ArticleParkinsonism & related disorders2015
Deficient vesicular storage: A common theme in catecholaminergic neurodegeneration.
Article in Parkinsonism & related disorders, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 36 citations in OpenAlex.
- Catecholamine metabolism revisited: from neurochemistry to integrative physiology and pathophysiology.Physiological reviews · 2026Review
- Serotonin content and uptake in platelets can distinguish Parkinson's disease from control patients and essential tremor.Journal of Parkinson's disease · 2026Article
- Putamen dopamine synthesis, vesicular storage, and metabolism in Parkinson disease.medRxiv : the preprint server for health sciences · 2026Article
- Preclinical Catecholaminergic Biomarkers of Central Lewy Body Diseases.Journal of clinical neurology (Seoul, Korea) · 2026Review
- 3,4-Dihydroxyphenylglycol levels separate multiple system atrophy from Parkinson disease with orthostatic hypotension.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025Observational
- Selective dopaminergic neurotoxicity modulated by inherent cell-type specific neurobiology.Neurotoxicology · 2024Review
- Cardiac noradrenergic deficiency revealed by 18F-dopamine positron emission tomography identifies preclinical central Lewy body diseases.The Journal of clinical investigation · 2024Article
- Dihydroxyphenylacetaldehyde Lowering Treatment Improves Locomotor and Neurochemical Abnormalities in the Rat Rotenone Model: Relevance to the Catecholaldehyde Hypothesis for the Pathogenesis of Parkinson's Disease.International journal of molecular sciences · 2023Article
- Midbrain dopamine oxidation links ubiquitination of glutathione peroxidase 4 to ferroptosis of dopaminergic neurons.The Journal of clinical investigation · 2023Article
- What new can we learn from cardiac sympathetic neuroimaging in synucleinopathies?Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2022Article
- Dynamic planar scintigraphy for the rapid kinetic measurement of myocardialEJNMMI research · 2021Article
- Stable expression of the human dopamine transporter in N27 cells as an in vitro model for dopamine cell trafficking and metabolism.Toxicology in vitro : an international journal published in association with BIBRA · 2021Article
- Do indices of baroreflex failure and peripheral noradrenergic deficiency predict the magnitude of orthostatic hypotension in Lewy body diseases?Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2021Article
- CardiacMovement disorders clinical practice · 2021Article
- "Sick-but-not-dead": multiple paths to catecholamine deficiency in Lewy body diseases.Stress (Amsterdam, Netherlands) · 2020Review
- Cardiac sympathetic innervation and vesicular storage in pure autonomic failure.Annals of clinical and translational neurology · 2020Article
- The "Sick-but-not-Dead" Phenomenon Applied to Catecholamine Deficiency in Neurodegenerative Diseases.Seminars in neurology · 2020Review
- Increased Noradrenaline as an Additional Cerebrospinal Fluid Biomarker in PSP-Like Parkinsonism.Frontiers in aging neuroscience · 2020Article
- Long-term trends in myocardial sympathetic innervation and function in synucleinopathies.Parkinsonism & related disorders · 2019Observational
- Computational modeling reveals multiple abnormalities of myocardial noradrenergic function in Lewy body diseases.JCI insight · 2019Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Several neurodegenerative diseases involve loss of catecholamine neurons--Parkinson's disease (PD) is a prototypical example. Catecholamine neurons are rare in the nervous system, and why they are lost has been mysterious. Accumulating evidence supports the concept of "autotoxicity"--inherent cytotoxicity caused by catecholamine metabolites. Since vesicular sequestration limits the buildup of toxic products of enzymatic and spontaneous oxidation of catecholamines, a vesicular storage defect could play a pathogenic role in the death of catecholaminergic neurons in a variety of neurodegenerative diseases. In putamen, deficient vesicular storage is revealed in vivo by accelerated loss of (18)F-DOPA-derived radioactivity and post-mortem by decreased tissue dopamine (DA):DOPA ratios; in myocardium in vivo by accelerated loss of (18)F-dopamine-derived radioactivity and post-mortem by increased 3,4-dihydroxyphenylglycol:norepinephrine (DHPG:NE) ratios; and in sympathetic noradrenergic nerves overall in vivo by increased plasma F-dihydroxyphenylacetic acid (F-DOPAC):DHPG ratios. We retrospectively analyzed data from 20 conditions with decreased or intact catecholaminergic innervation, involving different etiologies, pathogenetic mechanisms, and lesion locations. All conditions involving parkinsonism had accelerated loss of putamen (18)F-DOPA-derived radioactivity; in those with post-mortem data there were also decreased putamen DA:DOPA ratios. All conditions involving cardiac sympathetic denervation had accelerated loss of myocardial (18)F-dopamine-derived radioactivity; in those with post-mortem data there were increased myocardial DHPG:NE ratios. All conditions involving localized loss of catecholaminergic innervation had evidence of decreased vesicular storage specifically in the denervated regions. Thus, across neurodegenerative diseases, loss of catecholaminergic neurons seems to be associated with decreased vesicular storage in the residual neurons.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.