scholarly journals Alterations of Plasma Galectin-3 and C3 Levels in Patients with Parkinson’s Disease

2021 ◽  
Vol 11 (11) ◽  
pp. 1515
Author(s):  
Hsiu-Chuan Wu ◽  
Kuo-Hsuan Chang ◽  
Mu-Chun Chiang ◽  
Chiung-Mei Chen
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Peripheral Blood ◽  
Plasma Levels ◽  
Dopaminergic Neurons ◽  
Cathepsin D ◽  
The Other ◽  
Galectin 3 ◽  
Progressive Neurodegeneration ◽  
Normal Controls

Parkinson’s disease (PD) is characterized by progressive neurodegeneration of dopaminergic neurons in the ventral midbrain. The complement-phagosome pathway is involved in the pathogenesis of PD. Here we measured levels of complement-phagocytosis molecules, including galectin-3, C3, C4, and cathepsin D, in the plasma of 56 patients with PD, and 46 normal controls (NCs). Plasma levels of galectin-3 (9.93 ± 3.94 ng/mL) were significantly higher in PD patients compared with NCs (8.39 ± 1.95 ng/mL, p = 0.012), and demonstrated a positive correlation with Hoehn and Yahr stages in PD patients (R2 = 0.218, p < 0.001). On the other hand, plasma C3 levels were significantly lower in PD patients (305.27 ± 205.16 μg/mL) compared with NCs (444.34 ± 245.54 μg/mL, p = 0.002). However, the levels did not correlate with Hoehn and Yahr stages (R2 = 0.010, p = 0.469). Plasma levels of C4 and cathepsin D in PD patients were similar to those in NCs. Our results show possible altered complement-phagocytosis signals in the peripheral blood of PD patients, highlighting the potential of galectin-3 as a biomarker of PD.

scholarly journals Lipid-Mediated Oxidative Stress and Inflammation in the Pathogenesis of Parkinson's Disease

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Tahira Farooqui ◽  
Akhlaq A. Farooqui
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Platelet Activating Factor ◽  
Lipid Mediators ◽  
Unknown Etiology ◽  
Oxygen Species ◽  
Progressive Loss ◽  
Progressive Neurodegeneration

Parkinson's disease (PD) is a neurodegenerative movement disorder of unknown etiology. PD is characterized by the progressive loss of dopaminergic neurons in the substantia nigra, depletion of dopamine in the striatum, abnormal mitochondrial and proteasomal functions, and accumulation ofα-synuclein that may be closely associated with pathological and clinical abnormalities. Increasing evidence indicates that both oxidative stress and inflammation may play a fundamental role in the pathogenesis of PD. Oxidative stress is characterized by increase in reactive oxygen species (ROS) and depletion of glutathione. Lipid mediators for oxidative stress include 4-hydroxynonenal, isoprostanes, isofurans, isoketals, neuroprostanes, and neurofurans. Neuroinflammation is characterized by activated microglial cells that generate proinflammatory cytokines, such as TNF-αand IL-1β. Proinflammatory lipid mediators include prostaglandins and platelet activating factor, together with cytokines may play a prominent role in mediating the progressive neurodegeneration in PD.

Immune system and new avenues in Parkinson’s disease research and treatment

2019 ◽  
Vol 30 (7) ◽  
pp. 709-727 ◽  
Author(s):  
Ava Nasrolahi ◽  
Fatemeh Safari ◽  
Mehdi Farhoudi ◽  
Afra Khosravi ◽  
Fereshteh Farajdokht ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Neuronal Loss ◽  
Disease Research ◽  
Disease Modifying Therapies ◽  
Progressive Neurodegeneration ◽  
Disease Modifying ◽  
Clinical Description ◽  
Genetic And Environmental Factors

Abstract Parkinson’s disease (PD) is a progressive neurological disorder characterized by degeneration of dopaminergic neurons in the substantia nigra. However, although 200 years have now passed since the primary clinical description of PD by James Parkinson, the etiology and mechanisms of neuronal loss in this disease are still not fully understood. In addition to genetic and environmental factors, activation of immunologic responses seems to have a crucial role in PD pathology. Intraneuronal accumulation of α-synuclein (α-Syn), as the main pathological hallmark of PD, potentially mediates initiation of the autoimmune and inflammatory events through, possibly, auto-reactive T cells. While current therapeutic regimens are mainly used to symptomatically suppress PD signs, application of the disease-modifying therapies including immunomodulatory strategies may slow down the progressive neurodegeneration process of PD. The aim of this review is to summarize knowledge regarding previous studies on the relationships between autoimmune reactions and PD pathology as well as to discuss current opportunities for immunomodulatory therapy.

scholarly journals Two Types of Spheroid Bodies in the Nigral Neurons in Parkinson's Disease

1991 ◽  
Vol 18 (3) ◽  
pp. 287-294 ◽  
Author(s):  
Tatsuo Yamada ◽  
Haruhiko Akiyama ◽  
Patrick L. McGeer
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Staining Pattern ◽  
Lewy Bodies ◽  
Substantia Nigra Pars Compacta ◽  
Striatonigral Degeneration ◽  
Neurologically Normal ◽  
Normal Controls ◽  
Dystrophic Dendrites

ABSTRACT:Dendritic spheroid bodies (SBs) and Lewy bodies (LBs) were identified in comparable numbers in the substantia nigra pars compacta (SBC) of nine parkinsonian cases and one case of striatonigral degeneration but were not found irt cases of Huntington's disease or neurologically normal controls. The immunohistochemical profile of the SBs in dystrophic dendrites of nigrostriatal dopaminergic neurons was remarkably similar to that of the LBs found within dendrites or free of the SNC neuropil. Both types of inclusions stained positively with antibodies to tyrosine hydroxylase, ubiquitin and microtubule-associated protein-2 (MAP2), and negatively for Tau-2, although they had different ultrastructural appearances. A few intracellular LBs were stained by antibodies to neurofilament proteins (NFs) 68, 160, and 200 kD, but dendritic SBs and extracellular LBs were not so stained. These data indicate that dendritic SBs and extracellular LBs may have a common molecular pathogenetic origin in Parkinson's disease. On the other hand, the SBs seen in the pars reticulata (SNR) and in the distal nigrostriatal axons even in control cases were generally stained by antibodies to NFs and ubiquitin but not to MAP2. This latter staining pattern in similar to that shown by SBs in the anterior horn in ALS and in the cerebellum of neurologically normal brains and is believed typical of axonal as opposed to dendritic SBs.

scholarly journals Characterizing relevant microRNA editing sites in Parkinson’s disease

2020 ◽  
Author(s):  
Chenyu Lu ◽  
Shuchao Ren ◽  
Zhigang Zhao ◽  
Xingwang Wu ◽  
Angbaji Suo ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rna Sequencing ◽  
Small Rna ◽  
Small Rna Sequencing ◽  
Progressive Neurodegeneration ◽  
Functional Relevance ◽  
Human Brains ◽  
Mirna Editing ◽  
Normal Controls

AbstractMicroRNAs (miRNAs) are extensively edited in human brains. However, the functional relevance of miRNA editome is largely unknown in Parkinson’s disease (PD). By analyzed small RNA sequencing profiles of brain tissues of 43 PD patients and 88 normal controls, we totally identified 421 miRNA editing sites with significantly different editing levels in prefrontal cortices of PD patients (PD-PC). A-to-I edited miR-497-5p has significantly higher expression levels in PD-PC compared to normal controls and directly represses OPA1 and VAPB, which potentially contributes to the progressive neurodegeneration of PD patients. These results provide new insights into mechanistic understanding, novel diagnostic and therapeutic clues of PD.

scholarly journals Improvement of Blood Plasmalogens and Clinical Symptoms in Parkinson’s Disease by Oral Administration of Ether Phospholipids: A Preliminary Report

2020 ◽  
Vol 2020 ◽  
pp. 1-7 ◽  
Author(s):  
Shiro Mawatari ◽  
Shinji Ohara ◽  
Yoshihide Taniwaki ◽  
Yoshio Tsuboi ◽  
Toru Maruyama ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Oral Administration ◽  
Peripheral Blood ◽  
Sleep Problems ◽  
Clinical Symptoms ◽  
Blood Levels ◽  
Nonmotor Symptoms ◽  
Ether Phospholipids ◽  
Normal Controls

Introduction. Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease (AD). With the ageing of population, the frequency of PD is expected to increase dramatically in the coming decades. L-DOPA (1,3,4-dihydroxyalanine) is the most effective drug in the symptomatic treatment of PD. Nonmotor symptoms in PD include sleep problems, depression, and dementia, which are not adequately controlled with dopaminergic therapy. Here, we report the efficacy of oral administration of scallop-derived ether phospholipids to some nonmotor symptoms of PD. Methods. Ten (10) patients received oral administration of 1 mg/day of purified ether phospholipids derived from scallop for 24 weeks. Clinical symptoms and blood tests were checked at 0, 4, 12, 24, and 28 weeks. The blood levels of plasmalogens in patients with PD were compared with those of 39 age-matched normal controls. Results. Initial levels of plasma ethanolamine ether phospholipids in PD and ethanolamine plasmalogen of erythrocyte from PD were lower than those of age-matched normal controls. Oral administration of 1 mg/day of the purified ether phospholipids increased plasma ether phospholipids in PD and increased the relative composition of ether phospholipids of erythrocyte membrane in PD. The levels of ether phospholipids in peripheral blood reached to almost normal levels after 24 weeks. Furthermore, some clinical symptoms of PD improved concomitantly. Conclusion. 1 mg/day of oral administration of purified ether phospholipids derived from scallop can increase ether phospholipids in peripheral blood and concomitantly improve some clinical symptoms of PD.

scholarly journals No Country for Old Worms: A Systematic Review of the Application of C. elegans to Investigate a Bacterial Source of Environmental Neurotoxicity in Parkinson’s Disease

Metabolites ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 70 ◽  
Author(s):  
Kim Caldwell ◽  
Jennifer Thies ◽  
Guy Caldwell
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopaminergic Neurons ◽  
Ubiquitin Proteasome System ◽  
Genetic Associations ◽  
Cellular Mechanisms ◽  
Streptomyces Species ◽  
C Elegans ◽  
Progressive Neurodegeneration ◽  
Ubiquitin Proteasome

While progress has been made in discerning genetic associations with Parkinson’s disease (PD), identifying elusive environmental contributors necessitates the application of unconventional hypotheses and experimental strategies. Here, we provide an overview of studies that we conducted on a neurotoxic metabolite produced by a species of common soil bacteria, Streptomyces venezuelae (S. ven), indicating that the toxicity displayed by this bacterium causes stress in diverse cellular mechanisms, such as the ubiquitin proteasome system and mitochondrial homeostasis. This dysfunction eventually leads to age and dose-dependent neurodegeneration in the nematode Caenorhabditis elegans. Notably, dopaminergic neurons have heightened susceptibility, but all of the neuronal classes eventually degenerate following exposure. Toxicity further extends to human SH-SY5Y cells, which also degenerate following exposure. Additionally, the neurons of nematodes expressing heterologous aggregation-prone proteins display enhanced metabolite vulnerability. These mechanistic analyses collectively reveal a unique metabolomic fingerprint for this bacterially-derived neurotoxin. In considering that epidemiological distinctions in locales influence the incidence of PD, we surveyed soils from diverse regions of Alabama, and found that exposure to ~30% of isolated Streptomyces species caused worm dopaminergic neurons to die. In addition to aging, one of the few established contributors to PD appears to be a rural lifestyle, where exposure to soil on a regular basis might increase the risk of interaction with bacteria producing such toxins. Taken together, these data suggest that a novel toxicant within the Streptomyces genus might represent an environmental contributor to the progressive neurodegeneration that is associated with PD.

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