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Levodopa

Levodopa, also known as L-DOPA, is a medication primarily used to treat the symptoms of Parkinson's disease.
It is a precursor to the neurotransmitters dopamine, norepinephrine, and epinephrine, and is essential for the proper functioning of the central nervous system.
Levodopa helps to alleviate the motor symptoms associated with Parkinson's, such as tremors, rigidity, and slow movements.
It is often combined with other medications, such as carbidopa, to enhance its effectiveness and reduce side effects.
Researchers continue to explore new ways to optimize Levodopa therapy, including developing improved delivery methods and investigating novel treatment protocols.
PubCompare.ai can assist researchers in this endeavor by providing AI-driven comparisons that enhance reproducibility and accuracy, helping users find the best Levodopa research protocols and products.

Most cited protocols related to «Levodopa»

1
Early Parkinson's Disease Cohort Study
Cited 48 times
PD and HC subjects of similar age and gender from 24 study sites in the US (18), Europe (5) and Australia (1) were enrolled after obtaining informed consent. We acknowledge that the early PD cohort likely includes a small number of subjects with other DAT deficit parkinsonian syndromes such as progressive supranuclear palsy (PSP), multiple system atrophy (MSA) and cortical basal syndrome (CBS), which may be indistinguishable from PD at the earliest stages of disease. At each study visit, the investigators reassess the subject diagnosis to identify any non‐PD subjects.
This study was conducted in accordance with the Declaration of Helsinki and the Good Clinical Practice (GCP) guidelines after approval of the local ethics committees of the participating sites. At enrollment, PD subjects were required to be age 30 years or older, untreated with PD medications (levodopa, dopamine agonists, MAO‐B inhibitors, or amantadine), within 2 years of diagnosis, Hoehn and Yahr <3, and to have either at least two of resting tremor, bradykinesia, or rigidity (must have either resting tremor or bradykinesia) or a single asymmetric resting tremor or asymmetric bradykinesia. All PD subjects underwent dopamine transporter (DAT) imaging with 123I Ioflupane or vesicular monoamine transporter (VMAT‐2) imaging with 18F AV133 (Australia only) and were only eligible if DAT or VMAT‐2 imaging demonstrated dopaminergic deficit consistent with PD in addition to clinical features of the disease. Study investigators evaluated enrolled PD subjects to assess absence of current or imminent (6 months) disability requiring PD medications, though subjects could initiate PD medications at any time after enrollment if the subject or investigator deemed it clinically necessary. Those subjects screened as potential PD subjects who were ineligible due to DAT or VMAT‐2 scans without evidence of dopaminergic deficit (SWEDD) were eligible to be enrolled in a SWEDD cohort.4 HC subjects were required to be age 30 years or older without an active, clinically significant neurological disorder or a first‐degree relative with PD. All enrolled subjects agreed to complete all study evaluations, including lumbar puncture.
PD and SWEDD subjects were excluded if they had a clinical diagnosis of dementia or had taken PD medications within 60 days of baseline or for longer than 60 days in total. HC subjects were excluded if they had a Montreal Cognitive Assessment (MoCA) total score ≤26. All subjects were excluded if they were treated with neuroleptics, metoclopramide, alpha methyldopa, methylphenidate, reserpine, or amphetamine derivative within 6 months or were currently treated with anticoagulants that might preclude safe completion of the lumbar puncture.
Marek K., Chowdhury S., Siderowf A., Lasch S., Coffey C.S., Caspell‐Garcia C., Simuni T., Jennings D., Tanner C.M., Trojanowski J.Q., Shaw L.M., Seibyl J., Schuff N., Singleton A., Kieburtz K., Toga A.W., Mollenhauer B., Galasko D., Chahine L.M., Weintraub D., Foroud T., Tosun‐Turgut D., Poston K., Arnedo V., Frasier M, & Sherer T. (2018). The Parkinson's progression markers initiative (PPMI) – establishing a PD biomarker cohort. Annals of Clinical and Translational Neurology, 5(12), 1460-1477.
Publication 2018
123I-ioflupane Amantadine Amphetamine Anticoagulants Antipsychotic Agents Bradykinesia Cortex, Cerebral Dementia Diagnosis Disabled Persons Dopamine Agonists Gender Hydrochloride, Dopamine Levodopa Methyldopa Methylphenidate Metoclopramide Monoamine Oxidase Inhibitors Multiple System Atrophy Muscle Rigidity Nervous System Disorder Parkinsonian Disorders Pharmaceutical Preparations Progressive Supranuclear Palsy Punctures, Lumbar Radionuclide Imaging Regional Ethics Committees Reserpine Resting Tremor SLC6A3 protein, human Syndrome Vesicular Monoamine Transport Proteins Volumetric-Modulated Arc Therapy
2
Idiopathic Parkinson's Disease Evaluation
Cited 37 times
A convenience sample of 104 participants (see Table 1 for demographic and clinical characteristics) with idiopathic PD were assessed either as part of participation in an ICD clinical trial or through convenience sampling at the Parkinson’s Disease and Movement Disorders Center at the University of Pennsylvania between January 2010 and April 2011. The Institutional Review Board (IRB) at Penn approved the study, and written consent was obtained from participants prior to study participation. Disease severity was assessed with the Unified Parkinson’s Disease Rating Scale (UPDRS) and Hoehn and Yahr stage,13 and levodopa and dopamine agonist dosages were converted to levodopa equivalent daily dosages (LEDDs).14 (link)
Weintraub D., Mamikonyan E., Papay K., Shea J.A., Xie S.X, & Siderowf A. (2011). Questionnaire for Impulsive-Compulsive Disorders in Parkinson’s Disease–Rating Scale. Movement disorders : official journal of the Movement Disorder Society, 27(2), 242-247.
Publication 2011
Dopamine Agonists Ethics Committees, Research Levodopa Movement Disorders Parkinson Disease
3
Instrumental Learning Task Under Drug Influence
Cited 35 times
The study was approved by the local ethics committee. In all, 39 healthy subjects were scanned (19–37 years old; 23 males), including a single-blind initial study of 13 subjects treated with a placebo only (lactose) and a double-blind test study of 26 subjects, half treated with Haldol (haloperidol, 1mg) and half with Madopar (L-DOPA, 100mg, plus benserazide, 25mg). After a short practice, subjects had to perform three sessions of the same instrumental learning task, each proposing three new pairs of abstract stimuli. Each of the pairs of stimuli (gain, loss and neutral) was associated with pairs of outcomes (‘gain’ £1/nil, ‘loss’ £1/nil, ‘look’ £1/nil), the two stimuli corresponding to reciprocal probabilities (0.8/0.2 and 0.2/0.8). On each trial, one pair was randomly presented and the two stimuli were displayed on the screen, above and below a central fixation cross, their relative position being counterbalanced across trials. The subject was required to choose the upper stimulus by pressing a button (Go response), or the lower stimulus by doing nothing (NoGo response). The choice was then circled in red and the outcome was displayed on the screen. To win money the subjects had to learn, by trial and error, the stimulus–outcome associations. They were told that their winnings would be their remuneration for participation, but they all left with the same fixed amount. To assess for side effects of the drug, they were finally asked to rate their subjective feelings, using visual analogue scales. Behavioural performance was compared directly between the L-DOPA and haloperidol groups, with two-sample t-tests.
Pessiglione M., Seymour B., Flandin G., Dolan R.J, & Frith C.D. (2006). Dopamine-dependent prediction errors underpin reward-seeking behaviour in humans. Nature, 442(7106), 1042-1045.
Publication 2006
Benserazide Drug Reaction, Adverse Feelings Haldol Haloperidol Healthy Volunteers Lactose Levodopa madopar Males Placebos Regional Ethics Committees Visual Analog Pain Scale
4
Multivariate Distance Matrix Regression of Functional Connectivity
Cited 27 times

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Publication 2014
actinomycin D1 actinomycin D2 Blood Oxygen Levels Brain Brain Mapping cDNA Library Disorder, Attention Deficit-Hyperactivity fMRI Gray Matter indicine-N-oxide Levodopa Microtubule-Associated Proteins neuro-oncological ventral antigen 2, human Phenotype Python Tissues
5
Cerebral Small Vessel Disease Cohort
Cited 26 times
Cerebral SVD is characterized on neuroimaging by either WML or lacunar infarcts. Symptoms of SVD include acute symptoms, such as transient ischemic attack (TIA) or lacunar syndromes, but also subacute manifestations such as cognitive and motor (gait) disturbances [5 (link)]. As the onset of cerebral SVD is often insidious, clinically heterogeneous, and typically with mild symptoms, it has been suggested that the selection of subjects with cerebral SVD in clinical studies should be based on the more consistent brain imaging features [20 (link)].
Accordingly, in 2006, consecutive individuals referred to the Department of Neurology between October 2002 and November 2006, were selected for possible participation. Inclusion criteria were: (a) age between 50 and 85 years; (b) cerebral SVD on neuroimaging (WML and/or lacunar infarcts). Subsequently, the above mentioned acute and subacute clinical symptoms of SVD were assessed by standardized structured assessments (a questionnaire for TIA and stroke [21 (link)]; for cognition the Cognitive Failures Questionnaire [22 (link)]; for gait the Falls Questionnaire [23 (link)] and the Freezing of Gait Questionnaire [24 (link)]) Subjects who were eligible because of a lacunar syndrome were included only > 6 months after the event to avoid acute effects on the outcomes.
To be able to detect incident dementia and parkinsonism we applied the following exclusion criteria: (a) presence of dementia [25 ] and (b) parkinson(-ism)[26 (link),27 (link)]. In addition patients with (c)intracranial hemorrhage; (d) life expectancy of less than six months; (e) intracranial space occupying lesion; (f) (psychiatric) disease interfering with cognitive testing or follow-up; (g) recent or current use of acetylcholine-esterase inhibitors, neuroleptic agents, L-dopa or dopa-a(nta)gonists; (h) non-SVD related WML (e.g. multiple sclerosis); (i) prominent visual or hearing impairment; (j) language barrier; (k) MRI contraindications or known claustrophobia were excluded.
All participants signed an informed consent form. The Medical Review Ethics Committee region Arnhem-Nijmegen approved the study.
van Norden A.G., de Laat K.F., Gons R.A., van Uden I.W., van Dijk E.J., van Oudheusden L.J., Esselink R.A., Bloem B.R., van Engelen B.G., Zwarts M.J., Tendolkar I., Olde-Rikkert M.G., van der Vlugt M.J., Zwiers M.P., Norris D.G, & de Leeuw F.E. (2011). Causes and consequences of cerebral small vessel disease. The RUN DMC study: a prospective cohort study. Study rationale and protocol. BMC Neurology, 11, 29.
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Publication 2011
Acetylcholinesterase Inhibitors Antipsychotic Agents Brain Cerebrovascular Accident Claustrophobia Cognition Dementia Dopa Genetic Heterogeneity Hearing Impairment Infarction, Lacunar Intracranial Hemorrhage Levodopa Mental Disorders Multiple Sclerosis Neurobehavioral Manifestations Parkinsonian Disorders Patients Stroke, Lacunar Transient Ischemic Attack

Most recents protocols related to «Levodopa»

1
Parkinson's Disease Tremor Measurement Protocol
The research has been approved by the Chinese Clinical Trial Registry (Registration No.: ChiCTR2100054804) and the local Ethics Committee of Shanghai Jiao Tong University, China (Approved No. of Ethic Committee: 2019 Clinical Trial No. 136). All subjects provided written consent after being informed of the purpose and the procedures of the experiment. The overall experiment was strictly performed in accordance with all relevant guidelines and regulations of the institutional review board and the Declaration of Helsinki. Patients were recruited by the department of neurology of Rui Jin Hospital (Shanghai, China). All of them were out-patients with upper limb tremor resulted from Parkinson's disease (Excluded N = 11; Not meeting the inclusion criteria N = 7; Declined to participate N = 4) (Figure 1).
The inclusion criteria for subjects were: (1) age between 50 and 80 years old, (2) confirmed diagnosis of idiopathic Parkinson's disease according to the MDS clinical diagnostic criteria for PD (Postuma et al., 2015 (link)), (3) symptom of upper limb tremor (rest tremor or postural tremor) resulted from PD, and (4) modified Hoen & Yahr (H&Y) Stage 1 to 3 (Hoehn and Yahr, 1967 (link)). The exclusion criteria included: (1) history of other diseases that may lead to pathological tremor, such as essential tremor (Deuschl et al., 1998 (link)), (2) under the treatment of other neuromodulation therapy, such as DBS, within recent 1 month, (3) history of mental problems, including anxiety, dementia, hallucination or delusion etc., (4) strong reliance on anti-Parkinson medications, or (5) history of cognitive disorder [Mini-mental State Examination (MMSE) score ≤ 16] (Tombaugh and McIntyre, 1992 (link)).
The average disease duration of PD among all subjects [7M/6F, all right-handed, aged 67.5 ± 4.9 (mean ± SD)] were 4.38 ± 1.86 (mean ± SD) years. The Unified Parkinson's Disease Rating Scale (UPDRS) score ranged from 20 to 78 [31.7 ± 15.4 (mean ± SD)] while the modified H&Y stage ranged from 1.0 to 3.0 [1.8 ± 0.8 (mean ± SD)]. The tremor was found to be lateralized in all subjects. Throughout the manuscript, we refer to the more-affected side (MAS) as the side of body exhibiting more severe tremor, which was determined visually by an experienced physician, while the less-affected side (LAS)was defined as the other. Of all subjects, about half (n = 7) were found to be more-affected by tremor on the left side with the other half (n = 6) on the right side. The average levodopa-equivalent daily dose (LEDD) among all subjects was 278.8 ± 203.3 (mean ± SD) mg according to the calculation protocol provided by Tomlinson et al. (2010 (link)). In order to exclude drug effects, all subjects were told to discontinue anti-Parkinson medications on the day of the experiment, which ensured a withdrawal period of more than 12 h. Anti-Parkinson medications were resumed immediately after the experiment session of the day.
Zhang B., Huang F., Liu J, & Zhang D. (2023). Bilateral transcranial direct current stimulation may be a feasible treatment of Parkinsonian tremor. Frontiers in Neuroscience, 17, 1101751.
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Publication 2023
Anxiety Chinese Cognition Disorders Delusions Dementia Diagnosis Essential Tremor Ethics Committees Ethics Committees, Research Hallucinations Human Body Levodopa Mini Mental State Examination Outpatients Parkinson Disease Patients Pharmaceutical Preparations Physicians Regional Ethics Committees Reliance resin cement Respiratory Diaphragm Resting Tremor Static Tremor Therapeutics Tremor Tremor, Limb Upper Extremity
2
Parkinson's Disease Patients for STN-DBS
PD patients who were referred to our center for bilateral MER guided STN-DBS from July 2019 to December 2021, were included in this study. Exclusion criteria were: (a) previous PD related surgery; (b) medication history, which might have influences on MER signals; (c) MER data lost, incomplete, or with quality problems; (d) lost to follow-up within 6 months. The consort flow diagram was presented as Figure 1. All patients included in this study were preoperatively assessed with the application of Unified Parkinson Disease Rating Scale III (UPDRS-III), Hoehn and Yahr (H&Y) Staging, and Mini Mental State Examination (MMSE) under the condition of off-medication, which was defined as medication discontinued over 12 h. Preoperative levodopa equivalent daily dose (LEDD) was also recorded as the baseline.
Qian K., Wang J., Rao J., Zhang P., Sun Y., Hu W., Hao J., Jiang X, & Fu P. (2023). Intraoperative microelectrode recording under general anesthesia guided subthalamic nucleus deep brain stimulation for Parkinson's disease: One institution's experience. Frontiers in Neurology, 14, 1117681.
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Publication 2023
Levodopa Mini Mental State Examination Operative Surgical Procedures Parkinson Disease Patients Pharmaceutical Preparations
3
Tyrosinase Inhibition Assay Protocol

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Publication 2023
Agaricales Biological Assay kojic acid Levodopa Light Monophenol Monooxygenase Psychological Inhibition
4
Differentiation of Dopaminergic Neurons
For the L‐Dopa and Carbidopa studies, NPCs were seeded on top of mouse PA6 cells and maintained in N2B27 medium, as described above. DAn were treated after 20 days in culture with L‐Dopa (50 μM; 3,4‐dihydroxy‐L‐phenylalanine, Sigma) and Carbidopa (12.5 μM; Sigma) in a ratio of 4:1 (Burbulla et al, 2017 (link)) for 10 days. Each compound was added three times a week at each change of the medium. For the early L‐Dopa studies, treatment was started on day 6 during the neural induction of EBs and maintained until the end of differentiation on day 30, for a total of 24 days.
Tristán‐Noguero A., Fernández‐Carasa I., Calatayud C., Bermejo‐Casadesús C., Pons‐Espinal M., Colini Baldeschi A., Campa L., Artigas F., Bortolozzi A., Domingo‐Jiménez R., Ibáñez S., Pineda M., Artuch R., Raya Á., García‐Cazorla À, & Consiglio A. (2023). iPSC‐based modeling of THD recapitulates disease phenotypes and reveals neuronal malformation. EMBO Molecular Medicine, 15(3), e15847.
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Publication 2023
Carbidopa Cells Levodopa Mus Nervousness
5
Dopamine Quantification in Neuron Supernatants
The supernatant was collected from neurons differentiated on top of PA6 and kept directly at −80°C until the time of analysis. Before their analysis, the medium samples were previously deproteinized with 50 μl of homogenization medium (100 ml miliQ H2O, 100 mg of sodium metabisulphite (Sigma), 10 mg of EDTA‐Na (Sigma), 100 mg of cysteine (Sigma) and 3.5 ml of HClO4 concentrated (Scharlau, 70%)); centrifuged at 3,723 g for 30 min at 4°C, and the supernatant was filtered (0.45 μm, Millipore) for a posterior HPLC injection. The concentration of 3,4‐Dihydroxy‐L‐phenylalanine (L‐Dopa), dopamine (DA), and 3,4‐dihydroxyphenylacetic acid (DOPAC) in supernatant samples was determined using an HPLC system with a Waters 717 plus autosampler (Waters Cromatografia), a Waters 515 pump, a 5 μm particle size C18 column (100 × 46 mm, Kinetex EVO, Phenomenex), and a Waters 2465 amperometric detector set at an oxidation potential of 0.75 V. The mobile phase consisted of 0.15 M NaH2PO4.H2O, 0.57 mM 1‐octane sulfonic acid, 0.5 mM EDTA (pH 2.8, adjusted with phosphoric acid), and 7.4% methanol and was pumped at 0.9 ml/min. The total sample analysis time was of 50 min and the L‐Dopa, DA, and DOPAC retention times were 2.06, 3.94, and 4.25 min respectively. The detection limit was of 2–3 fmol (injection volume 60 μl). The corresponding content of the DA metabolite was normalized to the protein concentration previously determined by Bradford method detection.
Tristán‐Noguero A., Fernández‐Carasa I., Calatayud C., Bermejo‐Casadesús C., Pons‐Espinal M., Colini Baldeschi A., Campa L., Artigas F., Bortolozzi A., Domingo‐Jiménez R., Ibáñez S., Pineda M., Artuch R., Raya Á., García‐Cazorla À, & Consiglio A. (2023). iPSC‐based modeling of THD recapitulates disease phenotypes and reveals neuronal malformation. EMBO Molecular Medicine, 15(3), e15847.
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Publication 2023
3,4-Dihydroxyphenylacetic Acid Cysteine Dopamine Edetic Acid High-Performance Liquid Chromatographies Levodopa Methanol Neurons octane Phosphoric Acids Proteins Retention (Psychology) sodium metabisulfite Sulfonic Acids

Top products related to «Levodopa»

1
L dopa by Merck Group
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L-DOPA is a laboratory product manufactured by Merck Group. It is a chemical compound used as a precursor in the synthesis of various pharmaceutical and research-related substances. The core function of L-DOPA is to serve as a starting material or intermediate in chemical reactions and processes. No further details or interpretations are provided.
2
Mushroom tyrosinase by Merck Group
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Mushroom tyrosinase is a laboratory enzyme derived from mushrooms. It catalyzes the conversion of tyrosine to melanin, a pigment. The core function of mushroom tyrosinase is to facilitate this biochemical reaction in a controlled laboratory setting.
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6
Benserazide by Merck Group
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Benserazide is a pharmaceutical compound used as a component in the treatment of Parkinson's disease. It acts as a decarboxylase inhibitor, which helps to maintain higher levels of levodopa, the primary drug used to treat Parkinson's symptoms. Benserazide is typically administered in combination with levodopa.
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Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.
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Gallic acid is a naturally occurring organic compound that can be used as a laboratory reagent. It is a white to light tan crystalline solid with the chemical formula C6H2(OH)3COOH. Gallic acid is commonly used in various analytical and research applications.

More about "Levodopa"

Levodopa, also known as L-DOPA, is a critical medication used to treat the symptoms of Parkinson's disease, a neurodegenerative disorder affecting movement and coordination.
As a precursor to essential neurotransmitters like dopamine, norepinephrine, and epinephrine, Levodopa plays a vital role in the proper functioning of the central nervous system.
By helping to alleviate motor symptoms such as tremors, rigidity, and slow movements, Levodopa has become a mainstay of Parkinson's treatment.
Often combined with other drugs like carbidopa to enhance its effectiveness and reduce side effects, Levodopa therapy is continually being optimized by researchers.
Exploring new delivery methods and novel treatment protocols, scientists are leveraging AI-driven platforms like PubCompare.ai to enhance the reproducibility and accuracy of their Levodopa studies.
These platforms enable researchers to quickly identify the best research protocols and products, streamlining their investigations into this critical Parkinson's medication.
Beyond Levodopa, related compounds like L-DOPA, Mushroom tyrosinase, Kojic acid, DMSO, L-tyrosine, Benserazide, α-MSH, FBS, Triton X-100, and Gallic acid may also hold important insights for Parkinson's research and treatment.
By leveraging the power of AI-driven literature analysis, scientists can uncover these connections and optimize their work for maximum impact.