将应激、儿茶酚胺自毒性和应激反应与神经退行性疾病联系起来：纪念理查德·克维特南斯基的重点综述。
Linking Stress, Catecholamine Autotoxicity, and Allostatic Load with Neurodegenerative Diseases: A Focused Review in Memory of Richard Kvetnansky.
机构信息
Clinical Neurocardiology Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 9000 Rockville Pike MSC-1620, Building 10 Room 5N220, Bethesda, MD, 20892-1620, USA.
出版信息
Cell Mol Neurobiol. 2018 Jan;38(1):13-24. doi: 10.1007/s10571-017-0497-x. Epub 2017 May 9.
Abstract
In this Focused Review, we provide an update about evolving concepts that may link chronic stress and catecholamine autotoxicity with neurodegenerative diseases such as Parkinson's disease. Richard Kvetnansky's contributions to the field of stress and catecholamine systems inspired some of the ideas presented here. We propose that coordination of catecholaminergic systems mediates adjustments maintaining health and that senescence-related disintegration of these systems leads to disorders of regulation and to neurodegenerative diseases such as Parkinson's disease. Chronically repeated episodes of stress-related catecholamine release and reuptake, with attendant increases in formation of the toxic dopamine metabolite 3,4-dihydroxyphenylacetaldehyde, might accelerate this process.
摘要
在本次重点综述中，我们提供了一些最新的概念更新，这些概念可能将慢性应激和儿茶酚胺自毒性与帕金森病等神经退行性疾病联系起来。理查德·克维特南斯基（Richard Kvetnansky）对应激和儿茶酚胺系统领域的贡献激发了这里提出的一些观点。我们提出，儿茶酚胺能系统的协调介导了维持健康的调节，而与衰老相关的这些系统的解体导致调节障碍，并导致帕金森病等神经退行性疾病。与应激相关的儿茶酚胺释放和再摄取的慢性反复发作，伴随着毒性多巴胺代谢物 3,4-二羟基苯乙醛形成的增加，可能会加速这个过程。
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本文引用的文献
1
Are Dopamine Oxidation Metabolites Involved in the Loss of Dopaminergic Neurons in the Nigrostriatal System in Parkinson's Disease?
ACS Chem Neurosci. 2017 Apr 19;8(4):702-711. doi: 10.1021/acschemneuro.7b00034. Epub 2017 Mar 3.
2
Chronic mild stress augments MPTP induced neurotoxicity in a murine model of Parkinson's disease.
Physiol Behav. 2017 May 1;173:132-143. doi: 10.1016/j.physbeh.2017.01.046. Epub 2017 Feb 6.
3
DOPAL derived alpha-synuclein oligomers impair synaptic vesicles physiological function.
Sci Rep. 2017 Jan 13;7:40699. doi: 10.1038/srep40699.
4
Determinants of denervation-independent depletion of putamen dopamine in Parkinson's disease and multiple system atrophy.
Parkinsonism Relat Disord. 2017 Feb;35:88-91. doi: 10.1016/j.parkreldis.2016.12.011. Epub 2016 Dec 15.
5
Traumatic Brain Injury Leads to Development of Parkinson's Disease Related Pathology in Mice.
Front Neurosci. 2016 Oct 13;10:458. doi: 10.3389/fnins.2016.00458. eCollection 2016.
6
Association of Traumatic Brain Injury With Late-Life Neurodegenerative Conditions and Neuropathologic Findings.
JAMA Neurol. 2016 Sep 1;73(9):1062-9. doi: 10.1001/jamaneurol.2016.1948.
7
Antioxidant-Mediated Modulation of Protein Reactivity for 3,4-Dihydroxyphenylacetaldehyde, a Toxic Dopamine Metabolite.
Chem Res Toxicol. 2016 Jul 18;29(7):1098-107. doi: 10.1021/acs.chemrestox.5b00528. Epub 2016 Jun 15.
8
A physiologist's view of homeostasis.
Adv Physiol Educ. 2015 Dec;39(4):259-66. doi: 10.1152/advan.00107.2015.
9
Comparison of Monoamine Oxidase Inhibitors in Decreasing Production of the Autotoxic Dopamine Metabolite 3,4-Dihydroxyphenylacetaldehyde in PC12 Cells.
J Pharmacol Exp Ther. 2016 Feb;356(2):483-92. doi: 10.1124/jpet.115.230201. Epub 2015 Nov 16.
10
Selective genetic disruption of dopaminergic, serotonergic and noradrenergic neurotransmission: insights into motor, emotional and addictive behaviour.
J Psychiatry Neurosci. 2016 Apr;41(3):169-81. doi: 10.1503/jpn.150028.
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