scholarly journals Anti-Parkinsonian Activity of Ganoderma Lucidum in Experimentally Induced Parkinson’s Disease

2021 ◽  
pp. 266-275
Author(s):  
Sana Aslam ◽  
Muhammad Aslam ◽  
Hania Kauser ◽  
Sara Naqvi
Keyword(s):  
Parkinson’S Disease ◽  
Lipid Peroxidation ◽  
Parkinson's Disease ◽  
Superoxide Dismutase ◽  
Motor Neurons ◽  
Ganoderma Lucidum ◽  
Muscle Rigidity ◽  
Experimentally Induced

Background: Parkinson's illness has been proclaimed as the second most neurodegenerative problem on the planet. Ganoderma lucidum is considered as a genuine restorative mushroom. Aim: Our study was directed to assess the antiparkinsonian action of Ganoderma lucidum in rotenone-incited Parkinson’s disease in male Wistar rodents. Methods: The impacts of Ganoderma lucidum were concentrated on catalepsy, muscle rigidity. Results: Ganoderma lucidum fundamentally decreased the expanded length of catalepsy. Rotenone essentially initiated the disturbance of motor neurons as demonstrated by muscle rigidity of muscles and decreased locomotion. Ganoderma lucidum alleviated the disturbance of motor neurons by rotarod execution and locomotor action of the creatures. The exercises of cell reinforcement proteins catalase and superoxide dismutase, and the level of tripeptide glutathione were essentially diminished by rotenone. Besides, rotenone extended the level of lipid peroxidation thing malondialdehyde. Notwithstanding, Ganoderma lucidum supplementation to rotenone-infused rats essentially extended the degrees of superoxide dismutase, catalase, and glutathione, and diminished the level of malondialdehyde Conclusion: Our study firmly supports the notion that Ganoderma lucidum has neuroprotective and antiparkinsonian action.

Respiratory disorders of Parkinson's Disease

2021 ◽  
Author(s):  
Yasmin C Aquino ◽  
Lais M Cabral ◽  
Nicole C Miranda ◽  
Monique C Naccarato ◽  
Barbara Falquetto ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Sleep Disturbances ◽  
Respiratory Control ◽  
Muscle Rigidity ◽  
Upper Airways ◽  
Respiratory Disorders ◽  
Functional Deficits ◽  
History Of ◽  
Subject Making

Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, mainly affecting people over 60 years of age. Patients develop both classic symptoms (tremors, muscle rigidity, bradykinesia and postural instability) and nonclassical symptoms (orthostatic hypotension, neuropsychiatric deficiency, sleep disturbances and respiratory disorders). Thus, patients with PD can have a significantly impaired quality of life, especially when they do not have multi-modality therapeutic follow-up. The respiratory alterations associated with this syndrome are the main cause of mortality in PD. They can be classified as peripheral when caused by disorders of the upper airways or muscles involved in breathing and as central when triggered by functional deficits of important neurons located in the brainstem and involved in respiratory control. Currently, there is little research describing these disorders, and therefore, there is no well-established knowledge about the subject, making the treatment of patients with respiratory symptoms difficult. In this review, the history of the pathology and data about the respiratory changes in PD obtained thus far will be addressed.

scholarly journals Potential Role of Caffeine in the Treatment of Parkinson’s Disease

2016 ◽  
Vol 10 (1) ◽  
pp. 42-58 ◽  
Author(s):  
Mohsin H.K. Roshan ◽  
Amos Tambo ◽  
Nikolai P. Pace
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Randomized Clinical Trials ◽  
Neurodegenerative Disorder ◽  
Lewy Bodies ◽  
Substantia Nigra Pars Compacta ◽  
Muscle Rigidity ◽  
Therapeutic Effects ◽  
Motor Symptoms ◽  
Wide Range

Parkinson’s disease [PD] is the second most common neurodegenerative disorder after Alzheimer’s disease, affecting 1% of the population over the age of 55. The underlying neuropathology seen in PD is characterised by progressive loss of dopaminergic neurons in the substantia nigra pars compacta with the presence of Lewy bodies. The Lewy bodies are composed of aggregates of α-synuclein. The motor manifestations of PD include a resting tremor, bradykinesia, and muscle rigidity. Currently there is no cure for PD and motor symptoms are treated with a number of drugs including levodopa [L-dopa]. These drugs do not delay progression of the disease and often provide only temporary relief. Their use is often accompanied by severe adverse effects. Emerging evidence from bothin vivoandin vitrostudies suggests that caffeine may reduce parkinsonian motor symptoms by antagonising the adenosine A2Areceptor, which is predominately expressed in the basal ganglia. It is hypothesised that caffeine may increase the excitatory activity in local areas by inhibiting the astrocytic inflammatory processes but evidence remains inconclusive. In addition, the co-administration of caffeine with currently available PD drugs helps to reduce drug tolerance, suggesting that caffeine may be used as an adjuvant in treating PD. In conclusion, caffeine may have a wide range of therapeutic effects which are yet to be explored, and therefore warrants further investigation in randomized clinical trials.

scholarly journals Review on Parkinson’s Disease, a Neurodegenerative Disorder and The Role of Ceruloplasmin Protein in It

2021 ◽  
Vol 8 (4) ◽  
Author(s):  
Ajay Chaudhary ◽  
Noopur Khare ◽  
Yamini Dixit ◽  
Abhimanyu Kumar Jha
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Free Radical ◽  
Early Onset ◽  
Parenchymal Cell ◽  
Health Concern ◽  
Muscle Rigidity ◽  
Liver Parenchymal Cell ◽  
Mao B

Parkinson’s disease (PD), a neurodegenerative disease is becoming major health concern mainly for elder people of age over 60 years. The main cause of PD is permanent loss/death of dopaminergic nerve cells present in brain part called substantia nigra, which is responsible for dopamine synthesis. MAO-B, monoamine oxidase B, regulates dopamine metabolism and increased activity of MAO-B causes dopamine degradation which in turn promotes the accumulation of glutamate and oxidative stress with free radical liberation. Several factors like oxidative stress, free radical formation, increased cholesterol, mitochondrial dysfunction, nitric oxide toxicity, signal-mediated apoptosis, head trauma, and environmental toxins and gene mutations like VPS35, SNCA, EIF4G1, GBA, CHCHD, LRRK2, PINK1, DNAJC13 and SOD2 are associated with PD. Symptoms of PD include bradykinesia, muscle rigidity, resting tremors, postural instability and shuffling gait, constipation, sleep problems, fatigue, apathy, loss of smell and taste, excessive sweating, frequent nightmares, dream enacting behaviour, anxiety, depression, daytime drowsiness. In PD, low levels of ceruloplasmin were observed in people with early onset of PD. Ceruloplasmin, a ferroxidase enzyme which is synthesized in liver parenchymal cell, regulates iron metabolism and lower level of which causes iron accumulation in brain which is responsible for the early onset of PD. Levodopa-based preparations, Dopamine agonists, Catechol-o-methyltransferase (COMT) inhibitors, MOA-B inhibitors, Adjunctive therapy, Antiglutamatergics drugs are currently used for the treatment of PD.

DOES ABNORMAL SPINAL RECIPROCAL INHIBITION LEAD TO CO-CONTRACTION OF ANTAGONIST MOTOR UNITS? A MODELING STUDY

2007 ◽  
Vol 17 (04) ◽  
pp. 319-327 ◽  
Author(s):  
VASSILIS CUTSURIDIS
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Motor Neurons ◽  
Motor Units ◽  
Neural Model ◽  
Reciprocal Inhibition ◽  
Dopamine Depletion ◽  
Cortical Cells ◽  
Simulation Results ◽  
Modeling Study

It is suggested that co-contraction of antagonist motor units perhaps due to abnormal disynaptic I a reciprocal inhibition is responsible for Parkinsonian rigidity. A neural model of Parkinson's disease bradykinesia is extended to incorporate the effects of spindle feedback on key cortical cells and examine the effects of dopamine depletion on spinal activities. Simulation results show that although reciprocal inhibition is reduced in DA depleted case, it doesn't lead to co-contraction of antagonist motor neurons. Implications to Parkinsonian rigidity are discussed.

scholarly journals Effects of Ginkgo Biloba Extract on A53T α-Synuclein Transgenic Mouse Models of Parkinson’s Disease

2017 ◽  
Vol 45 (2) ◽  
pp. 182-187 ◽  
Author(s):  
Shaosong Kuang ◽  
Lin Yang ◽  
Ziliang Rao ◽  
Zhiyong Zhong ◽  
Jinfeng Li ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Superoxide Dismutase ◽  
Locomotor Activity ◽  
Tyrosine Hydroxylase ◽  
Glutathione Peroxidase ◽  
Transgenic Mice ◽  
Ginkgo Biloba ◽  
Ginkgo Biloba Extract ◽  
Dopamine Transporters

AbstractBackground: Parkinson’s disease (PD) is a degenerative disorder of the central nervous system mainly affecting the motor system. Presently, there is no effective and safe drug to treat patients with PD. Ginkgo biloba extract (GBE), obtained from leaves of the Ginkgo biloba tree, is a complex mixture of ingredients primarily containing two active components: flavonoids and terpenoids. In this study, we investigated the effects of GBE on A53T α-synuclein transgenic mice, a PD model that has better simulated the progression of PD patients than other models such as the 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine–induced PD model. Methods: Fifty α-synuclein A53T transgenic mice were fed and treated with GBE, and locomotor activity was detected by pole test, forced swim test, and wire-hang test. The expression of tyrosine hydroxylase and dopamine transporters was detected using immunohistochemistry. Superoxide dismutase activity, glutathione peroxidase activity, and malondialdehyde expression were detected using an assay kit. Results: Our results show that GBE treatment improved locomotor activity and that superoxide dismutase and glutathione peroxidase inhibited the expression of methane dicarboxylic aldehyde and recovered the expression of tyrosine hydroxylase and dopamine transporters. Conclusions: The GBE treatment improved locomotor activity and inhibited the development of PD in the A53T α-synuclein transgenic mice, which may be partly responsible for decreased oxidative damage and maintain the normal dopamine homeostasis.

scholarly journals A clinical rating scale of speech dysfunction on Parkinson's disease

1978 ◽  
Vol 25 (1) ◽  
Author(s):  
Alison K. Thompson
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rating Scale ◽  
Muscle Rigidity ◽  
Clinical Use ◽  
Clinical Notes ◽  
Clinical Rating ◽  
Research Findings ◽  
Clinical Rating Scale

The speech dysfunction of Parkinson's disease is complex and individually variable owing to the interaction of muscle rigidity, tremor and disturbance of movement. Eight speech dimensions which are characteristically disturbed in Parkinson's disease are discussed with reference to available research findings. In order to provide a more detailed description of the speech than could be obtained by clinical notes alone, a speech rating scale has been developed, and is presented in summarized form for clinical use. Incidence and progression of the speech dysfunction are considered in addition to the problems of assessment peculiar to the patient with Parkinson's disease.

Zoophilia in a Patient with Parkinson's Disease

2017 ◽  
Vol 41 (S1) ◽  
pp. S632-S632
Author(s):  
A. Fornelos ◽  
M. Roque
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Case Report ◽  
Educational Background ◽  
Muscle Rigidity ◽  
Motor Symptoms ◽  
Brain Disorder ◽  
Pubmed Database ◽  
Paraphilic Disorders ◽  
Clinical Records

IntroductionParkinson's disease (PD) is a neurodegenerative brain disorder characterized by Bradykinesia, muscle rigidity and resting tremor. Non-motor symptoms like neuropsychiatric manifestations can also cause significant morbidity. Common medications used in anti-Parkinsonian treatment such as dopaminergic agonists, may help motor symptoms but can also cause or contribute to adverse behavioral manifestations. These include dementia, depression, anxiety, insomnia, psychosis and paraphilic disorders. There are sporadic reports of zoophilia in association with dopaminergic therapy.ObjectivesReport of a clinical case of PD and zoophilia.Aimsclinicians must be aware of paraphilic disorders, namely zoophilia, in patients with dopaminergic medication.MethodSearch of the Pubmed database was conducted for articles published that had “zoophilia [All Fields] and Parkinson [All Fields]”, resulting in 3 eligible articles through October 2016. The patient's clinical records were also reviewed.Case ReportA 77-year-old man, living in a rural area and with a low educational background, with akinetic–rigid PD in an advanced stage and followed by neurology since 2003. His family physician sent him to a psychiatric assessment for hyper-sexuality with zoophilia. The psychiatrist found that these behaviors had begun a week after levodopa was increased along with the introduction of selegiline. The psychiatrist has introduced quetiapine with significant decrease of the hyper-sexuality and the end of zoophilic episodes.ConclusionDespite hyper-sexuality is found in just 2–6% of PD patients in connection with dopaminergic treatment. This case report emphasizes how crucial it is to evaluate PD patients’ sexuality as well as to explain these adverse effects to the families involved.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Experimental Parkinson's disease in monkeys. Effect of ergot alkaloid derivative on lipid peroxidation in different brain areas

1993 ◽  
Vol 18 (10) ◽  
pp. 1101-1106 ◽  
Author(s):  
Fulvio Marzatico ◽  
Carla Caf� ◽  
Monica Taborelli ◽  
Gianni Benzi
Keyword(s):  
Parkinson’S Disease ◽  
Lipid Peroxidation ◽  
Parkinson's Disease ◽  
Ergot Alkaloid ◽  
Brain Areas
Sign in / Sign up

Export Citation Format

Share Document