Too much for your own good: Excessive dopamine damages neurons and contributes to Parkinson's disease: An Editorial Highlight for "Enhanced tyrosine hydroxylase activity induces oxidative stress, causes accumulation of autotoxic catecholamine metabolites, and augments amphetamine effects in vivo".
Journal
Journal of neurochemistry
ISSN: 1471-4159
Titre abrégé: J Neurochem
Pays: England
ID NLM: 2985190R
Informations de publication
Date de publication:
08 2021
08 2021
Historique:
revised:
28
05
2021
received:
25
05
2021
accepted:
30
05
2021
pubmed:
30
6
2021
medline:
16
11
2021
entrez:
29
6
2021
Statut:
ppublish
Résumé
Dopamine dyshomeostasis is a driving factor of nigrostriatal degeneration in Parkinson's disease (PD). Accumulation of cytosolic dopamine at striatal projections results in the buildup of autoxidation products, which generates protein adducts and exacerbate oxidative stress. Moreover, an excessive rate of dopamine degradation results in accumulation of 3,4-dihydroxyphenylacetaldehyde (DOPAL), a toxic metabolite which rapidly reacts with other proteins. These events lead to protein misfolding and cross-linking as well as mitochondrial and lysosomal dysfunction, the main pathological mechanisms underscoring dopaminergic neuron loss in PD. In this issue of Journal of Neurochemistry, Vecchio et al. generated and characterized a new in vivo model of chronic dopamine accumulation through the overexpression of a hyperactive form of tyrosine hydroxylase (TH-HI), the rate-limiting step enzyme in dopamine biosynthesis. At 3-5 months of age, TH-HI mice displayed increased striatal dopamine content, exacerbated dopamine catabolism, and augmented responses to amphetamine. This correlated with enhanced oxidative stress and DOPAL buildup, highlighting a catechol-induced neurotoxic vicious cycle that may anticipate a parkinsonian-like phenotype in aged mice. This novel TH-HI animal model represents an exciting new tool to unravel the molecular mechanisms underlying dopamine disequilibrium, catecholamine autotoxicity, and neurodegeneration in PD.
Substances chimiques
Catecholamines
0
Amphetamine
CK833KGX7E
Tyrosine 3-Monooxygenase
EC 1.14.16.2
Dopamine
VTD58H1Z2X
Types de publication
Editorial
Research Support, Non-U.S. Gov't
Comment
Langues
eng
Sous-ensembles de citation
IM
Pagination
833-836Commentaires et corrections
Type : CommentOn
Informations de copyright
© 2021 International Society for Neurochemistry.
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