scholarly journals Schinus terebinthifolius administration prevented behavioral and biochemical alterations in a rotenone model of Parkinson's disease

2016 ◽  
Vol 26 (2) ◽  
pp. 240-245 ◽  
Author(s):  
Adriana Sereniki ◽  
Cybelle F.B. Linard-Medeiros ◽  
Shirliane N. Silva ◽  
Juciene B.R. Silva ◽  
Tadeu J.S. Peixoto Sobrinho ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Schinus Terebinthifolius ◽  
Biochemical Alterations

Beneficial effect of rice bran extract against rotenone-induced experimental Parkinson’s disease in rats

2021 ◽  
Vol 14 ◽  
Author(s):  
Sachin Kumar ◽  
Puneet Kumar
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Rice Bran ◽  
Motor Coordination ◽  
Hexane Extract ◽  
Brain Disorder ◽  
Biochemical Alterations ◽  
Transport Chain ◽  
Behavioral Parameters ◽  
Per Oral

Background: Neurodegenerative diseases have become the rising cause of various disabilities worldwide, followed by aging, including Parkinson’s disease (PD). Parkinson’s disease is a degenerative brain disorder distinguished by growing motor & non-motor failure due to the degeneration of medium-sized spiked neurons in the striatum region. Rotenone is often employed to originate the animal model of PD. It is a powerful blocker of mitochondrial complex-I, mitochondrial electron transport chain that reliably produces Parkinsonism-like symptoms in rats. Rice bran (RB) is very rich in polyunsaturated fatty acids (PUFA) and nutritionally beneficial compounds such as γ-oryzanol, tocopherols, and tocotrienols and sterols are believed to have favorable outcomes on oxidative stress & mitochondrial function. Objective: The present study has been designed to explore RB extract’s effect against rotenone-induced neurotoxicity in rats. Method: In the present study, Rotenone (2 mg/kg, s.c) was administered systemically for 28 days. The hexane extract of RB was prepared using Soxhlation. Hexane extract (250 & 500 mg/kg) was administered per oral for 28 days in rotenone treated groups. Behavioral parameters (grip strength, motor coordination, locomotion, and catalepsy) were conducted on the 7th, 14th, 21st, and 28th day. Animals were sacrificed on the 29th day for biochemical estimation in the striatum and cortex. Result: This study demonstrates significant alteration in behavioral parameters, oxidative burden (increased lipid peroxidation, nitrite concentration, and decreased glutathione, catalase, SOD) in rotenone treated animals. Administration of hexane extract of RB prevented the behavioral, biochemical alterations induced by rotenone. The current research has been sketched to inspect RB extract’s effect against rotenone-developed neurotoxicity in rats. Conclusion: The findings support that PD is associated with impairments in motor activity. The results also suggest that the nutraceutical rice bran that contains γ-oryzanol, Vitamin-E, ferulic acid etc., may underlie the adjuvant susceptibility towards rotenone-induced PD in experimental rats.

scholarly journals Iron Redox Chemistry and Implications in the Parkinson’s Disease Brain

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Dinendra L. Abeyawardhane ◽  
Heather R. Lucas
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Iron Homeostasis ◽  
Substantia Nigra Pars Compacta ◽  
Biochemical Alterations ◽  
Redox Active ◽  
Cellular Inclusions ◽  
Iron Redox ◽  
Presynaptic Protein

The etiology of Parkinson’s disease (PD) is linked with cellular inclusions in the substantia nigra pars compacta region of the brain that are enriched in the misfolded presynaptic protein α-synuclein (αS) and death of the dopaminergic neurons. Brain iron homeostasis governs both neurotransmission and neurodegeneration; hence, the role of iron in PD progression and neuronal health is apparent. Elevated iron deposits become prevalent in the cerebral region upon aging and even more so in the PD brain. Structural as well as oxidative modifications can result from coordination of αS with redox active iron, which could have functional and/or pathological implications. In this review, we will discuss iron-mediated αS aggregation, alterations in iron metabolism, and the role of the iron-dopamine couple. Moreover, iron interactions with N-terminally acetylated αS, the physiologically relevant form of the human protein, will be addressed to shed light on the current understanding of protein dynamics and the physiological environment in the disease state. Oxidative pathways and biochemical alterations resulting from aberrant iron-induced chemistry are the principal focus of this review in order to highlight the plethora of research that has uncovered this emerging dichotomy of iron playing both functional and disruptive roles in PD pathology.

scholarly journals Ubiquitin and Parkinson's disease through the looking glass of genetics

2017 ◽  
Vol 474 (9) ◽  
pp. 1439-1451 ◽  
Author(s):  
Helen Walden ◽  
Miratul M.K. Muqit
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Quality Control ◽  
Protein Misfolding ◽  
Protein Quality ◽  
Neuronal Loss ◽  
Protein Quality Control ◽  
Biochemical Alterations ◽  
Ubiquitin System ◽  
Novel Therapeutic Strategies

Biochemical alterations found in the brains of Parkinson's disease (PD) patients indicate that cellular stress is a major driver of dopaminergic neuronal loss. Oxidative stress, mitochondrial dysfunction, and ER stress lead to impairment of the homeostatic regulation of protein quality control pathways with a consequent increase in protein misfolding and aggregation and failure of the protein degradation machinery. Ubiquitin signalling plays a central role in protein quality control; however, prior to genetic advances, the detailed mechanisms of how impairment in the ubiquitin system was linked to PD remained mysterious. The discovery of mutations in the α-synuclein gene, which encodes the main protein misfolded in PD aggregates, together with mutations in genes encoding ubiquitin regulatory molecules, including PTEN-induced kinase 1 (PINK1), Parkin, and FBX07, has provided an opportunity to dissect out the molecular basis of ubiquitin signalling disruption in PD, and this knowledge will be critical for developing novel therapeutic strategies in PD that target the ubiquitin system.

scholarly journals The Genetic Link between Parkinson’s Disease and the Kynurenine Pathway Is Still Missing

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Nóra Török ◽  
Rita Török ◽  
Zoltán Szolnoki ◽  
Ferenc Somogyvári ◽  
Péter Klivényi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Age At Onset ◽  
Kynurenine Pathway ◽  
Regulatory Proteins ◽  
Nucleotide Polymorphisms ◽  
Single Nucleotide ◽  
Genetic Link ◽  
Biochemical Alterations ◽  
The Brain

Background. There is substantial evidence that the kynurenine pathway (KP) plays a role in the normal physiology of the brain and is involved in the pathology of neurodegenerative disorders such as Huntington’s disease and Parkinson’s disease (PD).Objective. We set out to investigate the potential roles in PD of single nucleotide polymorphisms (SNPs) from one of the key enzymes of the KP, kynurenine 3-monooxygenase (KMO).Methods. 105 unrelated, clinically definitive PD patients and 131 healthy controls were enrolled to investigate the possible effects of the different alleles of KMO. Fluorescently labeled TaqMan probes were used for allele discrimination.Results. None of the four investigated SNPs proved to be associated with PD or influenced the age at onset of the disease.Conclusions. The genetic link between the KP and PD is still missing. The investigated SNPs presumably do not appear to influence the function of KMO and probably do not contain binding sites for regulatory proteins of relevance in PD. This is the first study to assess the genetic background behind the biochemical alterations of the kynurenine pathway in PD, directing the attention to this previously unexamined field.

Biochemical alterations of the striatum in an MPTP-treated mouse model of Parkinson’s disease

2010 ◽  
Vol 25 (2) ◽  
pp. 177-183 ◽  
Author(s):  
Hayato Kuroiwa ◽  
Hironori Yokoyama ◽  
Hiroki Kimoto ◽  
Hiroyuki Kato ◽  
Tsutomu Araki
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Treated Mouse ◽  
Biochemical Alterations

scholarly journals Measurements of morphological and biochemical alterations in individual neuron cells associated with early neurotoxic effects in Parkinson’s disease

2016 ◽  
Author(s):  
Su-A Yang ◽  
Jonghee Yoon ◽  
Kyoohyun Kim ◽  
YongKeun Park
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Optical Diffraction ◽  
Optical Measurements ◽  
Diffraction Tomography ◽  
Biochemical Alterations ◽  
Optical Diffraction Tomography ◽  
Neurotoxic Effects ◽  
Index Distribution

AbstractParkinson’s disease (PD) is a common neurodegenerative disease. However, therapeutic methods of PD are still limited due to complex pathophysiology in PD. Here, we present optical measurements of individual neurons fromin vitroPD model using optical diffraction tomography (ODT). By measuring 3-D refractive index distribution of neurons, morphological and biochemical alterations inin-vitroPD model are quantitatively investigated. We found that neurons show apoptotic features in early PD progression. The present approach will open up new opportunities for quantitative investigation of the pathophysiology of various neurodegenerative diseases.

Evaluation of Efferent Auditory System and Hearing Quality in Parkinson's Disease: Is the Difficulty in Speech Understanding in Complex Listening Conditions Related to Neural Degeneration or Aging?

2020 ◽  
pp. 1-9
Author(s):  
Nuriye Yıldırım Gökay ◽  
Bülent Gündüz ◽  
Fatih Söke ◽  
Recep Karamert
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Auditory System ◽  
Otoacoustic Emissions ◽  
Pure Tone ◽  
Pure Tone Audiometry ◽  
Auditory Pathway ◽  
Normal Hearing ◽  
System Function ◽  
Distortion Product

Purpose The effects of neurological diseases on the auditory system have been a notable issue for investigators because the auditory pathway is closely associated with neural systems. The purposes of this study are to evaluate the efferent auditory system function and hearing quality in Parkinson's disease (PD) and to compare the findings with age-matched individuals without PD to present a perspective on aging. Method The study included 35 individuals with PD (mean age of 48.50 ± 8.00 years) and 35 normal-hearing peers (mean age of 49 ± 10 years). The following tests were administered for all participants: the first section of the Speech, Spatial and Qualities of Hearing Scale; pure-tone audiometry, speech audiometry, tympanometry, and acoustic reflexes; and distortion product otoacoustic emissions (DPOAEs) and contralateral suppression of DPOAEs. SPSS Version 25 was used for statistical analyses, and values of p < .05 were considered statistically significant. Results There were no statistically significant differences in the pure-tone audiometry thresholds and DPOAE responses between the individuals with PD and their normal-hearing peers ( p = .732). However, statistically significant differences were found between the groups in suppression levels of DPOAEs and hearing quality ( p < .05). In addition, a statistically significant and positive correlation was found between the amount of suppression at some frequencies and the Speech, Spatial and Qualities of Hearing Scale scores. Conclusions This study indicates that medial olivocochlear efferent system function and the hearing quality of individuals with PD were affected adversely due to the results of PD pathophysiology on the hearing system. For optimal intervention and follow-up, tasks related to hearing quality in daily life can also be added to therapies for PD.

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