ArticleProgress in neuro-psychopharmacology & biological psychiatry2013
Genotype-independent decrease in plasma dopamine beta-hydroxylase activity in Alzheimer's disease.
Article in Progress in neuro-psychopharmacology & biological psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- The catecholamine biosynthetic enzyme dopamine β-hydroxylase (DBH): first genome-wide search positions trait-determining variants acting additively in the proximal promoter.Human molecular genetics · 2014Pooled it
- Associations Between Dopamine Beta-Hydroxylase Gene Polymorphisms and Restless Legs Syndrome: A Case-Control Study.Medical science monitor : international medical journal of experimental and clinical research · 2025Article
- Proteo-metabolomic insights for early dual physical and cognitive impairments: A search for biomarkers of healthy aging based on muscle-brain crosstalk.Aging cell · 2025Article
- The regulatory role of AP-2β in monoaminergic neurotransmitter systems: insights on its signalling pathway, linked disorders and theragnostic potential.Cell & bioscience · 2022Review
- Pathogenesis and Personalized Interventions for Pharmacological Treatment-Resistant Neuropsychiatric Symptoms in Alzheimer's Disease.Journal of personalized medicine · 2022Review
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
- The Cholinergic System, the Adrenergic System and the Neuropathology of Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Modelling the pathogenesis of X-linked distal hereditary motor neuropathy using patient-derived iPSCs.Disease models & mechanisms · 2020Article
- Relationships of Cerebrospinal Fluid Alzheimer's Disease Biomarkers and COMT, DBH, and MAOB Single Nucleotide Polymorphisms.Journal of Alzheimer's disease : JAD · 2020Article
- Complex noradrenergic dysfunction in Alzheimer's disease: Low norepinephrine input is not always to blame.Brain research · 2019Article
- Monoaminergic neuropathology in Alzheimer's disease.Progress in neurobiology · 2017Review
- Epigenetic dysregulation of brainstem nuclei in the pathogenesis of Alzheimer's disease: looking in the correct place at the right time?Cellular and molecular life sciences : CMLS · 2017Review
- The influence of dopamine-beta-hydroxylase and catecholDiabetology & metabolic syndrome · 2017Article
- Genetics of Aggression in Alzheimer's Disease (AD).Frontiers in aging neuroscience · 2017Article
- Monoaminergic and Histaminergic Strategies and Treatments in Brain Diseases.Frontiers in neuroscience · 2016Review
- Catecholamine-Based Treatment in AD Patients: Expectations and Delusions.Frontiers in aging neuroscience · 2015Review
- Update on the core and developing cerebrospinal fluid biomarkers for Alzheimer disease.Croatian medical journal · 2014Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The noradrenergic system is involved in the etiology and progression of Alzheimer's disease (AD) but its role is still unclear. Dopamine beta-hydroxylase (DBH) as a catecholamine-synthesizing enzyme plays a central role in noradrenaline (NA) synthesis and turnover. Plasma DBH (pDBH) activity shows wide inheritable interindividual variability that is under genetic control. The aim of this study was to determine pDBH activity, DBH (C-970T; rs1611115) and DBH (C1603T; rs6271) gene polymorphisms in 207 patients with AD and in 90 healthy age-matched controls. Plasma DBH activity was lower, particularly in the early stage of AD, compared to values in middle and late stages of the disease, as well as to control values. Two-way ANOVA revealed significant effect of both diagnosis and DBH (C-970T) or DBH (C1603T) genotypes on pDBH activity, but without significant diagnosis×genotype interaction. No association was found between AD and DBH C-970T (OR=1.08, 95% CI 1.13-4.37; p=0.779) and C1603T (OR=0.89; 95% CI 0.36-2.20; p=0.814) genotypes controlled for age, gender, and ApoE4 allele. The decrease in pDBH activity, found in early phase of AD suggests that alterations in DBH activity represent a compensatory mechanism for the loss of noradrenergic neurons, and that treatment with selective NA reuptake inhibitors may be indicated in early stages of AD to compensate for loss of noradrenergic activity in the locus coeruleus.
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Registered trials
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