scholarly journals Reward learning deficits in Parkinson’s disease depend on depression

2016 ◽  
Author(s):  
Monique H.M. Timmer ◽  
Guillaume Sescousse ◽  
Marieke E. van der Schaaf ◽  
Rianne A.J. Esselink ◽  
Roshan Cools
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Reversal Learning ◽  
Learning Deficits ◽  
Medication Withdrawal ◽  
History Of ◽  
Depression History ◽  
Non Motor Symptoms ◽  
History Of Depression

AbstractBackgroundDepression is one of the most common and debilitating non-motor symptoms of Parkinson’s disease (PD). The neurocognitive mechanisms underlying depression in PD are unclear and treatment is often suboptimal.MethodsWe investigated the role of striatal dopamine in reversal learning from reward and punishment by combining a controlled medication withdrawal procedure with functional magnetic resonance imaging (fMRI) in 22 non-depressed PD patients and 19 PD patients with past or present PD-related depression.ResultsPD patients with a PD-related depression (history) exhibited impaired reward versus punishment reversal learning as well as reduced reward versus punishment-related BOLD signal in the striatum (putamen) compared with non-depressed PD patients. No effects of dopaminergic medication were observed.ConclusionsThe present findings demonstrate that impairments in reversal learning from reward versus punishment and associated reward-related striatal signalling depend on the presence of (a history of) depression in PD.

scholarly journals Reward learning deficits in Parkinson's disease depend on depression

2017 ◽  
Vol 47 (13) ◽  
pp. 2302-2311 ◽  
Author(s):  
M. H. M. Timmer ◽  
G. Sescousse ◽  
M. E. van der Schaaf ◽  
R. A. J. Esselink ◽  
R. Cools
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Reversal Learning ◽  
Learning Deficits ◽  
Medication Withdrawal ◽  
History Of ◽  
Depression History ◽  
Non Motor Symptoms ◽  
History Of Depression

BackgroundDepression is one of the most common and debilitating non-motor symptoms of Parkinson's disease (PD). The neurocognitive mechanisms underlying depression in PD are unclear and treatment is often suboptimal.MethodsWe investigated the role of striatal dopamine in reversal learning from reward and punishment by combining a controlled medication withdrawal procedure with functional magnetic resonance imaging in 22 non-depressed PD patients and 19 PD patients with past or present depression.ResultsPD patients with a depression (history) exhibited impaired reward v. punishment reversal learning as well as reduced reward v. punishment-related BOLD signal in the striatum (putamen) compared with non-depressed PD patients. No effects of dopaminergic medication were observed.ConclusionsThe present findings demonstrate that impairments in reversal learning from reward v. punishment and associated striatal signalling depend on the presence of (a history of) depression in PD.

Treatment of Parkinson’s Disease by MAO-B Inhibitors, New Therapies and Future Challenges - A Mini-Review

2020 ◽  
Vol 23 (9) ◽  
pp. 847-861
Author(s):  
Della G.T. Parambi
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Clinical Evidence ◽  
Significant Rise ◽  
Glutamate Toxicity ◽  
Mao B ◽  
Pharmacokinetic Properties ◽  
Future Challenges ◽  
Non Motor Symptoms

Background: One of the most prevalent neurodegenerative diseases with increasing age is Parkinson’s disease (PD). Its pathogenesis is unclear and mainly confined to glutamate toxicity and oxidative stress. The dyskinesia and motor fluctuations and neuroprotective potential are the major concerns which are still unmet in PD therapy. Objective: This article is a capsulization of the role of MAO-B in the treatment of PD, pharmacological properties, safety and efficiency, clinical evidence through random trials, future therapies and challenges. Conclusion: : MAO-B inhibitors are well tolerated for the treatment of PD because of their pharmacokinetic properties and neuroprotective action. Rasagiline and selegiline were recommended molecules for early PD and proven safe and provide a modest to significant rise in motor function, delay the use of levodopa and used in early PD. Moreover, safinamide is antiglutamatergic in action. When added to Levodopa, these molecules significantly reduce the offtime with a considerable improvement of non-motor symptoms. This review also discusses the new approaches in therapy like the use of biomarkers, neurorestorative growth factors, gene therapy, neuroimaging, neural transplantation, and nanotechnology. Clinical evidence illustrated that MAOB inhibitors are recommended as monotherapy and added on therapy to levodopa. A large study and further evidence are required in the field of future therapies to unwind the complexity of the disease.

scholarly journals Association of fall risk factors and non-motor symptoms in patients with early Parkinson’s disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kyum-Yil Kwon ◽  
Suyeon Park ◽  
Eun Ji Lee ◽  
Mina Lee ◽  
Hyunjin Ju
Keyword(s):  
Risk Factors ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Freezing Of Gait ◽  
Prior History ◽  
Motor Symptoms ◽  
Related Factors ◽  
Related Risk ◽  
History Of ◽  
Non Motor Symptoms

AbstractThe association of non-motor symptoms (NMSs) with fall-related factors in patients with Parkinson’s disease (PD) remains to be further elucidated in the early stages of the disease. Eighty-six patients with less than 5 years of the onset of PD were retrospectively enrolled in the study. We assessed potential fall-related risk factors including (1) a history of falls during the past year (faller versus non-faller), (2) the fear of falling (FoF), and (3) the freezing of gait (FoG). Different types of NMSs were measured using the Montreal Cognitive Assessment (MoCA), the Beck Depression Inventory (BDI), the Beck Anxiety Inventory (BAI), the Parkinson’s disease Fatigue Scale (PFS), and the Scales for Outcomes in Parkinson’s disease—Autonomic dysfunction (SCOPA-AUT). The faller group (37.2%) showed higher scores for BDI, BAI, PFS, and SCOPA-AUT, compared to the non-faller group. From logistic regression analyses, the prior history of falls was related to the gastrointestinal domain of SCOPA-AUT, FoF was associated with BAI, and gastrointestinal and urinary domains of SCOPA-AUT, and FoG was linked to BAI and gastrointestinal domain of SCOPA-AUT. In conclusion, we found that fall-related risk factors in patients with early PD were highly connected with gastrointestinal dysautonomia.

scholarly journals Possible Link between SARS-CoV-2 Infection and Parkinson’s Disease: The Role of Toll-Like Receptor 4

2021 ◽  
Vol 22 (13) ◽  
pp. 7135
Author(s):  
Carmela Conte
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cerebrovascular Diseases ◽  
Substantia Nigra Pars Compacta ◽  
Motor Disorder ◽  
Nigrostriatal Pathway ◽  
Contributing Factors ◽  
Toll Like Receptor 4 ◽  
Non Motor Symptoms

Parkinson’s disease (PD) is the most common neurodegenerative motor disorder characterized by selective degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) of the midbrain, depletion of dopamine (DA), and impaired nigrostriatal pathway. The pathological hallmark of PD includes the aggregation and accumulation α-synuclein (α-SYN). Although the precise mechanisms underlying the pathogenesis of PD are still unknown, the activation of toll-like receptors (TLRs), mainly TLR4 and subsequent neuroinflammatory immune response, seem to play a significant role. Mounting evidence suggests that viral infection can concur with the precipitation of PD or parkinsonism. The recently identified coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of ongoing pandemic coronavirus disease 2019 (COVID-19), responsible for 160 million cases that led to the death of more than three million individuals worldwide. Studies have reported that many patients with COVID-19 display several neurological manifestations, including acute cerebrovascular diseases, conscious disturbance, and typical motor and non-motor symptoms accompanying PD. In this review, the neurotropic potential of SARS-CoV-2 and its possible involvement in the pathogenesis of PD are discussed. Specifically, the involvement of the TLR4 signaling pathway in mediating the virus entry, as well as the massive immune and inflammatory response in COVID-19 patients is explored. The binding of SARS-CoV-2 spike (S) protein to TLR4 and the possible interaction between SARS-CoV-2 and α-SYN as contributing factors to neuronal death are also considered.

The Role of Monoamine Oxidase B Inhibitors in the Treatment of Parkinson’s Disease – An Update

2021 ◽  
Vol 21 ◽  
Author(s):  
Zhi Xin Chew ◽  
Chooi Ling Lim ◽  
Khuen Yen Ng ◽  
Soi Moi Chye ◽  
Anna Pick Kiong Ling ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Monoamine Oxidase ◽  
Neuropsychiatric Symptoms ◽  
European Medicines Agency ◽  
Dopamine Level ◽  
Mao B ◽  
Sensory Disturbances ◽  
Non Motor Symptoms

Abstract: Parkinson's disease (PD) is a progressive neurodegenerative disease characterised by reduced dopamine level in the substantial nigra. This may lead to typical motor features such as bradykinesia, resting tremors and rigid muscles; as well as non-motor symptoms such as neuropsychiatric symptoms, sleep disorders, autonomic dysfunction, and sensory disturbances. Inhibitors of MAO-B are used to alleviate symptoms by reducing monoamine oxidase-catalysed degradation of dopamine; hence, preserving functional levels of dopamine. The very first MAO-B used therapeutically was selegiline, followed by rasagiline, its indane derivative which has superior efficacy and selectivity. Both inhibitors can be used as monotherapy or in combination with other anti-Parkinson drugs. Safinamide, a reversible MAO-B inhibitor that utilises both dopaminergic and non-dopaminergic mechanisms, was recently approved by the European Medicines Agency (EMA) (2015) and U.S. FDA (2017) as an add-on therapy for patients with mid- or late-stage Parkinson’s disease. Furthermore, MAO-B inhibitors were found to be associated with potential neuroprotective and disease modifying effects. However, evidence of their efficacy and role in PD models are scarce and warrants further investigation.

scholarly journals CRITICAL REVIEW OF PHARMACOGENOMICS IN ANTIPARKINSONIAN DRUG THERAPY: IMPACT ON CLINICAL MANAGEMENT OF PARKINSON’S DISEASE

2016 ◽  
Vol 9 (6) ◽  
pp. 24
Author(s):  
Poornima R ◽  
Sabreen Bashir
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Critical Review ◽  
Neurodegenerative Disorder ◽  
Future Research ◽  
Comt Inhibitors ◽  
Gait Dysfunction ◽  
Non Motor Symptoms ◽  
Antiparkinsonian Drugs

Parkinson’s disease is a progressive neurodegenerative disorder characterized by rest tremors, bradykinesia , rigidity , postural instability , gait dysfunction and several non motor symptoms . The marked difference in drug response and adverse effect profile among patients led to search of genetic markers and polymorphism associated with response to antiparkinsonian drugs which will enable us to predict an individuals   response to drugs in terms of both efficacy and toxicity. Hence efforts to define the role of genetic polymorphism in optimizing pharmacotherapy of Parkinson’s disease have been undertaken and some promising genetic loci for the treatment have been determined. Therefore we aim to present a critical review of  pharmacogenetic aspects of levodopa ,  dopamine agonists and COMT inhibitors and describe gene polymorphism of interest for future research. 

Bupropion in the treatment of depression in Parkinson's disease

2010 ◽  
Vol 23 (2) ◽  
pp. 325-327 ◽  
Author(s):  
Maria Załuska ◽  
Agnieszka Dyduch
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Successful Treatment ◽  
Double Blind ◽  
Motor Abilities ◽  
Unsuccessful Treatment ◽  
Treatment Of Depression ◽  
History Of ◽  
History Of Depression

ABSTRACTA 78-year-old female with a nine-year history of depression was hospitalized due to worsening depression and symptoms associated with Parkinson's disease (PD). Her motor abilities improved on levodopa and the depression improved after a trial of bupropion, following unsuccessful treatment with other antidepressants. We found four reports on successful treatment of depression in PD with bupropion. However, no controlled double-blind studies have been conducted so clinicians should be cautious when administering bupropion in depression in PD.

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