Database : MEDLINE
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[PMID]: 29524600
[Au] Autor:Vitale F; Capozzo A; Mazzone P; Scarnati E
[Ad] Address:Department of Biotechnological and Applied Clinical Sciences (DISCAB), University of L'Aquila, Via Vetoio 2, 67100 L'Aquila, Italy.
[Ti] Title:Neurophysiology of the pedunculopontine tegmental nucleus.
[So] Source:Neurobiol Dis;, 2018 Mar 07.
[Is] ISSN:1095-953X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The interest in the pedunculopontine tegmental nucleus (PPTg), a structure located in the brainstem at the level of the pontomesencephalic junction, has greatly increased in recent years because it is involved in the regulation of physiological functions that fail in Parkinson's disease and because it is a promising target for deep brain stimulation in movement disorders. The PPTg is highly interconnected with the main basal ganglia nuclei and relays basal ganglia activity to thalamic and brainstem nuclei and to spinal effectors. In this review, we address the functional role of the main PPTg outputs directed to the basal ganglia, thalamus, cerebellum and spinal cord. Together, the data that we discuss show that the PPTg may influence thalamocortical activity and spinal motoneuron excitability through its ascending and descending output fibers, respectively. Cerebellar nuclei may also relay signals from the PPTg to thalamic and brainstem nuclei. In addition to participating in motor functions, the PPTg participates in arousal, attention, action selection and reward mechanisms. Finally, we discuss the possibility that the PPTg may be involved in excitotoxic degeneration of the dopaminergic neurons of the substantia nigra through the glutamatergic monosynaptic input that it provides to these neurons.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 25131 MEDLINE  
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[PMID]: 29524599
[Au] Autor:Chen AY; Tully T
[Ad] Address:Cold Spring Harbor Laboratory, 1 Bungtown Rd, Cold Spring Harbor, NY 11724, USA; Graduate Program in Neuroscience, Life Sciences 550, SUNY at Stony Brook, Stony Brook, NY 11794, USA; Dart Neuroscience LLC, 12278 Scripps Summit Dr., San Diego, CA 92131, USA. Electronic address: Alexchenns@gmail.com.
[Ti] Title:A stress-enhanced model for discovery of disease-modifying gene: Ece1-suppresses the toxicity of α-synuclein A30P.
[So] Source:Neurobiol Dis;, 2018 Mar 07.
[Is] ISSN:1095-953X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Parkinson's disease (PD) is a progressive motor neurodegenerative disorder, characterized by a selective loss of dopaminergic neurons in the substantia nigra. The complexity of disease etiology includes both genetic and environmental factors. No effective drug that can modify disease progression and protect dopamine neurons from degeneration is presently available. Human α-Synuclein A30P (A30P) is a mutant gene identified in early onset PD and showed to result selective dopamine neuron loss in transgenic A30P flies and mice. Paraquat (PQ) is an herbicide and an oxidative stress generator, linked to sporadic PD. We hypothesized that vital PD modifier genes are conserved across species and would show unique transcriptional changes to oxidative stress in animals expressing a PD-associated gene, such as A30P. We also hypothesized that manipulation of PD modifier genes would provide neuroprotection across species. To identify disease modifier genes, we performed two independently-duplicated experiments of microarray, capturing genome-wide transcriptional changes in A30P flies, chronically fed with PQ-contaminated food. We hypothesized that the best time point of identifying a disease modifier gene is at time when flies showed maximal combined toxicity of A30P transgene and PQ treatment during an early stage of disease and that effective disease modifiers gene are those showing transcriptional changes to oxidative stress in A30P expressing and not in wild type animals. Fly Neprilysin3 (Nep3) is one identified gene that is highly conserved. Its mouse and human homolog is endothelin-converting enzyme-1 (Ece1). To investigate the neuroprotective effect of Ece1, we used NS1 cells and mouse midbrain neurons expressing A30P, treated with or without PQ. We found that ECE1 expression protected against A30P toxicity on cell viability, on neurite outgrowth and ameliorated A30P accumulation in vitro. Expression of ECE1 in vivo suppressed dopamine neuron loss and alleviated the corresponding motor deficits in mice with A30P-expression. Our study leverages a new approach to identify disease modifier genes using a stress-enhanced PD animal model.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 25131 MEDLINE  
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[PMID]: 29522838
[Au] Autor:Gan L; Ma D; Li M; Yang FC; Rogers RS; Wheatley JL; Koch LG; Britton SL; Thyfault JP; Geiger PC; Stanford JA
[Ad] Address:Department of Neurology, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China; Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA.
[Ti] Title:Region-specific differences in bioenergetic proteins and protein response to acute high fat diet in brains of low and high capacity runner rats.
[So] Source:Neurosci Lett;, 2018 Mar 06.
[Is] ISSN:1872-7972
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Aerobic capacity is a strong predictor of mortality. Low capacity runner (LCR) rats exhibit reduced mitochondrial function in peripheral organs. A high fat diet (HFD) can worsen metabolic phenotype in LCR rats. Little is known about metabolic changes in the brains of these rats, however. This study examined protein markers of mitochondrial function and metabolism as a function of aerobic running capacity and an acute HFD in four brain regions: the striatum, hippocampus, hypothalamus, and substantia nigra. After 3 days HFD or chow diets, we measured peroxisome proliferator-activated receptor-γ coactivator 1α (PGC1-α), nuclear respiratory factors 1 (Nrf-1), mitochondrial transcription factor A (TFAM), and phosphorylated (activated) AMP-activated protein kinase (p-AMPK) protein levels in the four brain regions. LCR rats exhibited lower levels of mitochondrial proteins (PGC1-α, Nrf-1, TFAM), and greater p-AMPK, in striatum, but not in the other brain regions. Mitochondrial protein levels were greater in HFD LCR striatum, while p-AMPK was lower in this group. Markers of lower mitochondrial biogenesis and increased metabolic demand were limited to the LCR striatum, which nevertheless maintained the capacity to respond to an acute HFD challenge.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  4 / 25131 MEDLINE  
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[PMID]: 29501454
[Au] Autor:Sharma S; Kumar P; Deshmukh R
[Ad] Address:Neuropharmacology Division, Department of Pharmacology, I.S.F. College of Pharmacy, Moga 142001, Punjab, India.
[Ti] Title:Neuroprotective potential of spermidine against rotenone induced Parkinson's disease in rats.
[So] Source:Neurochem Int;, 2018 Mar 06.
[Is] ISSN:1872-9754
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Parkinson's disease is a leading hypokinetic disorder characterized by selective loss of dopaminergic neurons in substantia nigra pars compacta (SNpc) region of mid-brain. Degeneration of dopaminergic neurons is considered to be due to oxidative stress, neuroinflammation, disturbed calcium homeostasis and glutamate excitotoxicity etc. Spermidine is a polyamine which counteracts age associated cell death by scavenging free radical formation, activates authophagic machinery by enhancing formation of autophagosome, and antagonizes NMDA receptor. In the current study we investigated the neuroprotective potential of spermidine against rotenone induced PD in rats. Rats were treated subcutaneously with rotenone 1.5 mg/kg daily for 28 days. Spermidine 5&10 mg/kg was administered orally 1 h prior to rotenone administration from 15 to 28. Rotenone caused significant reduction in motor functioning and elevated levels of oxidative stress markers and proinflammatory cytokines levels (IL-1, IL6 and TNF-α). The neurochemical analysis revealed a significant decrease in serotonin, norepinephrine, dopamine and their metabolites accompanied by a significant loss of dopaminergic neurons in the SNpc following ROT injection. However, treatment with spermidine rescued DAergic neurons in SNpc and nerve terminals in the striatum following ROT insult. Spermidine treatment also attenuated oxidative stress, neuroinflammation and restored striatal neurochemistry. Results of our study suggest that spermidine has promising neuroprotective effect against degenerative changes in experimental PD, and the protective effects are mediated through its antioxidant and anti-inflammatory properties.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 25131 MEDLINE  
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[PMID]: 29496635
[Au] Autor:Kelm-Nelson CA; Trevino MA; Ciucci MR
[Ad] Address:Department of Surgery, Division of Otolaryngology, University of Wisconsin-Madison, Madison, WI, USA. Electronic address: CAKelm@wisc.edu.
[Ti] Title:Quantitative Analysis of Catecholamines in the Pink1 -/- Rat Model of Early-onset Parkinson's Disease.
[So] Source:Neuroscience;, 2018 Feb 27.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Parkinson's disease (PD) related to homozygous mutations in the Pink1 gene is associated with nigrostriatal dopamine depletion and a wide range of sensorimotor deficits. In humans and animal models of PD, not all sensorimotor deficits are levodopa-responsive. We hypothesized that the underlying mechanisms of locomotion, limb control, and vocal communication behavior include other pathologies. Here, Pink1 -/- rats were treated with an oral dose of levodopa and limb motor and vocal communication behaviors were measured. Levodopa significantly improved some aspects of locomotion but did not improve ultrasonic vocalization intensity or frequency. Catecholamine concentrations in the striatum (SR), substantia nigra (SN), and locus coeruleus (LC) were analyzed to test the hypothesis that behavioral deficits would correlate to altered protein levels. There were no differences in dopamine concentrations in the SR and SN of Pink1 -/- animals compared to wild-type controls. There was a significant increase in norepinephrine concentration in the SN of Pink1 -/- animals. Moreover, an observed decrease in norepinephrine concentrations in the LC is consistent with the hypothesis that early-stage PD includes noradrenergic loss in the brainstem, and is congruent with a significant increase in catechol-O-methyltransferase expression in the LC of Pink1 -/- animals. Pearson's correlations showed that increases in time to traverse a tapered balance beam are significantly associated with reductions in striatal dopamine. Ultrasonic vocalization complexity was positively correlated with LC norepinephrine concentrations. These data support the evolving hypothesis that differences in neural substrates and early-onset noradrenergic mechanisms in the brainstem may contribute to pathogenesis in the Pink1 -/- rat.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  6 / 25131 MEDLINE  
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[PMID]: 29462643
[Au] Autor:Christensen AB; Srensen JCH; Ettrup KS; Orlowski D; Bjarkam CR
[Ad] Address:Department of Anesthesiology, Institute of Clinical Medicine, Aalborg University Hospital, Hobrovej 18-22, 9100 Aalborg, Denmark. Electronic address: a.bro@rn.dk.
[Ti] Title:Pirouetting pigs: A large non-primate animal model based on unilateral 6-hydroxydopamine lesioning of the nigrostriatal pathway.
[So] Source:Brain Res Bull;139:167-173, 2018 Feb 17.
[Is] ISSN:1873-2747
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:INTRODUCTION: The rotating 6-hydroxydopamine (6-OHDA) rat model has long been important when developing new treatment strategies for Parkinson's disease (PD). Similar non-human primate models have been developed for translational research purposes as large animal models are required by regulatory bodies as an intermediate "phase 0" trial step. However, experimental research in non-human primates encounters several economical and regulatory issues, which may be avoided by the alternative use of pigs as a large animal model for experimental brain research. OBJECTIVE: The primary aim of this study was to examine if unilateral injections of 6-OHDA into the Gttingen minipig nigrostriatal pathway would lead to dopaminergic imbalance and rotational behavior similar to the 6-OHDA unilateral symptomatic model of PD created in other species. The secondary aim was to attempt to verify the rotational behavior as a parkinsonian symptom using subthalamic deep brain stimulation (STN-DBS) to minimize the elicited rotational pattern. MATERIALS AND METHODS: Using an MRI-based stereotactic procedure, ten female Gttingen minipigs were injected unilaterally with 6-OHDA in the nigrostriatal pathway. Postoperatively, an MRI was performed, and the animals were injected with amphetamine and apomorphine and observed for rotational behavior. After a survival period of three months the brains were removed and immunohistochemically stained for tyrosine hydroxylase (TH). One week before sacrifice two animals had DBS electrodes unilaterally implanted in the subthalamic nucleus and various stimulation protocols were conducted during amphetamine challenge. RESULTS: As expected most animals rotated towards the side of the lesion when given amphetamine (3.5-4.0 mg/kg), whereas the predicted opposite response to apomorphine were much harder to reproduce. T1- and T2-weighted postoperative MRI could demonstrate the size and the location of the 6-OHDA injection. Postmortem TH-staining of the final two animals receiving a medial and a lateral injection of 25 L of 6-OHDA (8 g/L, injection rate 5 L/min) into the diencephalic nigrostriatal pathway showed a prominent unilateral decrease in TH-staining of the substantia nigra pars compacta, the ventral tegmental area and the nigrostriatal pathway on the lesioned side. These two animals displayed spontaneous rotational behavior toward the lesioned side for the first 2-3 days postoperatively, and this behavior could later on be reelicited by amphetamine and attenuated by ipsilateral STN-DBS. CONCLUSION: Female Gttingen minipigs are susceptible to unilateral dopaminergic degeneration when properly injected unilaterally with sufficient amounts of 6-OHDA in the nigrostriatal pathway. The location of the 6-OHDA injections and thus the accuracy of the employed stereotaxy can be verified in vivo using MRI postoperatively. The injected minipigs display unilateral parkinsonism with a well-defined rotational response to amphetamine that may be ameliated by STN-DBS performed on the lesioned side. The response to apomorphine was, however, not consistent, illustrating that further work on this promising non-primate large animal model is needed, before it is fully similar to the established 6-OHDA models in other species.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  7 / 25131 MEDLINE  
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[PMID]: 29420861
[Au] Autor:Chu Y; Buchman AS; Olanow CW; Kordower JH
[Ad] Address:Department of Neurological Sciences, Rush University Medical Center, Chicago, IL.
[Ti] Title:Do subjects with minimal motor features have prodromal Parkinson disease?
[So] Source:Ann Neurol;, 2018 Feb 08.
[Is] ISSN:1531-8249
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Understanding the pathological changes underlying mild motor features of the eldery and defining a patient population with prodromal Parkinson disease (PD) are of great clinical importance. It remains unclear, however, how to accurately and specifically diagnose prodromal PD. We examined whether older adults with minimal parkinsonian motor features have nigrostriatal degeneration and α-synuclein pathology consistent with prodromal PD. METHODS: Brain sections were obtained from older adults with a clinical diagnosis of PD (n = 21) and without a clinical diagnosis of PD (n = 27) who underwent motor examination proximate to death. Cases without PD were further dichotomized into no motor deficit (n = 9) or minimal motor features (n = 18) groups using a modified Unified Parkinson's Disease Rating Scale. We performed quantitative unbiased stereological analyses of dopaminergic neurons/terminals and α-synuclein accumulation in the nigrostriatal system. RESULTS: In all subjects with minimal motor features, there were significant reductions in dopaminergic neurons and terminals in the substantia nigra and putamen that were intermediate between subjects with no motor deficit and PD. Phosphorylated α-synuclein inclusions were observed in the substantia nigra that were of similar density to what was seen in PD. Furthermore, there was greater Lewy neuritic pathology in the putamen relative to PD patients. Lastly, neurons with α-synuclein inclusions displayed reductions in tyrosine hydroxylase expression that were comparable in subjects with both minimal motor features and PD. INTERPRETATION: Minimal motor features in older adults may represent prodromal PD and identify at-risk individuals for testing putative neuroprotective interventions that could slow or prevent PD progression. Ann Neurol 2018.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1002/ana.25179

  8 / 25131 MEDLINE  
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[PMID]: 29378222
[Au] Autor:Lins LCRF; Souza MF; Bispo JMM; Gois AM; Melo TCS; Andrade RAS; Quintans-Junior LJ; Ribeiro AM; Silva RH; Santos JR; Marchioro M
[Ad] Address:Department of Physiology, Federal University of Sergipe, So Cristvo, SE, Brazil.
[Ti] Title:Carvacrol prevents impairments in motor and neurochemical parameters in a model of progressive parkinsonism induced by reserpine.
[So] Source:Brain Res Bull;139:9-15, 2018 Jan 30.
[Is] ISSN:1873-2747
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Parkinson's disease (PD) is a neurodegenerative disease characterized by a progressive degeneration of dopaminergic neurons in the substantia nigra pars compact (SNpc), with consequent depletion of dopamine in the striatum, which gives rise to the characteristic motor symptoms of PD. Although its etiology is unknown, several studies have suggested that oxidative stress plays a critical function in the pathophysiology of PD, and antioxidant agents could be helpful to slown down the dopaminergic neurodegeneration. Carvacrol (CA) is a phenolic monoterpene found in essential oils of many aromatic plants that presents antioxidant and neuroprotective effects. This study aimed to assess the effect of CA in a reserpine (RES)-induced rat model of PD. Male Wistar rats received 15 s.c. injections of 0.1 mg/kg RES or vehicle, every other day, concomitantly to daily i.p. injections of CA (12.5 or 25 mg/kg) or vehicle. Across the treatment, the animals were submitted to behavioral evaluation in the catalepsy test (performed daily), open field test (7th day) and assessment of vacuous chewing movements (12th, 20th and 30th days). Upon completion of behavioral tests, rats were perfused and their brains underwent tyrosine hydroxylase (TH) immunohistochemical analysis. Our results showed that CA (12.5 e 25 mg/kg) prevented the increase in catalepsy behavior and number of vacuous chewing movements, but failed to revert the decreased open-field locomotor activity induced by RES. In addition, CA in both doses prevented the decrease in TH immunostaining induced by RES in the SNpc and dorsal striatum. Taken together, our results suggest that CA shows a protective effect in a rat model of PD, preventing motor and neurochemical impairments induced by RES. Thus, the use of CA as a promising new strategy for the prevention and/or treatment of PD may be considered.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  9 / 25131 MEDLINE  
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[PMID]: 29520900
[Au] Autor:Wang J; Li Y; Huang Z; Wan W; Zhang Y; Wang C; Cheng X; Ye F; Liu K; Fei G; Zeng M; Jin L
[Ad] Address:Department of Radiology, Zhongshan Hospital, Fudan University.
[Ti] Title:Neuromelanin-sensitive MRI features of the substantia nigra and locus coeruleus in de novo Parkinson's disease and its phenotypes.
[So] Source:Eur J Neurol;, 2018 Mar 09.
[Is] ISSN:1468-1331
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Neuromelanin of the brainstem, which is considered a marker of neurodegeneration in Parkinson's disease (PD), can be detected by T1-weighted neuromelanin-sensitive magnetic resonance imaging (NM-MRI). We aimed to investigate the NM-MRI features of de novo PD and to determine whether these features are associated with motor and non-motor symptoms in de novo PD patients. METHODS: Fifty-one patients with de novo PD (Hoehn and Yahr stage 1-2) and 28 healthy controls were recruited. All subjects underwent clinical and MRI examinations including NM-MRI sequence. The width and contrast-to-noise ratio (CNR) of the substantia nigra pars compacta (SNc) and the CNR of the locus coeruleus (LC) were measured on NM-MRI images. RESULTS: Both the width and CNR values of the high-intensity signals in the SNc were significantly decreased in the lateral, central and medial SNc parts in de novo PD patients compared to control subjects. The changes in the SNc on NM-MRI were not significantly different among the motor subgroups. The CNR values of the left LC were significantly lower in the PD group than in the control group. Specifically, the subtype of PD patients with depressive symptoms exhibited a significantly lower CNR in the left LC than the control group and PD patients without depressive symptoms. CONCLUSIONS: SNc neuromelanin changes occur across both motor and non-motor (with and without depressive symptoms) subtypes, while LC changes are more notable in PD patients with depressive symptoms. Our results may provide new evidence to understand the pathophysiology of non-motor symptoms in PD. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1111/ene.13628

  10 / 25131 MEDLINE  
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[PMID]: 29520721
[Au] Autor:Medeiros-Linard CFB; Andrade-da-Costa BLDS; Augusto RL; Sereniki A; Trevisan MTS; Perreira RCR; de Souza FTC; Braz GRF; Lagranha CJ; de Souza IA; Wanderley AG; Smailli SS; Lafayette SSL
[Ad] Address:Departamento de Fisiologia e Farmacologia, Centro de Biocincias, Universidade Federal de Pernambuco, Av. da Engenharia, s/n, Cidade Universitria, Recife, Pernambuco, CEP 50740600, Brazil.
[Ti] Title:Anacardic Acids from Cashew Nuts Prevent Behavioral Changes and Oxidative Stress Induced by Rotenone in a Rat Model of Parkinson's Disease.
[So] Source:Neurotox Res;, 2018 Mar 08.
[Is] ISSN:1476-3524
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Anacardic acids (AAs) are alkyl phenols mainly presenting in cashew nuts. The antioxidant effects of these compounds have been an area of interest in recent research, with findings suggesting potential therapeutic use for certain diseases. Nevertheless, none of these studies were performed in order to test the hypothesis of whether anacardic acids are capable of preventing behavioral changes and oxidative stress induced by the pesticide rotenone in experimental model of Parkinson's disease. In our research, adult male rats were treated orally with AAs (1, 3, 10, 25, 50, or 100mg/kg/day) 1h before rotenone (3mg/kg; s.c.) for five consecutive days. The behavioral testing strategies, including tests for general locomotor activity (open field), motor coordination (rotarod), and spatial memory performance (elevated T-maze), were carried out. Lipoperoxidation levels and total superoxide dismutase (t-SOD) activity, as well as cytoplasmic and mitochondrial SOD gene expression, were assessed in the substantia nigra (SN), striatum, and cerebral cortex. The results showed that AAs dose-dependently prevented the rotenone-induced learning and motor impairment from 10mg/kg/day. AAs also precluded rotenone-induced lipoperoxidation in all doses, acting directly on the mitochondria, and improved the t-SOD activity in the doses 25-100mg/kg/day. AAs per se (100mg/kg/day) increased SOD gene expression and t-SOD activity. Our findings indicate that the oral administration of AAs prevents rotenone-induced behavioral changes and oxidative stress, in part due to a modulatory action on the mitochondria and SOD gene expression. These data suggest that AAs have promising neuroprotective action against degenerative changes in Parkinson's disease.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1007/s12640-018-9882-6


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