{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T22:15:00Z","timestamp":1787004900514,"version":"build-2736575974"},"reference-count":200,"publisher":"Georg Thieme Verlag KG","issue":"05","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Semin Neurol"],"published-print":{"date-parts":[[2020,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The catecholamines dopamine and norepinephrine are key central neurotransmitters that participate in many neurobehavioral processes and disease states. Norepinephrine is also the main neurotransmitter mediating regulation of the circulation by the sympathetic nervous system. Several neurodegenerative disorders feature catecholamine deficiency. The most common is Parkinson's disease (PD), in which putamen dopamine content is drastically reduced. PD also entails severely decreased myocardial norepinephrine content, a feature that characterizes two other Lewy body diseases\u2014pure autonomic failure and dementia with Lewy bodies. It is widely presumed that tissue catecholamine depletion in these conditions results directly from loss of catecholaminergic neurons; however, as highlighted in this review, there are also important functional abnormalities in extant residual catecholaminergic neurons. We refer to this as the \u201csick-but-not-dead\u201d phenomenon. The malfunctions include diminished dopamine biosynthesis via tyrosine hydroxylase (TH) and L-aromatic-amino-acid decarboxylase (LAAAD), inefficient vesicular sequestration of cytoplasmic catecholamines, and attenuated neuronal reuptake via cell membrane catecholamine transporters. A unifying explanation for catecholaminergic neurodegeneration is autotoxicity exerted by 3,4-dihydroxyphenylacetaldehyde (DOPAL), an obligate intermediate in cytoplasmic dopamine metabolism. In PD, putamen DOPAL is built up with respect to dopamine, associated with a vesicular storage defect and decreased aldehyde dehydrogenase activity. Probably via spontaneous oxidation, DOPAL potently oligomerizes and forms quinone-protein adducts with (\u201cquinonizes\u201d) \u03b1-synuclein (AS), a major constituent in Lewy bodies, and DOPAL-induced AS oligomers impede vesicular storage. DOPAL also quinonizes numerous intracellular proteins and inhibits enzymatic activities of TH and LAAAD. Treatments targeting DOPAL formation and oxidation therefore might rescue sick-but-not-dead catecholaminergic neurons in Lewy body diseases.<\/jats:p>","DOI":"10.1055\/s-0040-1713874","type":"journal-article","created":{"date-parts":[[2020,9,9]],"date-time":"2020-09-09T19:03:41Z","timestamp":1599678221000},"page":"502-514","source":"Crossref","is-referenced-by-count":20,"title":["The \u201cSick-but-not-Dead\u201d Phenomenon Applied to Catecholamine Deficiency in Neurodegenerative Diseases"],"prefix":"10.1055","volume":"40","author":[{"given":"David S.","family":"Goldstein","sequence":"additional","affiliation":[{"name":"Autonomic Medicine Section, Clinical Neurosciences Program, Division of Intramural Research, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"194","published-online":{"date-parts":[[2020,9,9]]},"reference":[{"key":"ref1","volume-title":"Catecholamines: Bridging Basic Science with Clinical Medicine","author":"D S Goldstein","year":"1998"},{"key":"ref2","doi-asserted-by":"crossref","DOI":"10.1007\/978-1-4757-3538-3","volume-title":"Catecholamine Research: From Molecular Insights to Clinical Medicine","author":"T Nagatsu","year":"2002"},{"key":"ref3","volume-title":"A New Era of Catecholamines in the Laboratory and Clinic","author":"L E Eiden","year":"2013"},{"issue":"07","key":"ref4","first-page":"611","article-title":"The sympathetic nervous system through the ages: from Thomas Willis to resistant hypertension","volume":"96","author":"M Esler","year":"2011","journal-title":"Exp Physiol"},{"issue":"06","key":"ref5","doi-asserted-by":"crossref","first-page":"976","DOI":"10.1161\/CIRCRESAHA.116.303604","article-title":"The sympathetic nervous system alterations in human hypertension","volume":"116","author":"G Grassi","year":"2015","journal-title":"Circ Res"},{"issue":"06","key":"ref6","doi-asserted-by":"crossref","first-page":"293","DOI":"10.1056\/NEJM197702102960601","article-title":"The sympathetic-nervous-system defect in primary orthostatic hypotension","volume":"296","author":"M G Ziegler","year":"1977","journal-title":"N Engl J Med"},{"issue":"08","key":"ref7","doi-asserted-by":"crossref","first-page":"1327","DOI":"10.1212\/01.WNL.0000058766.46428.F3","article-title":"Plasma levels of catechols and metanephrines in neurogenic orthostatic hypotension","volume":"60","author":"D S Goldstein","year":"2003","journal-title":"Neurology"},{"issue":"07","key":"ref8","doi-asserted-by":"crossref","first-page":"914","DOI":"10.1136\/jnnp.51.7.914","article-title":"Low lumbar CSF levels of homovanillic acid and 5-hydroxyindoleacetic acid in multiple system atrophy with autonomic failure","volume":"51","author":"R J Polinsky","year":"1988","journal-title":"J Neurol Neurosurg Psychiatry"},{"key":"ref9","doi-asserted-by":"crossref","first-page":"88","DOI":"10.1016\/j.parkreldis.2016.12.011","article-title":"Determinants of denervation-independent depletion of putamen dopamine in Parkinson's disease and multiple system atrophy","volume":"35","author":"D S Goldstein","year":"2017","journal-title":"Parkinsonism Relat Disord"},{"issue":"02","key":"ref10","doi-asserted-by":"crossref","first-page":"216","DOI":"10.1016\/0022-510X(95)00155-U","article-title":"Decrease of medullary catecholaminergic neurons in multiple system atrophy and Parkinson's disease and their preservation in amyotrophic lateral sclerosis","volume":"132","author":"S Kato","year":"1995","journal-title":"J Neurol Sci"},{"key":"ref11","doi-asserted-by":"crossref","first-page":"15","DOI":"10.1016\/j.jns.2005.08.011","article-title":"Impaired myocardial 123I-metaiodobenzylguanidine uptake in Lewy body disease: comparison between dementia with Lewy bodies and Parkinson's disease","volume":"240","author":"M Suzuki","year":"2006","journal-title":"J Neurol Sci"},{"key":"ref12","first-page":"1236","article-title":"Distribution of noradrenaline and dopamine (3-hydroxytyramine) in the human brain and their behavior in diseases of the extrapyramidal system [in German]","volume":"38","author":"H Ehringer","year":"1960","journal-title":"Wien Klin Wochenschr"},{"issue":"04","key":"ref13","doi-asserted-by":"crossref","first-page":"415","DOI":"10.1016\/0022-510X(73)90175-5","article-title":"Brain dopamine and the syndromes of Parkinson and Huntington. 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