Adverse effects produced by different drugs used in the treatment of Parkinson's disease: A mixed treatment comparison

Li, Baodong; Bi, Zhen-Yun; Liu, Jingfeng; Si, Weijun; Shi, Qianqian; Xue, Lipeng; Bai, Jing

doi:10.1111/cns.12727

Cited by 43 publications

(28 citation statements)

References 52 publications

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“…For example, it is recommended that all individuals receive a cardiac evaluation before beginning treatment with a stimulant (The American Heart Association) (Thomas et al, 2011). In patients with Parkinson’s disease, chronic L-DOPA treatment has been shown to cause motor side effects, like dyskinesia, dystonia, and wearing off effects at the end of dose (Li et al, 2017) (Katzenschlager and Lees, 2002), and systemic side effects, like insomnia, gastrointestinal symptoms, and hallucinations (Foster and Hoffer, 2004). These sides effects are greatly reduced when treating with dopamine agonists instead of L-DOPA, though dyskinesia and other side effects can still occur (Li et al, 2017) (Katzenschlager and Lees, 2002).…”

Section: Dopamine Based Therapiesmentioning

confidence: 99%

“…In patients with Parkinson’s disease, chronic L-DOPA treatment has been shown to cause motor side effects, like dyskinesia, dystonia, and wearing off effects at the end of dose (Li et al, 2017) (Katzenschlager and Lees, 2002), and systemic side effects, like insomnia, gastrointestinal symptoms, and hallucinations (Foster and Hoffer, 2004). These sides effects are greatly reduced when treating with dopamine agonists instead of L-DOPA, though dyskinesia and other side effects can still occur (Li et al, 2017) (Katzenschlager and Lees, 2002). Similar side effects are observed in children given L-DOPA for myopia and in children given drugs that increase extracellular dopamine in the brain (Adderall, Ritalin, etc.)…”

Section: Dopamine Based Therapiesmentioning

confidence: 99%

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Neuroprotective strategies for retinal disease

Pardue

Allen

2018

Progress in Retinal and Eye Research

189

160

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Diseases that affect the eye, including photoreceptor degeneration, diabetic retinopathy, and glaucoma, affect 11.8 million people in the US, resulting in vision loss and blindness. Loss of sight affects patient quality of life and puts an economic burden both on individuals and the greater healthcare system. Despite the urgent need for treatments, few effective options currently exist in the clinic. Here, we review research on promising neuroprotective strategies that promote neuronal survival with the potential to protect against vision loss and retinal cell death. Due to the large number of neuroprotective strategies, we restricted our review to approaches that we had direct experience with in the laboratory. We focus on drugs that target survival pathways, including bile acids like UDCA and TUDCA, steroid hormones like progesterone, therapies that target retinal dopamine, and neurotrophic factors. In addition, we review rehabilitative methods that increase endogenous repair mechanisms, including exercise and electrical stimulation therapies. For each approach, we provide background on the neuroprotective strategy, including history of use in other diseases; describe potential mechanisms of action; review the body of research performed in the retina thus far, both in animals and in humans; and discuss considerations when translating each treatment to the clinic and to the retina, including which therapies show the most promise for each retinal disease. Despite the high incidence of retinal diseases and the complexity of mechanisms involved, several promising neuroprotective treatments provide hope to prevent blindness. We discuss attractive candidates here with the goal of furthering retinal research in critical areas to rapidly translate neuroprotective strategies into the clinic.

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Section: Dopamine Based Therapiesmentioning

confidence: 99%

Section: Dopamine Based Therapiesmentioning

confidence: 99%

Neuroprotective strategies for retinal disease

Pardue

Allen

2018

Progress in Retinal and Eye Research

189

160

View full text Add to dashboard Cite

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“…In particular, Parkinson’s disease (PD) is defined by a clinical picture that consists in impaired motor functions and cognitive deficits caused by the progressive loss of dopaminergic neuronal cells in the substantia nigra pars compacta (SNpc) that leads to the depletion of dopamine fibers in the striatum [ 1 , 2 ] and other catecholaminergic systems [ 3 ]. Since the current pharmacological treatments for PD are being controlled in order to reduce motor symptoms [ 4 ], new studies are focused on the design of non-pharmacological strategies to avoid side effects caused by drug administration [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Effect of NAC treatment and physical activity on neuroinflammation in subchronic Parkinsonism; is physical activity essential?

Gil-Martínez

Cuenca

Sánchez

et al. 2018

J Neuroinflammation

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BackgroundNeuroprotective strategies are becoming relevant to slow down dopaminergic cell death and inflammatory processes related to the progressive neurodegeneration in Parkinson’s disease (PD). Interestingly, among others, physical activity (PA) or anti-oxidant agents (such as N-acetyl-L-cysteine, NAC) are common therapeutic strategies. Therefore, this study aims to analyze if there is a synergistic effect of physical activity along with NAC treatment on dopaminergic degeneration and neuroinflammatory response in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism model after subchronic intoxication.MethodsTo ascertain this possibility, 48 8-week-old male mice (C57BL/6 strain) were used. Twenty four of them were placed individually in cages where voluntary physical activity was automatically monitored during 30 days and were divided into groups: (i) control; (ii) NAC; (iii) MPTP, and (iv) MPTP+NAC. The other 24 mice were divided into the same four groups but without physical activity.ResultsThe data collected during the treatment period showed that there was an overall increase in the total running distance in all groups under physical activity, including Parkinsonian animals. However, the monitoring data per day showed that the activity routine by MPTP and MPTP+NAC groups was disrupted by alterations in the circardian rhythm because of MPTP intoxication. Results from post-mortem studies in the substantia nigra pars compacta (SNpc) showed significant decrease in the number of TH+ cells in all MPTP groups. Moreover, TH+ expression in the striatum was significantly decreased in all MPTP groups. Thus, PA + NAC treatment do not protect dopaminergic neurons against a subchronic intoxication of MPTP. Regarding glial response, the results obtained from microglial analysis do not show significant increase in the number of Iba-1+ cell in MPTP+NAC and MPTP+PA + NAC. In the striatum, a significant decrease is observed only in the MPTP+NAC group compared with that of the MPTP group. The microglial results are reinforced by those obtained from the analysis of astroglial response, in which a decrease in the expression of GFAP+ cells are observed in MPTP+NAC and MPTP+PA + NAC compared with MPTP groups both in the SNpc and in the striatum. Finally, from the study of the astroglial response by the co-localization of GFAP/S100b, we described some expression patterns observed based on the severity of the damage produced by the MPTP intoxication in the different treated groups.ConclusionsThese results suggest that the combination of physical activity with an anti-oxidant agent does not have a synergistic neuroprotective effect in the nigrostriatal pathway. Our results show a potential positive effect, only due to NAC treatment, on the neuroinflammatory response after subchronic MPTP intoxication. Thus, physical activity is not essential, under these conditions. However, we believe that physical activity, used for therapeutic purposes, has a beneficial long-term effect. In this line, these results open the d...

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“…Although there is currently no cure for PD, a combination of pharmacological (e.g., levodopa, dopamine receptor agonists, anticholinergics) and non-pharmacological (e.g., physiotherapy, deep brain stimulation) therapies are the only available treatment options. However, such interventions only ameliorate the symptoms of the illness, and their long term use is associated with adverse side effects in some patients [26,27], which in turn result in suboptimal medication compliance and low quality of life. Research seeking to identify the disease's genetic components that contribute to drug response variability could lead to the discovery of personalised disease-modifying therapies with great potential to improve PD patients' well-being and quality of life.…”

Section: Introductionmentioning

confidence: 99%

The Australian Parkinson’s Genetics Study (APGS) - pilot (N = 1,532)

Bivol

Mellick

Gratten

et al. 2021

Preprint

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Purpose: Parkinson's disease (PD) is a neurodegenerative disorder associated with progressive disability. While the precise aetiology is unknown, there is evidence of significant genetic and environmental influences on individual risk. The Australian Parkinson's Genetics Study (APGS) seeks to study patient-reported data from a large cohort of individuals with PD in Australia to understand the sociodemographic, genetic, and environmental basis of PD susceptibility, symptoms and progression. Participants: In the pilot phase reported here, 1,819 participants were recruited through assisted mailouts facilitated by Services Australia (formerly known as the Australian Government Department of Human Services), based on having three or more prescriptions for anti-PD medications in their Pharmaceutical Benefits Scheme (PBS) records. The average age at the time of the questionnaire was 64 +/- 6 years. We collected patient-reported PD information and socio-demographic variables via an online (93% of the cohort) or paper-based (7%) questionnaire. 1,532 participants (84.2%) had a current PD diagnosis and consented to provide a DNA sample via a saliva sampling kit sent by traditional post. Of these, 1435 (94%) returned the saliva samples for genotyping. Findings to date: 65% of participants were male, and 92% identified as being of European descent. A previous traumatic brain injury was reported by 16% of participants and was associated with a younger age of symptom onset. At the time of the questionnaire, constipation (36% of participants), depression (34%), anxiety (17%), melanoma (16%) and diabetes (10%) were the most commonly reported comorbid conditions. Future plans: We are actively seeking funding to expand the project's scope and reach, including recruiting unaffected controls, and a follow-up questionnaire focused on non-motor symptoms and cognitive function assessment. Future work will explore the role of genetic and environmental factors in the aetiology of PD susceptibility, onset, symptoms and progression, including as part of international PD research consortia.

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Adverse effects produced by different drugs used in the treatment of Parkinson's disease: A mixed treatment comparison

Cited by 43 publications

References 52 publications

Neuroprotective strategies for retinal disease

Neuroprotective strategies for retinal disease

Effect of NAC treatment and physical activity on neuroinflammation in subchronic Parkinsonism; is physical activity essential?

The Australian Parkinson’s Genetics Study (APGS) - pilot (N = 1,532)

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