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Erschienen in: Journal of Neural Transmission 2/2020

05.12.2019 | Neurology and Preclinical Neurological Studies - Review Article

The catecholaldehyde hypothesis: where MAO fits in

verfasst von: David S. Goldstein

Erschienen in: Journal of Neural Transmission | Ausgabe 2/2020

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Abstract

Monoamine oxidase (MAO) plays a central role in the metabolism of the neurotransmitters dopamine, norepinephrine, and serotonin. This brief review focuses on 3,4-dihydroxyphenylacetaldehyde (DOPAL), which is the immediate product of MAO acting on cytoplasmic dopamine. DOPAL is toxic; however, normally DOPAL is converted via aldehyde dehydrogenase (ALDH) to 3,4-dihydroxyphenylacetic acid (DOPAC), which rapidly exits the neurons. In addition to vesicular uptake of dopamine via the vesicular monoamine transporter (VMAT), the two-enzyme sequence of MAO and ALDH keeps cytoplasmic dopamine levels low. Dopamine oxidizes readily to form toxic products that could threaten neuronal homeostasis. The catecholaldehyde hypothesis posits that diseases featuring catecholaminergic neurodegeneration result from harmful interactions between DOPAL and the protein alpha-synuclein, a major component of Lewy bodies in diseases such as Parkinson disease, dementia with Lewy bodies, and pure autonomic failure. DOPAL potently oligomerizes alpha-synuclein, and alpha-synuclein oligomers impede vesicular functions, shifting the fate of cytoplasmic dopamine toward MAO-catalyzed formation of DOPAL—a vicious cycle. When MAO deaminates dopamine to form DOPAL, hydrogen peroxide is generated; and DOPAL, hydrogen peroxide, and divalent metal cations react to form hydroxyl radicals, which peroxidate lipid membranes. Lipid peroxidation products in turn inhibit ALDH, causing DOPAL to accumulate—another vicious cycle. MAO inhibition decreases DOPAL formation but concurrently increases the spontaneous oxidation of dopamine, potentially trading off one form of toxicity for another. These considerations rationalize a neuroprotection strategy based on concurrent treatment with an MAO inhibitor and an anti-oxidant.
Literatur
Zurück zum Zitat Amino T, Orimo S, Takahashi A, Uchihara T, Mizusawa H (2005) Profound cardiac sympathetic denervation occurs in Parkinson disease. Brain Path 15:29–34CrossRef Amino T, Orimo S, Takahashi A, Uchihara T, Mizusawa H (2005) Profound cardiac sympathetic denervation occurs in Parkinson disease. Brain Path 15:29–34CrossRef
Zurück zum Zitat Aminoff MJ, Wilcox CS (1971) Assessment of autonomic function in patients with a Parkinsonian syndrome. Br Med J 4(779):80–84CrossRef Aminoff MJ, Wilcox CS (1971) Assessment of autonomic function in patients with a Parkinsonian syndrome. Br Med J 4(779):80–84CrossRef
Zurück zum Zitat Appenzeller O, Goss JE (1971) Autonomic deficits in Parkinson’s syndrome. Arch Neurol 24:50–57CrossRef Appenzeller O, Goss JE (1971) Autonomic deficits in Parkinson’s syndrome. Arch Neurol 24:50–57CrossRef
Zurück zum Zitat Arai K, Kato N, Kashiwado K, Hattori T (2000) Pure autonomic failure in association with human alpha-synucleinopathy. Neurosci Lett 296:171–173CrossRef Arai K, Kato N, Kashiwado K, Hattori T (2000) Pure autonomic failure in association with human alpha-synucleinopathy. Neurosci Lett 296:171–173CrossRef
Zurück zum Zitat Baba M, Nakajo S, Tu PH, Tomita T, Nakaya K, Lee VM, Trojanowski JQ, Iwatsubo T (1998) Aggregation of alpha-synuclein in Lewy bodies of sporadic Parkinson’s disease and dementia with Lewy bodies. Am J Pathol 152(4):879–884PubMedPubMedCentral Baba M, Nakajo S, Tu PH, Tomita T, Nakaya K, Lee VM, Trojanowski JQ, Iwatsubo T (1998) Aggregation of alpha-synuclein in Lewy bodies of sporadic Parkinson’s disease and dementia with Lewy bodies. Am J Pathol 152(4):879–884PubMedPubMedCentral
Zurück zum Zitat Banerjee K, Munshi S, Sen O, Pramanik V, Roy Mukherjee T, Chakrabarti S (2014) Dopamine cytotoxicity involves both oxidative and nonoxidative pathways in SH-SY5Y cells: potential role of alpha-synuclein overexpression and proteasomal inhibition in the etiopathogenesis of Parkinson’s disease. Parkinsons Dis 2014:878935. https://doi.org/10.1155/2014/878935 CrossRefPubMedPubMedCentral Banerjee K, Munshi S, Sen O, Pramanik V, Roy Mukherjee T, Chakrabarti S (2014) Dopamine cytotoxicity involves both oxidative and nonoxidative pathways in SH-SY5Y cells: potential role of alpha-synuclein overexpression and proteasomal inhibition in the etiopathogenesis of Parkinson’s disease. Parkinsons Dis 2014:878935. https://​doi.​org/​10.​1155/​2014/​878935 CrossRefPubMedPubMedCentral
Zurück zum Zitat Benarroch EE (2003) Brainstem in multiple system atrophy: clinicopathological correlations. Cell Mol Neurobiol 23(4–5):519–526CrossRef Benarroch EE (2003) Brainstem in multiple system atrophy: clinicopathological correlations. Cell Mol Neurobiol 23(4–5):519–526CrossRef
Zurück zum Zitat Bonuccelli U, Lucetti C, Del Dotto P, Ceravolo R, Gambaccini G, Bernardini S, Rossi G, Piaggesi A (2003) Orthostatic hypotension in de novo Parkinson disease. Arch Neurol 60:1400–1404CrossRef Bonuccelli U, Lucetti C, Del Dotto P, Ceravolo R, Gambaccini G, Bernardini S, Rossi G, Piaggesi A (2003) Orthostatic hypotension in de novo Parkinson disease. Arch Neurol 60:1400–1404CrossRef
Zurück zum Zitat Braak H, de Vos RA, Bohl J, Del Tredici K (2006) Gastric alpha-synuclein immunoreactive inclusions in Meissner’s and Auerbach’s plexuses in cases staged for Parkinson’s disease-related brain pathology. Neurosci Lett 396(1):67–72CrossRef Braak H, de Vos RA, Bohl J, Del Tredici K (2006) Gastric alpha-synuclein immunoreactive inclusions in Meissner’s and Auerbach’s plexuses in cases staged for Parkinson’s disease-related brain pathology. Neurosci Lett 396(1):67–72CrossRef
Zurück zum Zitat Burke WJ, Li SW, Williams EA, Nonneman R, Zahm DS (2003) 3,4-Dihydroxyphenylacetaldehyde is the toxic dopamine metabolite in vivo: implications for Parkinson’s disease pathogenesis. Brain Res 989(2):205–213CrossRef Burke WJ, Li SW, Williams EA, Nonneman R, Zahm DS (2003) 3,4-Dihydroxyphenylacetaldehyde is the toxic dopamine metabolite in vivo: implications for Parkinson’s disease pathogenesis. Brain Res 989(2):205–213CrossRef
Zurück zum Zitat Carlsson A, Fornstedt B (1991) Possible mechanisms underlying the special vulnerability of dopaminergic neurons. Acta Neurol Scand Suppl 136:16–18CrossRef Carlsson A, Fornstedt B (1991) Possible mechanisms underlying the special vulnerability of dopaminergic neurons. Acta Neurol Scand Suppl 136:16–18CrossRef
Zurück zum Zitat Eisenhofer G, Goldstein DS, Stull R, Keiser HR, Sunderland T, Murphy DL, Kopin IJ (1986) Simultaneous liquid-chromatographic determination of 3,4-dihydroxyphenylglycol, catecholamines, and 3,4-dihydroxyphenylalanine in plasma, and their responses to inhibition of monoamine oxidase. Clin Chem 32:2030–2033CrossRef Eisenhofer G, Goldstein DS, Stull R, Keiser HR, Sunderland T, Murphy DL, Kopin IJ (1986) Simultaneous liquid-chromatographic determination of 3,4-dihydroxyphenylglycol, catecholamines, and 3,4-dihydroxyphenylalanine in plasma, and their responses to inhibition of monoamine oxidase. Clin Chem 32:2030–2033CrossRef
Zurück zum Zitat Eisenhofer G, Aneman A, Friberg P, Hooper D, Fandriks L, Lonroth H, Hunyady B, Mezey E (1997) Substantial production of dopamine in the human gastrointestinal tract. J Clin Endocrinol Metab 82(11):3864–3871CrossRef Eisenhofer G, Aneman A, Friberg P, Hooper D, Fandriks L, Lonroth H, Hunyady B, Mezey E (1997) Substantial production of dopamine in the human gastrointestinal tract. J Clin Endocrinol Metab 82(11):3864–3871CrossRef
Zurück zum Zitat Fitzmaurice AG, Rhodes SL, Lulla A, Murphy NP, Lam HA, O’Donnell KC, Barnhill L, Casida JE, Cockburn M, Sagasti A, Stahl MC, Maidment NT, Ritz B, Bronstein JM (2013) Aldehyde dehydrogenase inhibition as a pathogenic mechanism in Parkinson disease. Proc Natl Acad Sci USA 110(2):636–641. https://doi.org/10.1073/pnas.1220399110 CrossRefPubMed Fitzmaurice AG, Rhodes SL, Lulla A, Murphy NP, Lam HA, O’Donnell KC, Barnhill L, Casida JE, Cockburn M, Sagasti A, Stahl MC, Maidment NT, Ritz B, Bronstein JM (2013) Aldehyde dehydrogenase inhibition as a pathogenic mechanism in Parkinson disease. Proc Natl Acad Sci USA 110(2):636–641. https://​doi.​org/​10.​1073/​pnas.​1220399110 CrossRefPubMed
Zurück zum Zitat Fornai F, Giorgi FS, Bassi L, Ferrucci M, Alessandri MG, Corsini GU (2000) Modulation of dihydroxyphenylacetaldehyde extracellular levels in vivo in the rat striatum after different kinds of pharmacological treatment. Brain Res 861(1):126–134CrossRef Fornai F, Giorgi FS, Bassi L, Ferrucci M, Alessandri MG, Corsini GU (2000) Modulation of dihydroxyphenylacetaldehyde extracellular levels in vivo in the rat striatum after different kinds of pharmacological treatment. Brain Res 861(1):126–134CrossRef
Zurück zum Zitat Fornstedt B, Carlsson A (1989) A marked rise in 5-S-cysteinyl-dopamine levels in guinea-pig striatum following reserpine treatment. J Neural Transm 76(2):155–161CrossRef Fornstedt B, Carlsson A (1989) A marked rise in 5-S-cysteinyl-dopamine levels in guinea-pig striatum following reserpine treatment. J Neural Transm 76(2):155–161CrossRef
Zurück zum Zitat Fornstedt B, Carlsson A (1991) Effects of inhibition of monoamine oxidase on the levels of 5-S-cysteinyl adducts of catechols in dopaminergic regions of the brain of the guinea pig. Neuropharmacology 30(5):463–468CrossRef Fornstedt B, Carlsson A (1991) Effects of inhibition of monoamine oxidase on the levels of 5-S-cysteinyl adducts of catechols in dopaminergic regions of the brain of the guinea pig. Neuropharmacology 30(5):463–468CrossRef
Zurück zum Zitat Fowler JS, Logan J, Volkow ND, Shumay E, McCall-Perez F, Jayne M, Wang GJ, Alexoff DL, Apelskog-Torres K, Hubbard B, Carter P, King P, Fahn S, Gilmor M, Telang F, Shea C, Xu Y, Muench L (2015) Evidence that formulations of the selective MAO-B inhibitor, selegiline, which bypass first-pass metabolism, also inhibit MAO-A in the human brain. Neuropsychopharmacology 40(3):650–657. https://doi.org/10.1038/npp.2014.214 CrossRefPubMed Fowler JS, Logan J, Volkow ND, Shumay E, McCall-Perez F, Jayne M, Wang GJ, Alexoff DL, Apelskog-Torres K, Hubbard B, Carter P, King P, Fahn S, Gilmor M, Telang F, Shea C, Xu Y, Muench L (2015) Evidence that formulations of the selective MAO-B inhibitor, selegiline, which bypass first-pass metabolism, also inhibit MAO-A in the human brain. Neuropsychopharmacology 40(3):650–657. https://​doi.​org/​10.​1038/​npp.​2014.​214 CrossRefPubMed
Zurück zum Zitat Fumagalli F, Gainetdinov RR, Wang YM, Valenzano KJ, Miller GW, Caron MG (1999) Increased methamphetamine neurotoxicity in heterozygous vesicular monoamine transporter 2 knock-out mice. J Neurosci 19(7):2424–2431CrossRef Fumagalli F, Gainetdinov RR, Wang YM, Valenzano KJ, Miller GW, Caron MG (1999) Increased methamphetamine neurotoxicity in heterozygous vesicular monoamine transporter 2 knock-out mice. J Neurosci 19(7):2424–2431CrossRef
Zurück zum Zitat Gainetdinov RR, Fumagalli F, Wang YM, Jones SR, Levey AI, Miller GW, Caron MG (1998) Increased MPTP neurotoxicity in vesicular monoamine transporter 2 heterozygote knockout mice. J Neurochem 70:1973–1978CrossRef Gainetdinov RR, Fumagalli F, Wang YM, Jones SR, Levey AI, Miller GW, Caron MG (1998) Increased MPTP neurotoxicity in vesicular monoamine transporter 2 heterozygote knockout mice. J Neurochem 70:1973–1978CrossRef
Zurück zum Zitat Goldstein DS, Holmes C, Cannon RO 3rd, Eisenhofer G, Kopin IJ (1997) Sympathetic cardioneuropathy in dysautonomias. N Engl J Med 336(10):696–702CrossRef Goldstein DS, Holmes C, Cannon RO 3rd, Eisenhofer G, Kopin IJ (1997) Sympathetic cardioneuropathy in dysautonomias. N Engl J Med 336(10):696–702CrossRef
Zurück zum Zitat Goldstein DS, Sullivan P, Holmes C, Miller GW, Sharabi Y, Kopin IJ (2014) A vesicular sequestration to oxidative deamination shift in myocardial sympathetic nerves in Parkinson disease. J Neurochem 131:219–228CrossRef Goldstein DS, Sullivan P, Holmes C, Miller GW, Sharabi Y, Kopin IJ (2014) A vesicular sequestration to oxidative deamination shift in myocardial sympathetic nerves in Parkinson disease. J Neurochem 131:219–228CrossRef
Zurück zum Zitat Group PS (1996) Impact of deprenyl and tocopherol treatment on Parkinson’s disease in DATATOP subjects not requiring levodopa. Parkinson Study Group. Ann Neurol 39:29–36CrossRef Group PS (1996) Impact of deprenyl and tocopherol treatment on Parkinson’s disease in DATATOP subjects not requiring levodopa. Parkinson Study Group. Ann Neurol 39:29–36CrossRef
Zurück zum Zitat Kaufmann H, Hague K, Perl D (2001) Accumulation of alpha-synuclein in autonomic nerves in pure autonomic failure. Neurology 56(7):980–981CrossRef Kaufmann H, Hague K, Perl D (2001) Accumulation of alpha-synuclein in autonomic nerves in pure autonomic failure. Neurology 56(7):980–981CrossRef
Zurück zum Zitat Kish SJ, Shannak K, Hornykiewicz O (1988) Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson’s disease. Pathophysiologic and clinical implications. N Engl J Med 318:876–880CrossRef Kish SJ, Shannak K, Hornykiewicz O (1988) Uneven pattern of dopamine loss in the striatum of patients with idiopathic Parkinson’s disease. Pathophysiologic and clinical implications. N Engl J Med 318:876–880CrossRef
Zurück zum Zitat Kristal BS, Conway AD, Brown AM, Jain JC, Ulluci PA, Li SW, Burke WJ (2001) Selective dopaminergic vulnerability: 3,4-dihydroxyphenylacetaldehyde targets mitochondria. Free Radic Biol Med 30(8):924–931CrossRef Kristal BS, Conway AD, Brown AM, Jain JC, Ulluci PA, Li SW, Burke WJ (2001) Selective dopaminergic vulnerability: 3,4-dihydroxyphenylacetaldehyde targets mitochondria. Free Radic Biol Med 30(8):924–931CrossRef
Zurück zum Zitat Lamensdorf I, Eisenhofer G, Harvey-White J, Hayakawa Y, Kirk K, Kopin IJ (2000a) Metabolic stress in PC12 cells induces the formation of the endogenous dopaminergic neurotoxin, 3,4-dihydroxyphenylacetaldehyde. J Neurosci Res 60(4):552–558CrossRef Lamensdorf I, Eisenhofer G, Harvey-White J, Hayakawa Y, Kirk K, Kopin IJ (2000a) Metabolic stress in PC12 cells induces the formation of the endogenous dopaminergic neurotoxin, 3,4-dihydroxyphenylacetaldehyde. J Neurosci Res 60(4):552–558CrossRef
Zurück zum Zitat Lamensdorf I, Eisenhofer G, Harvey-White J, Nechustan A, Kirk K, Kopin IJ (2000b) 3,4-Dihydroxyphenylacetaldehyde potentiates the toxic effects of metabolic stress in PC12 cells. Brain Res 868(2):191–201CrossRef Lamensdorf I, Eisenhofer G, Harvey-White J, Nechustan A, Kirk K, Kopin IJ (2000b) 3,4-Dihydroxyphenylacetaldehyde potentiates the toxic effects of metabolic stress in PC12 cells. Brain Res 868(2):191–201CrossRef
Zurück zum Zitat Lamensdorf I, Hrycyna C, He LP, Nechushtan A, Tjurmina O, Harvey-White J, Eisenhofer G, Rojas E, Kopin IJ (2000c) Acidic dopamine metabolites are actively extruded from PC12 cells by a novel sulfonylurea-sensitive transporter. Naunyn Schmiedebergs Arch Pharmacol 361(6):654–664CrossRef Lamensdorf I, Hrycyna C, He LP, Nechushtan A, Tjurmina O, Harvey-White J, Eisenhofer G, Rojas E, Kopin IJ (2000c) Acidic dopamine metabolites are actively extruded from PC12 cells by a novel sulfonylurea-sensitive transporter. Naunyn Schmiedebergs Arch Pharmacol 361(6):654–664CrossRef
Zurück zum Zitat Li SW, Lin TS, Minteer S, Burke WJ (2001) 3,4-Dihydroxyphenylacetaldehyde and hydrogen peroxide generate a hydroxyl radical: possible role in Parkinson’s disease pathogenesis. Brain Res Mol Brain Res 93(1):1–7CrossRef Li SW, Lin TS, Minteer S, Burke WJ (2001) 3,4-Dihydroxyphenylacetaldehyde and hydrogen peroxide generate a hydroxyl radical: possible role in Parkinson’s disease pathogenesis. Brain Res Mol Brain Res 93(1):1–7CrossRef
Zurück zum Zitat Lohr KM, Bernstein AI, Stout KA, Dunn AR, Lazo CR, Alter SP, Wang M, Li Y, Fan X, Hess EJ, Yi H, Vecchio LM, Goldstein DS, Guillot TS, Salahpour A, Miller GW (2014) Increased vesicular monoamine transporter enhances dopamine release and opposes Parkinson disease-related neurodegeneration in vivo. Proc Natl Acad Sci USA 111(27):9977–9982. https://doi.org/10.1073/pnas.1402134111 CrossRefPubMed Lohr KM, Bernstein AI, Stout KA, Dunn AR, Lazo CR, Alter SP, Wang M, Li Y, Fan X, Hess EJ, Yi H, Vecchio LM, Goldstein DS, Guillot TS, Salahpour A, Miller GW (2014) Increased vesicular monoamine transporter enhances dopamine release and opposes Parkinson disease-related neurodegeneration in vivo. Proc Natl Acad Sci USA 111(27):9977–9982. https://​doi.​org/​10.​1073/​pnas.​1402134111 CrossRefPubMed
Zurück zum Zitat Mandel S, Grunblatt E, Riederer P, Amariglio N, Jacob-Hirsch J, Rechavi G, Youdim MB (2005) Gene expression profiling of sporadic Parkinson’s disease substantia nigra pars compacta reveals impairment of ubiquitin-proteasome subunits, SKP1A, aldehyde dehydrogenase, and chaperone HSC-70. Ann N Y Acad Sci 1053:356–375CrossRef Mandel S, Grunblatt E, Riederer P, Amariglio N, Jacob-Hirsch J, Rechavi G, Youdim MB (2005) Gene expression profiling of sporadic Parkinson’s disease substantia nigra pars compacta reveals impairment of ubiquitin-proteasome subunits, SKP1A, aldehyde dehydrogenase, and chaperone HSC-70. Ann N Y Acad Sci 1053:356–375CrossRef
Zurück zum Zitat Mattammal MB, Haring JH, Chung HD, Raghu G, Strong R (1995) An endogenous dopaminergic neurotoxin: implication for Parkinson’s disease. Neurodegeneration 4(3):271–281CrossRef Mattammal MB, Haring JH, Chung HD, Raghu G, Strong R (1995) An endogenous dopaminergic neurotoxin: implication for Parkinson’s disease. Neurodegeneration 4(3):271–281CrossRef
Zurück zum Zitat Micieli G, Martignoni E, Cavallini A, Sandrini G, Nappi G (1987) Postprandial and orthostatic hypotension in Parkinson’s disease. Neurology 37(3):386–393CrossRef Micieli G, Martignoni E, Cavallini A, Sandrini G, Nappi G (1987) Postprandial and orthostatic hypotension in Parkinson’s disease. Neurology 37(3):386–393CrossRef
Zurück zum Zitat Molochnikov L, Rabey JM, Dobronevsky E, Bonucelli U, Ceravolo R, Frosini D, Grunblatt E, Riederer P, Jacob C, Aharon-Peretz J, Bashenko Y, Youdim MB, Mandel SA (2012) A molecular signature in blood identifies early Parkinson’s disease. Molec Neurodegen 7:26. https://doi.org/10.1186/1750-1326-7-26 CrossRef Molochnikov L, Rabey JM, Dobronevsky E, Bonucelli U, Ceravolo R, Frosini D, Grunblatt E, Riederer P, Jacob C, Aharon-Peretz J, Bashenko Y, Youdim MB, Mandel SA (2012) A molecular signature in blood identifies early Parkinson’s disease. Molec Neurodegen 7:26. https://​doi.​org/​10.​1186/​1750-1326-7-26 CrossRef
Zurück zum Zitat Nagatsu T (1997) Isoquinoline neurotoxins in the brain and Parkinson’s disease. Neurosci Res 29:99–111CrossRef Nagatsu T (1997) Isoquinoline neurotoxins in the brain and Parkinson’s disease. Neurosci Res 29:99–111CrossRef
Zurück zum Zitat Orimo S, Amino T, Takahashi A, Kojo T, Uchihara T, Mori F, Wakabayashi K, Takahashi H (2006) Cardiac sympathetic denervation in Lewy body disease. Parkinsonism Relat Disord 12(Suppl 2):S99–S105CrossRef Orimo S, Amino T, Takahashi A, Kojo T, Uchihara T, Mori F, Wakabayashi K, Takahashi H (2006) Cardiac sympathetic denervation in Lewy body disease. Parkinsonism Relat Disord 12(Suppl 2):S99–S105CrossRef
Zurück zum Zitat Polymeropoulos MH, Lavedan C, Leroy E, Ide SE, Dehejia A, Dutra A, Pike B, Root H, Rubenstein J, Boyer R, Stenroos ES, Chandrasekharappa S, Athanassiadou A, Papapetropoulos T, Johnson WG, Lazzarini AM, Duvoisin RC, Di Iorio G, Golbe LI, Nussbaum RL (1997) Mutation in the alpha-synuclein gene identified in families with Parkinson’s disease. Science 276:2045–2047CrossRef Polymeropoulos MH, Lavedan C, Leroy E, Ide SE, Dehejia A, Dutra A, Pike B, Root H, Rubenstein J, Boyer R, Stenroos ES, Chandrasekharappa S, Athanassiadou A, Papapetropoulos T, Johnson WG, Lazzarini AM, Duvoisin RC, Di Iorio G, Golbe LI, Nussbaum RL (1997) Mutation in the alpha-synuclein gene identified in families with Parkinson’s disease. Science 276:2045–2047CrossRef
Zurück zum Zitat Rajput AH, Rozdilsky B (1976) Dysautonomia in Parkinsonism: a clinicopathological study. J Neurol Neurosurg Psychiatry 39:1092–1100CrossRef Rajput AH, Rozdilsky B (1976) Dysautonomia in Parkinsonism: a clinicopathological study. J Neurol Neurosurg Psychiatry 39:1092–1100CrossRef
Zurück zum Zitat Staal RG, Sonsalla PK (2000) Inhibition of brain vesicular monoamine transporter (VMAT2) enhances 1-methyl-4-phenylpyridinium neurotoxicity in vivo in rat striata. J Pharmacol Exp Ther 293(2):336–342PubMed Staal RG, Sonsalla PK (2000) Inhibition of brain vesicular monoamine transporter (VMAT2) enhances 1-methyl-4-phenylpyridinium neurotoxicity in vivo in rat striata. J Pharmacol Exp Ther 293(2):336–342PubMed
Zurück zum Zitat Storch A, Ott S, Hwang YI, Ortmann R, Hein A, Frenzel S, Matsubara K, Ohta S, Wolf HU, Schwarz J (2002) Selective dopaminergic neurotoxicity of isoquinoline derivatives related to Parkinson’s disease: studies using heterologous expression systems of the dopamine transporter. Biochem Pharmacol 63(5):909–920CrossRef Storch A, Ott S, Hwang YI, Ortmann R, Hein A, Frenzel S, Matsubara K, Ohta S, Wolf HU, Schwarz J (2002) Selective dopaminergic neurotoxicity of isoquinoline derivatives related to Parkinson’s disease: studies using heterologous expression systems of the dopamine transporter. Biochem Pharmacol 63(5):909–920CrossRef
Zurück zum Zitat Wakabayashi K, Yoshimoto M, Tsuji S, Takahashi H (1998) Alpha-synuclein immunoreactivity in glial cytoplasmic inclusions in multiple system atrophy. Neurosci Lett 249(2–3):180–182CrossRef Wakabayashi K, Yoshimoto M, Tsuji S, Takahashi H (1998) Alpha-synuclein immunoreactivity in glial cytoplasmic inclusions in multiple system atrophy. Neurosci Lett 249(2–3):180–182CrossRef
Zurück zum Zitat Ward CD (1994) Does selegiline delay progression of Parkinson’s disease? A critical re-evaluation of the DATATOP study. J Neurol Neurosurg Psychiatry 57(2):217–220CrossRef Ward CD (1994) Does selegiline delay progression of Parkinson’s disease? A critical re-evaluation of the DATATOP study. J Neurol Neurosurg Psychiatry 57(2):217–220CrossRef
Zurück zum Zitat Weingarten P, Zhou QY (2001) Protection of intracellular dopamine cytotoxicity by dopamine disposition and metabolism factors. J Neurochem 77(3):776–785CrossRef Weingarten P, Zhou QY (2001) Protection of intracellular dopamine cytotoxicity by dopamine disposition and metabolism factors. J Neurochem 77(3):776–785CrossRef
Zurück zum Zitat Wey M, Fernandez E, Martinez PA, Sullivan P, Goldstein DS, Strong R (2012) Neurodegeneration and motor dysfunction in mice lacking cytosolic and mitochondrial aldehyde dehydrogenases: implications for Parkinson’s disease. PLoS ONE 7:e31522CrossRef Wey M, Fernandez E, Martinez PA, Sullivan P, Goldstein DS, Strong R (2012) Neurodegeneration and motor dysfunction in mice lacking cytosolic and mitochondrial aldehyde dehydrogenases: implications for Parkinson’s disease. PLoS ONE 7:e31522CrossRef
Zurück zum Zitat Winner B, Jappelli R, Maji SK, Desplats PA, Boyer L, Aigner S, Hetzer C, Loher T, Vilar M, Campioni S, Tzitzilonis C, Soragni A, Jessberger S, Mira H, Consiglio A, Pham E, Masliah E, Gage FH, Riek R (2011) In vivo demonstration that alpha-synuclein oligomers are toxic. Proc Natl Acad Sci USA 108(10):4194–4199. https://doi.org/10.1073/pnas.1100976108 CrossRefPubMed Winner B, Jappelli R, Maji SK, Desplats PA, Boyer L, Aigner S, Hetzer C, Loher T, Vilar M, Campioni S, Tzitzilonis C, Soragni A, Jessberger S, Mira H, Consiglio A, Pham E, Masliah E, Gage FH, Riek R (2011) In vivo demonstration that alpha-synuclein oligomers are toxic. Proc Natl Acad Sci USA 108(10):4194–4199. https://​doi.​org/​10.​1073/​pnas.​1100976108 CrossRefPubMed
Metadaten
Titel
The catecholaldehyde hypothesis: where MAO fits in
verfasst von
David S. Goldstein
Publikationsdatum
05.12.2019
Verlag
Springer Vienna
Erschienen in
Journal of Neural Transmission / Ausgabe 2/2020
Print ISSN: 0300-9564
Elektronische ISSN: 1435-1463
DOI
https://doi.org/10.1007/s00702-019-02106-9

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