The simultaneous assay of levodopa and dopamine is essential for diagnosis and treatment of neurodegenerative diseases and brain cancer. 3D stochastic microsensors based on multi-walled carbon nanotubes (MWCNTs), gold nanoparticles (AuNPs) and 1-adamantyloleamide (AOA) was used for the simultaneous molecular recognition of levodopa and dopamine in biological samples (whole blood, urine, and brain tissue). The proposed 3D stochastic microsensors presented low limits of quantification, and high sensitivities. High selectivity was recorded versus neurotransmitters such as epinephrine, norepinephrine, serotonin, and glutamate. High recoveries were obtained for the assay of both levodopa and dopamine in whole blood, urine, and tumor tissue samples.
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| http://dx.doi.org/10.1016/j.jpba.2021.114292 | DOI Listing |
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The degeneration of midbrain dopamine (DA) neurons disrupts the neural control of natural behavior, such as walking, posture, and gait in Parkinson's disease. While some aspects of motor symptoms can be managed by dopamine replacement therapies, others respond poorly. Recent advancements in machine learning-based technologies offer opportunities for unbiased segmentation and quantification of natural behavior in both healthy and diseased states.
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RSC Adv
January 2025
Key Laboratory of Tropical Biological Resources of Ministry of Education, School of Pharmaceutical Sciences, Collaborative Innovation Center of One Health, Hainan University Haikou 570228 China
Levodopa (l-Dopa), a precursor drug for dopamine has been widely used to treat Parkinson's disease. However, excess accumulation of l-Dopa in the body may cause movement disorders and uncontrollable emotions. Therefore, it is vital to monitor l-Dopa levels in patients.
View Article and Find Full Text PDFCoherent Changes in Neural Motor Network Activity during Levodopa-Induced Dyskinesia in a Rat Model of Parkinson's Disease.
J Integr Neurosci
December 2024
Federal State Budgetary Educational Institution, Institute of Theoretical and Experimental Biophysics, 142290 Pushchino, Russia.
Background: Long-term use of levodopa, a metabolic precursor of dopamine (DA) for alleviation of motor symptoms in Parkinson's disease (PD), can cause a serious side effect known as levodopa-induced dyskinesia (LID). With the development of LID, high-frequency gamma oscillations (~100 Hz) are registered in the motor cortex (MCx) in patients with PD and rats with experimental PD. Studying alterations in the activity within major components of motor networks during transition from levodopa-off state to dyskinesia can provide useful information about their contribution to the development of abnormal gamma oscillations and LID.
View Article and Find Full Text PDFCanagliflozin attenuates neurodegeneration and ameliorates dyskinesia through targeting the NLRP3/Nurr1/GSK-3β/SIRT3 pathway and autophagy modulation in rotenone-lesioned rats.
Int Immunopharmacol
December 2024
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Sinai University- Arish Branch, Arish 45511, Egypt.
Unlabelled: Despite a deep understanding of Parkinson's disease (PD) and levodopa-induced dyskinesia (LID) pathogenesis, current therapies are insufficient to effectively manage the progressive nature of PD or halt LID. Growing hypotheses suggested the NOD-like receptor 3 (NLRP3) inflammasome and orphan nuclear receptor-related 1 (Nurr1)/glycogen synthase kinase-3β (GSK-3β) and peroxisome proliferator-activated receptor γ (PPARγ) coactivator-1α (PGC-1α)/sirtuin 3 (SIRT3) pathways as potential avenues for halting neuroinflammation and oxidative stress in PD.
Aims: This study investigated for the first time the neuroprotective effect of canagliflozin against PD and LID in rotenone-intoxicated rats, emphasizing the crosstalk among the NLRP3/caspase-1 cascade, PGC-1α/SIRT3 pathway, mammalian target of rapamycin (mTOR)/beclin-1, and Nurr1/β-catenin/GSK-3β pathways as possible treatment strategies in PD and LID.
Sustained effects of repeated levodopa (L-DOPA) administration on reward circuitry, effort-based motivation, and anhedonia in depressed patients with higher inflammation.
Brain Behav Immun
December 2024
Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, GA 30322, USA; The Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA, 30322. Electronic address:
Inflammatory biomarkers like C-reactive protein (CRP) are elevated in a subset of patients with depression and associated with lower functional connectivity (FC) in a ventral striatum (VS) to ventromedial prefrontal cortex (vmPFC) reward circuit and symptoms of anhedonia. Evidence linking these relationships to the effects of inflammation on dopamine is consistent with our recent findings that acute levodopa (L-DOPA) increased VS-vmPFC FC in association with deceased anhedonia in depressed patients with higher but not lower CRP (>2 versus ≤ 2 mg/L). To determine whether repeated L-DOPA administration caused sustained effects on FC and behavior in these patients, medically stable depressed outpatients with CRP > 2 mg/L and anhedonia (n = 18) received one week of three doses of L-DOPA (150-450 mg/day/week with carbidopa) or placebo in a randomized order.
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