3,4-dihydroxyphenylacetic acid has been researched along with Degenerative Diseases, Central Nervous System in 11 studies
3,4-Dihydroxyphenylacetic Acid: A deaminated metabolite of LEVODOPA.
(3,4-dihydroxyphenyl)acetic acid : A dihydroxyphenylacetic acid having the two hydroxy substituents located at the 3- and 4-positions. It is a metabolite of dopamine.
dihydroxyphenylacetic acid : A dihydroxy monocarboxylic acid consisting of phenylacetic acid having two phenolic hydroxy substituents.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Tolcapone treatment enhanced CSF DOPAC concentrations in unlesioned animals (by approximately four times) as well as monkeys rendered parkinsonian after severe nigrostriatal dopaminergic injury caused by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)." | 1.32 | Cerebrospinal fluid 3,4-dihydroxyphenylacetic acid level after tolcapone administration as an indicator of nigrostriatal degeneration. ( Di Monte, DA; Langston, JW; Thiffault, C, 2003) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 5 (45.45) | 29.6817 |
| 2010's | 5 (45.45) | 24.3611 |
| 2020's | 1 (9.09) | 2.80 |
| Authors | Studies |
|---|---|
| Goldstein, DS | 3 |
| Kopin, IJ | 1 |
| Sharabi, Y | 1 |
| Plotegher, N | 1 |
| Bubacco, L | 1 |
| Sgadò, P | 1 |
| Viaggi, C | 1 |
| Pinna, A | 1 |
| Marrone, C | 1 |
| Vaglini, F | 1 |
| Pontis, S | 1 |
| Mercuri, NB | 1 |
| Morelli, M | 1 |
| Corsini, GU | 1 |
| Wey, MC | 1 |
| Fernandez, E | 1 |
| Martinez, PA | 1 |
| Sullivan, P | 1 |
| Strong, R | 1 |
| Choi, DY | 1 |
| Lee, MK | 1 |
| Hong, JT | 1 |
| Thiffault, C | 1 |
| Langston, JW | 1 |
| Di Monte, DA | 1 |
| Burke, WJ | 1 |
| Li, SW | 1 |
| Chung, HD | 1 |
| Ruggiero, DA | 1 |
| Kristal, BS | 1 |
| Johnson, EM | 1 |
| Lampe, P | 1 |
| Kumar, VB | 1 |
| Franko, M | 1 |
| Williams, EA | 1 |
| Zahm, DS | 1 |
| Youdim, MB | 1 |
| Stephenson, G | 1 |
| Ben Shachar, D | 1 |
| Andreassen, OA | 1 |
| Ferrante, RJ | 1 |
| Dedeoglu, A | 1 |
| Albers, DW | 1 |
| Klivenyi, P | 1 |
| Carlson, EJ | 1 |
| Epstein, CJ | 1 |
| Beal, MF | 1 |
| Kirik, D | 1 |
| Rosenblad, C | 1 |
| Burger, C | 1 |
| Lundberg, C | 1 |
| Johansen, TE | 1 |
| Muzyczka, N | 1 |
| Mandel, RJ | 1 |
| Björklund, A | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Does N-Acetylcysteine Decrease Spontaneous Oxidation of Central Neural Dopamine in Parkinson's Disease?[NCT03104725] | Phase 1 | 6 participants (Actual) | Interventional | 2017-09-25 | Terminated (stopped due to Difficulty with recruitment and participant accrual due to study eligibility criteria and required study procedures (e.g., multiple lumbar punctures).) | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Patients with Parkinson's Disease (PD) who took N-acetylcysteine (NAC), and healthy volunteers who did not take NAC, each had two separate lumbar punctures (LPs) to obtain spinal fluid. The spinal fluid samples were used to measure the ratio of the brain chemical called 5-S-cysteinyl-dopamine (Cys-DA) to the brain chemical called 3,4-Dihydroxyphenylacetic acid (Cys-DOPAC). Dopamine has 2 metabolic fates. One is the breakdown of dopamine by an enzyme to form DOPAC. The other is spontaneous oxidation to form Cys-DA. The ratio of Cys-DA/DOPAC may reflect these relative fates. If NAC reduced spontaneous oxidation to Cys-DA, then the ratio Cys-DA/DOPAC would decrease between LP 1 and LP 2, which would be reflected as a percent decrease. (NCT03104725)
Timeframe: All participants underwent a baseline LP. For PD participants, the second LP occurred approximately 2 hours after the participant had taken NAC the last NAC dose. For HV participants the second LP takes place approximately 48 hours after the first LP.
| Intervention | percent change (Mean) |
|---|---|
| Healthy Volunteers (HVs) | 50.1 |
| Parkinson's Disease (PD) Patients | 27.2 |
Patients with Parkinson's Disease (PD) who took N-acetylcysteine (NAC), and healthy volunteers who did not take NAC, each had two separate lumbar punctures (LP 1 and LP 2) to obtain spinal fluid. The spinal fluid samples were used to measure the amount of a brain chemical called 5-S-cysteinyl-dopamine (Cys-DA). The primary outcome measure is the mean change in CSF Cys-DA levels between pre and post-NAC treatment, which is calculated as the difference of CSF Cys-DA levels at pre-treatment (LP 1) and post-treatment (LP 2) divided by CSF Cys-DA at pre-treatment (LP 1). A greater percent decrease in Cys-DA levels in the brain would suggest that NAC may contribute to a reduction in the oxidation of brain dopamine, while a smaller percent decrease would suggest that NAC had no effect on the oxidation of brain dopamine. (NCT03104725)
Timeframe: All participants underwent a baseline LP. For PD participants, the second LP occurred approximately 2 hours after the participant had taken NAC the last NAC dose. For HV participants the second LP takes place approximately 48 hours after the first LP.
| Intervention | percent change (Mean) |
|---|---|
| Healthy Volunteers (HVs) | 45.7 |
| Parkinson's Disease (PD) Patients | 20.1 |
Patients with Parkinson's Disease (PD) who took N-acetylcysteine (NAC), and healthy volunteers who did not take NAC, each had two separate lumbar punctures (LPs) to obtain spinal fluid. The spinal fluid samples were used to measure the ratio of the brain chemical called 5-S-cysteinyl-dopamine (Cys-DA) to the brain chemical called 3,4-Dihydroxyphenylacetic acid (Cys-DOPAC). Dopamine has 2 possible metabolic fates or processes of degradation. One fate is the breakdown of Dopamine by an enzyme to form DOPAC. The other fate is spontaneous oxidation to form Cys-DA. The ratio of Cys-DA to DOPAC may reflect these relative fates. If NAC reduced spontaneous oxidation to Cys-DA, then the ratio Cys-DA/DOPAC ratio would decrease between LP 1 and LP 2. (NCT03104725)
Timeframe: All participants underwent a baseline LP. For PD participants, the second LP occurred approximately 2 hours after the participant had taken NAC the last NAC dose. For HV participants the second LP takes place approximately 48 hours after the first LP.
| Intervention | ratio (Mean) | |
|---|---|---|
| Cys-DA/DOPAC LP1 | Cys-DA/DOPAC LP2 | |
| Healthy Volunteers (HVs) | 0.12 | 0.05 |
| Parkinson's Disease (PD) Patients | 0.16 | 0.13 |
4 reviews available for 3,4-dihydroxyphenylacetic acid and Degenerative Diseases, Central Nervous System
| Article | Year |
|---|---|
The catecholaldehyde hypothesis: where MAO fits in.
Topics: 3,4-Dihydroxyphenylacetic Acid; Aldehyde Dehydrogenase; Animals; Dopamine; Humans; Monoamine Oxidase | 2020 |
Catecholamine autotoxicity. Implications for pharmacology and therapeutics of Parkinson disease and related disorders.
Topics: 3,4-Dihydroxyphenylacetic Acid; alpha-Synuclein; Animals; Apoptosis; Catecholamines; Humans; Lipid P | 2014 |
Lysines, Achilles' heel in alpha-synuclein conversion to a deadly neuronal endotoxin.
Topics: 3,4-Dihydroxyphenylacetic Acid; Aldehydes; alpha-Synuclein; Brain; Dopamine; Humans; Lysine; Metabol | 2016 |
Neurotoxicity of MAO metabolites of catecholamine neurotransmitters: role in neurodegenerative diseases.
Topics: 3,4-Dihydroxyphenylacetic Acid; Aldehydes; Animals; Apoptosis; Catecholamines; Catechols; Humans; Ne | 2004 |
7 other studies available for 3,4-dihydroxyphenylacetic acid and Degenerative Diseases, Central Nervous System
| Article | Year |
|---|---|
Behavioral, neurochemical, and electrophysiological changes in an early spontaneous mouse model of nigrostriatal degeneration.
Topics: 3,4-Dihydroxyphenylacetic Acid; Age Factors; Analysis of Variance; Animals; Behavior, Animal; Brain | 2011 |
Neurodegeneration and motor dysfunction in mice lacking cytosolic and mitochondrial aldehyde dehydrogenases: implications for Parkinson's disease.
Topics: 3,4-Dihydroxyphenylacetic Acid; Aldehyde Dehydrogenase; Animals; Body Weight; Cognition Disorders; C | 2012 |
Lack of CCR5 modifies glial phenotypes and population of the nigral dopaminergic neurons, but not MPTP-induced dopaminergic neurodegeneration.
Topics: 3,4-Dihydroxyphenylacetic Acid; Animals; Corpus Striatum; Disease Models, Animal; Dopaminergic Neuro | 2013 |
Cerebrospinal fluid 3,4-dihydroxyphenylacetic acid level after tolcapone administration as an indicator of nigrostriatal degeneration.
Topics: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; 3,4-Dihydroxyphenylacetic Acid; Animals; Antiparkinson | 2003 |
Ironing iron out in Parkinson's disease and other neurodegenerative diseases with iron chelators: a lesson from 6-hydroxydopamine and iron chelators, desferal and VK-28.
Topics: 3,4-Dihydroxyphenylacetic Acid; Analysis of Variance; Animals; Behavior, Animal; Brain; Brocresine; | 2004 |
Mice with a partial deficiency of manganese superoxide dismutase show increased vulnerability to the mitochondrial toxins malonate, 3-nitropropionic acid, and MPTP.
Topics: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; 3,4-Dihydroxyphenylacetic Acid; Animals; Carrier Prote | 2001 |
Parkinson-like neurodegeneration induced by targeted overexpression of alpha-synuclein in the nigrostriatal system.
Topics: 3,4-Dihydroxyphenylacetic Acid; alpha-Synuclein; Animals; Behavior, Animal; Cell Count; Cell Death; | 2002 |