scholarly journals Recommendations for the Treatment of Parkinson's Disease

2018 ◽  
Vol 65 (2) ◽  
pp. 41-45
Author(s):  
Cori Gray ◽  
Craig Stern
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Smooth Muscle ◽  
Lewy Bodies ◽  
Pathological Feature ◽  
Intracytoplasmic Inclusions ◽  
Chemical Messenger ◽  
Impaired Balance ◽  
Progressive Disorder

Parkinson's disease is a progressive disorder of the nervous system characterized by trembling or shaking of a limb, rigidity or stiffness of limbs, an inability to move, and impaired balance and coordination. Most symptoms begin to occur when neurons that produce dopamine in the substantia nigra of our brain die or become impaired. Dopamine is a chemical messenger that sends signals to our brain to produce smooth muscle movements. Without the neurons that create dopamine, our brain becomes unable to produce these muscle movements. Another pathological feature is the appearance of intracytoplasmic inclusions (Lewy bodies) in the remaining, intact nigral neurons.

scholarly journals Dysfunction of mitochondria as the basis of Parkinson’s disease

2018 ◽  
Vol 6 (4) ◽  
pp. 174-181
Author(s):  
Małgorzata Popis
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Dopaminergic Neurons ◽  
Genetic Factors ◽  
Lewy Bodies ◽  
Main Ingredient ◽  
Mitochondrial Dynamic ◽  
Factors Affecting

AbstractParkinson's disease is the second most common neurodegenerative disease, affecting about 0,15-0,3% of the world's population. Its characteristic feature is a loss of dopaminergic neurons in the substantia nigra. PD leads to dopamine deficiency and formation of intracellular inclusions called Lewy bodies, whose main ingredient is α-synuclein. Other types of nervous system cells are also affected by changes associated with that disease. The underlying molecular pathogenesis involves multiple pathways and mechanisms: mitochondrial function, oxidative stress, genetic factors, α-synuclein proteostasis, mitochondrial dynamic impairment, and disorders of the mitophagy process. This review summarizes the factors affecting the functioning of the mitochondria and their connection to the development of Parkinson's disease.

scholarly journals C-terminal α-synuclein truncations are linked to cysteine cathepsin activity in Parkinson's disease

2019 ◽  
Vol 294 (25) ◽  
pp. 9973-9984 ◽  
Author(s):  
Ryan P. McGlinchey ◽  
Shannon M. Lacy ◽  
Katherine E. Huffer ◽  
Nahid Tayebi ◽  
Ellen Sidransky ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Amino Acids ◽  
Parkinson's Disease ◽  
Amyloid Fibrils ◽  
Lewy Bodies ◽  
Amyloid Formation ◽  
Pathological Feature ◽  
Cysteine Cathepsins ◽  
Cathepsin Activity ◽  
Cysteine Cathepsin

A pathological feature of Parkinson's disease (PD) is Lewy bodies (LBs) composed of α-synuclein (α-syn) amyloid fibrils. α-Syn is a 140 amino acids–long protein, but truncated α-syn is enriched in LBs. The proteolytic processes that generate these truncations are not well-understood. On the basis of our previous work, we propose that these truncations could originate from lysosomal activity attributable to cysteine cathepsins (Cts). Here, using a transgenic SNCAA53T mouse model, overexpressing the PD-associated α-syn variant A53T, we compared levels of α-syn species in purified brain lysosomes from nonsymptomatic mice with those in age-matched symptomatic mice. In the symptomatic mice, antibody epitope mapping revealed enrichment of C-terminal truncations, resulting from CtsB, CtsL, and asparagine endopeptidase. We did not observe changes in individual cathepsin activities, suggesting that the increased levels of C-terminal α-syn truncations are because of the burden of aggregated α-syn. Using LC-MS and purified α-syn, we identified C-terminal truncations corresponding to amino acids 1–122 and 1–90 from the SNCAA53T lysosomes. Feeding rat dopaminergic N27 cells with exogenous α-syn fibrils confirmed that these fragments originate from incomplete fibril degradation in lysosomes. We mimicked these events in situ by asparagine endopeptidase degradation of α-syn fibrils. Importantly, the resulting C-terminally truncated fibrils acted as superior seeds in stimulating α-syn aggregation compared with that of the full-length fibrils. These results unequivocally show that C-terminal α-syn truncations in LBs are linked to Cts activities, promote amyloid formation, and contribute to PD pathogenesis.

Parkinsonism and other extrapyramidal diseases

2020 ◽  
pp. 5946-5956
Author(s):  
Elisaveta Sokolov ◽  
Vinod K. Metta ◽  
K. Ray Chaudhuri
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dementia With Lewy Bodies ◽  
Functional Organization ◽  
Lewy Bodies ◽  
Pathological Feature ◽  
Nigrostriatal Pathway ◽  
Drug Induced ◽  
Beneficial Effects ◽  
Clinical Syndromes

The human basal ganglia is a complex functional organization, with important interconnections with the nigrostriatal pathway, which dominates the dopaminergic innervation of the striatum (caudate nucleus and the putamen). The principal clinical syndromes affecting it are Parkinson’s disease; other syndromes with parkinsonian features (including drug-induced parkinsonism); progressive supranuclear palsy; multisystem atrophy; dementia with Lewy bodies; neuroacanthosis; torsion dystonia; and chorea. Apart from the use of dopaminergic agents, several drugs have beneficial effects in the management of parkinsonism and other extrapyramidal diseases. Parkinson’s disease affects about 0.2% of the population, including 2% of those over 80 years of age. The main pathological feature is degeneration of neuromelanin-containing neurons and Lewy body inclusions in the pars compacta of the substantia nigra, which leads directly and indirectly to excessive inhibition of the thalamus and consequent bradykinesia.

Parkinson's Disease: Distribution of Lewy Bodies in the Peripheral Autonomic Nervous System

1994 ◽  
Vol 14 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Shigeki Takeda ◽  
Kazunori Yamazaki ◽  
Teruo Miyakawa ◽  
Hiroyuki Arai
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Autonomic Nervous System ◽  
Lewy Bodies ◽  
Autonomic Nervous

scholarly journals Lewy bodies in the enteric nervous system in Parkinson's disease.

1989 ◽  
Vol 52 (Suppl) ◽  
pp. 191-194 ◽  
Author(s):  
Koichi WAKABAYASHI ◽  
Hitoshi TAKAHASHI ◽  
Shigeki TAKEDA ◽  
Eisaku OHAMA ◽  
Fusahiro IKUTA
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Enteric Nervous System ◽  
Lewy Bodies

scholarly journals Cortical Lewy Body Dementia

1990 ◽  
Vol 3 (3) ◽  
pp. 189-196 ◽  
Author(s):  
W. R. G. Gibb
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Lewy Body ◽  
Age Of Onset ◽  
Lewy Bodies ◽  
Lewy Body Dementia ◽  
Survival Duration ◽  
Visual Hallucinations ◽  
Alzheimer Pathology

In cortical Lewy body dementia the distribution of Lewy bodies in the nervous system follows that of Parkinson's disease, except for their greater profusion in the cerebral cortex. The cortical tangles and plaques of Alzheimer pathology are often present, the likely explanation being that Alzheimer pathology provokes dementia in many patients. Pure cortical Lewy body dementia without Alzheimer pathology is uncommon. The age of onset reflects that of Parkinson's disease, and clinical features, though not diagnostic, include aphasias, apraxias, agnosias, paranoid delusions and visual hallucinations. Parkinsonism may present before or after the dementia, and survival duration is approximately half that seen in Parkinson's disease without dementia.

scholarly journals The gut-brain axis in the pathogenesis of Parkinson’s disease

2019 ◽  
Vol 5 (2) ◽  
pp. 73-81 ◽  
Author(s):  
Lanxia Meng ◽  
Xin Yuan ◽  
Xuebing Cao ◽  
Zhentao Zhang
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Nervous System ◽  
Substantia Nigra ◽  
Enteric Nervous System ◽  
Lewy Bodies ◽  
Motor Symptoms ◽  
Gastrointestinal Dysfunction ◽  
Neurodegenerative Process ◽  
The Central Nervous System

Parkinson’s disease (PD) is the second most common neurodegenerative disease. Its pathological markers include Lewy bodies and Lewy neuritis, which primarily affect the substantia nigra. However, in recent years, mounting evidence suggests that PD is a multifocal neurodegenerative process that influences several neuronal structures aside from the substantia nigra, one of which is the enteric nervous system. Many clinical studies have reported that patients with PD experience gastrointestinal dysfunction for many years before the onset of motor symptoms. Emerging evidence indicates that α-synuclein deposition may start in the enteric nervous system and then propagate to the central nervous system. The gut-brain axis plays an important role in PD pathogenesis. Recent evidence suggests that these interactions may be primarily affected by the intestinal microbiota. In this review, the authors discuss recent research, and illustrate how changes in the composition of the gut microbiota may trigger inflammation, thus contributing to neurodegeneration in PD.

Differences in glucose metabolism between dementia with Lewy bodies and dementia associated with Parkinson's disease

2005 ◽  
Vol 32 (S 4) ◽  
Author(s):  
P Häussermann ◽  
A.O Ceballos-Baumann ◽  
H Förstl ◽  
R Feurer ◽  
B Conrad ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Glucose Metabolism ◽  
Dementia With Lewy Bodies ◽  
Lewy Bodies
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