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dc.contributor.authorHomaei, Selina Cannon
dc.contributor.authorBarone, Helene
dc.contributor.authorKleppe, Rune
dc.contributor.authorBetari, Nibal
dc.contributor.authorReif, Andreas
dc.contributor.authorHaavik, Jan
dc.date.accessioned2021-12-09T08:00:58Z
dc.date.available2021-12-09T08:00:58Z
dc.date.created2021-12-02T15:48:03Z
dc.date.issued2021
dc.identifier.issn0149-7634
dc.identifier.urihttps://hdl.handle.net/11250/2833487
dc.description.abstractNeurometabolic diseases (NMDs) are typically caused by genetic abnormalities affecting enzyme functions, which in turn interfere with normal development and activity of the nervous system. Although the individual disorders are rare, NMDs are collectively relatively common and often lead to lifelong difficulties and high societal costs. Neuropsychiatric manifestations, including ADHD symptoms, are prominent in many NMDs, also when the primary biochemical defect originates in cells and tissues outside the nervous system. ADHD symptoms have been described in phenylketonuria, tyrosinemias, alkaptonuria, succinic semialdehyde dehydrogenase deficiency, X-linked ichthyosis, maple syrup urine disease, and several mitochondrial disorders, but are probably present in many other NMDs and may pose diagnostic and therapeutic challenges. Here we review current literature linking NMDs with ADHD symptoms. We cite emerging evidence that many NMDs converge on common neurochemical mechanisms that interfere with monoamine neurotransmitter synthesis, transport, metabolism, or receptor functions, mechanisms that are also considered central in ADHD pathophysiology and treatment. Finally, we discuss the therapeutic implications of these findings and propose a path forward to increase our understanding of these relationships.en_US
dc.language.isoengen_US
dc.publisherElsevieren_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleADHD symptoms in neurometabolic diseases: Underlying mechanisms and clinical implicationsen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2021 The Author(s).en_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode2
dc.identifier.doi10.1016/j.neubiorev.2021.11.012
dc.identifier.cristin1963666
dc.source.journalNeuroscience and Biobehavioral Reviewsen_US
dc.identifier.citationNeuroscience and Biobehavioral Reviews, 2021.en_US


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Navngivelse 4.0 Internasjonal
Except where otherwise noted, this item's license is described as Navngivelse 4.0 Internasjonal