroplasticity neurogenesis. Despite promising results studies, there still challenges be addressed, such identifying direct binding targets, assessing toxicologic effects, understanding pharmacokinetics. Furthermore, well-designed controlled clinical trials should conducted validate safety treating various conditions. provides compelling evidence supporting natural agent.

Language: Английский

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Novel non-stimulants rescue hyperactive phenotype in an adgrl3.1 mutant zebrafish model of ADHD

Neuropsychopharmacology, Journal Year: 2022, Volume and Issue: 48(8), P. 1155 - 1163

Published: Nov. 18, 2022

Abstract ADHD is a highly prevalent neurodevelopmental disorder. The first-line therapeutic for ADHD, methylphenidate, can cause serious side effects including weight loss, insomnia, and hypertension. Therefore, the development of non-stimulant-based therapeutics has been prioritized. However, many these also other effects, most notably somnolence. Here, we have used uniquely powerful genetic model unbiased drug screen to identify novel non-stimulant therapeutics. We first found that adgrl3.1 null ( −/− ) zebrafish larvae showed robust hyperactive phenotype. Although hyperactivity was rescued by three therapeutics, all interfered significantly with sleep. Second, wild-type characterize simple behavioral phenotype generated atomoxetine screened 1200 compound Prestwick Chemical Library® matching profile resulting in 67 hits. These hits were re-assayed . Using previously identified non-stimulants as positive control, four compounds matched effect atomoxetine: aceclofenac, amlodipine, doxazosin, moxonidine. additionally demonstrated cognitive moxonidine mice using T-maze spontaneous alternation task. Moxonidine, high affinity imidazoline 1 receptors. We, therefore, assayed pure agonist, LNP599, which an closely suggesting role this receptor system ADHD. In summary, introduce five putative findings offer tool understanding neural circuits suggest mechanism its etiology,

Language: Английский

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Sex-specific neurobehavioral and prefrontal cortex gene expression alterations following developmental acetaminophen exposure in mice

Neurobiology of Disease, Journal Year: 2022, Volume and Issue: 177, P. 105970 - 105970

Published: Dec. 19, 2022

Acetaminophen (N-acetyl-p-aminophenol (APAP), also known as paracetamol) is one of the most common medications used by general population, including pregnant people. Although many human observational and animal model studies have shown associations between prenatal early postnatal APAP exposure attention deficit hyperactivity disorder, autism spectrum disorders, altered neurodevelopment, existing literature limited. In particular, no mouse investigated offspring deficits in behavioral tasks specifically designed to measure attention, prior rodent utilized 'omics' technologies, such transcriptomics, for an untargeted exploration potential mechanisms. We randomly assigned mice (starting embryonic day 4-10) receive (150 mg/kg/day) or vehicle control through 14. evaluated 111 a battery tests, pup ultrasonic vocalizations, elevated plus-maze, open field test, CatWalk (gait), pre-pulse inhibition, automated 5-choice serial reaction time task. Prefrontal cortex was collected at birth from 24 pups RNA sequencing. Developmental treatment resulted increased hastened separation-induced vocalizations days 2 11, well decreased ambulation vertical rearings male but not female adult offspring. associated with sex-specific prefrontal gene expression relating glutathione cytochrome p450 metabolism, DNA damage, endocrine immune systems. This study provides additional evidence neurodevelopmental harm generates hypotheses underlying molecular pathways via

Language: Английский

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