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Review Article Natural Compounds for the Management of Parkinson's

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Review Article Natural Compounds for the Management of Parkinson's Hindawi BioMed Research International Volume 2018, Article ID 4067597, 12 pages https://doi.org/10.1155/2018/4067597 Review Article Natural Compounds for the Management of Parkinson’s Disease and Attention-Deficit/Hyperactivity Disorder Juan Carlos Corona Laboratory of Neurosciences, Hospital Infantil de Mexico´ Federico Gomez,´ Mexico Correspondence should be addressed to Juan Carlos Corona; [email protected] Received 28 June 2018; Revised 31 October 2018; Accepted 11 November 2018; Published 22 November 2018 Guest Editor: Francesco Facchiano Copyright © 2018 Juan Carlos Corona. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Parkinson’s disease (PD) is the second most common neurodegenerative disorder with an unknown aetiology. Te pathogenic mechanisms include oxidative stress, mitochondrial dysfunction, protein dysfunction, infammation, autophagy, apoptosis, and abnormal deposition of �-synuclein. Currently, the existing pharmacological treatments for PD cannot improve fundamentally the degenerative process of dopaminergic neurons and have numerous side efects. On the other hand, attention-defcit/hyperactivity disorder (ADHD) is the most common neurodevelopmental disorder of childhood and is characterised by hyperactivity, impulsiv- ity, and inattention. Te aetiology of ADHD remains unknown, although it has been suggested that its pathophysiology involves abnormalities in several brain regions, disturbances of the catecholaminergic pathway, and oxidative stress. Psychostimulants and nonpsychostimulants are the drugs prescribed for the treatment of ADHD; however, they have been associated with increased risk of substance use and have several side efects. Today, there are very few tools available to prevent or to counteract the progression of such neurological disorders. Tus, therapeutic approaches with high efciency and fewer side efects are needed. Tis review presents a brief overview of the two neurological disorders and their current treatments, followed by a discussion of the natural compounds which have been studied as therapeutic agents and the mechanisms underlying the benefcial efects, in particular, the decrease in oxidative stress. 1. Introduction characterised by the progressive loss of dopaminergic neurons in the substantia nigra (SN) and their projections to For many years, natural compounds have provided an ef- the striatum. Tus, the function of the nigrostriatal pathway cient resource for the discovery of potential therapeutic becomes reduced and causes the development of movement agents. Among them, many natural products possess antiox- disorder [1]. Te basic characteristics of PD include tremor, idative, antiapoptotic and anti-infammatory activities. In this rigidity, bradykinesia, and impaired balance; depression is review,wesummarizetheroleofnaturalcompoundsand also present in patients, afecting the quality of life. One their therapeutic use for the management of dopamine- of the pathological features of PD is the presence of Lewy related diseases, divided into part 1 for Parkinson’sdisease and bodies, which are intraneuronal proteinaceous cytoplasmic part 2 for attention-defcit/hyperactivity disorder. In addi- inclusions and include �-synuclein, ubiquitin, and neuro- tion, the current knowledge of the mechanisms underlying flaments found in all afected brain regions [2]. Te the potential benefcial efects of diverse natural compounds pathogenic mechanisms of PD include oxidative stress, capable of counteracting the progression of this type of dis- mitochondrial dysfunction, protein dysfunction, infam- eases is reviewed, as demonstrated by their antioxidative mation, autophagy, and apoptosis [3]. PD occurs 95 % as efects. a sporadic form, while familial forms involve mutations in proteins that include PINK1, DJ-1, PARKIN, FBXO7, and 2. Parkinson’s Disease LRRK2 [4], even though pesticides, chemicals, and metals may increase the risk of developing PD. Currently, the Parkinson’s disease (PD) is the second most common treatment of PD includes drugs such as L-DOPA, which is progressive and chronic neurodegenerative disorder, catalysed primarily by dopa decarboxylase in the brain and is 2 BioMed Research International converted into dopamine, producing its therapeutic efects. iron homeostasis [16]. In low-dose whole-body �-irradiation Another treatment includes anticholinergic drugs that can in the reserpine model of PD, EGb761 was protective by block striatal cholinergic receptors inhibiting the excitability ameliorating the reserpine-induced state of oxidative stress, of cholinergic nerves; it has also been demonstrated that mitochondrial dysfunction, and apoptosis in the brain [15]. they can inhibit dopamine reuptake to enhance the function Te pretreatment with ginkgolide B or bilobalide protected of dopaminergic neurons [5]. At present, there are also SH-SY5Y cells against �-synuclein-induced cell injury and other drugs in Phase III clinical trials. Nevertheless, the apoptosis [17]. Ultimately, the G. biloba extract treatment current drugs used for the PD treatment have some side improved locomotor activity, decreased oxidative damage, efects, limiting their clinical applications [6]. Drugs used maintained the dopamine homeostasis, and inhibited the for the PD treatment and their side efects are shown in development of PD in A53T �-synuclein transgenic mice [18]. Table 1. Tus, the growing interest in alternative therapies for neurodegenerative disorders, including PD, has focused 2.2. Ginseng. Ginseng is a traditional Chinese herb con- on the neuroprotective and antioxidant efects of natural taining more than 30 ginsenosides, the active ingredients products that may provide alternatives, since they can have of ginseng. Ginsenosides Rb1 and Rg1 are regarded as the high efciency and fewer side efects. Natural compounds main compounds responsible for the therapeutic actions used as alternative therapies for the management of PD are of ginseng. Previous studies have shown that, in SN-K-SH shown in Table 2. cells, both ginsenosides Rb1 and Rg1 reversed MPTP-induced cell death [19]. Te protective efect of Rg1 against MPTP- 2.1. Ginkgo biloba. Ginkgo biloba is an ancient tree native to induced apoptosis was attributed to enhancing Bcl-2 and China and has been extensively used in traditional Chinese Bcl-xl expression, reducing Bax and iNOS expression, and medicine to manage symptoms associated with dysfunctions inhibiting activation of caspase-3 [20]. Te ginseng extract oftheheartandlungs.G.bilobausuallycontainsthreeingre- G115 signifcantly blocked tyrosine hydroxylase- (TH-) dients, which include favonoids, terpenoids, and ginkgolic positive cell loss in the SN and reduced the appearance of acid [81]. Ginkgolides well-known plant extracts obtained locomotor dysfunction in two rodent models of PD [21]. from leaves from G. biloba, especially in the preparation Pretreatments of Rg1 or N-acetylcysteine were found to EGb761, which contains ginkgolide B and bilobalide, have protect against MPTP-induced SN neuron loss by preventing emerged as natural therapeutic compounds, in part due to glutathione (GSH) reduction, attenuate the phosphorylations their antioxidant activity. Tese efects have been observed in of JNK and c-Jun, and activate superoxide dismutase (SOD) + the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- (MPTP-) [22]. MPP -induced cytotoxicity in SH-SY5Y was inhibited treated mouse model of PD, where chronic ingestion of by water extract of ginseng, as demonstrated by the inhibitory EGb761 prevented MPTP-induced reduction in the dopamin- efect on cell death, overproduction of ROS, elevated Bax/Bcl- ergic nerve endings [9]. In addition, EGb761 administered 2 ratio, release of cytochrome c, and activation of caspase- before or afer MPTP treatment protected against MPTP- 3 expression [23]. It was demonstrated that ginsenosides induced dopaminergic neurotoxicity [10]. Moreover, EGb761 protect by reducing intracellular ROS levels, enhancing attenuated the neurotoxic efect of levodopa in the 6- antioxidant activity, preserving the activity of complex I, sta- hydroxydopamine (6-OHDA) model of PD, indicated that bilising the û Ψm, and increasing intracellular ATP levels. Rg1 levodopa is neurotoxic and that EGb761 may decrease this treatment restored motor functions in MPTP-treated mice toxicity [11]. Te neuroprotective efects of EGb761 were and these behavioural ameliorations were accompanied by demonstrated in the 6-OHDA rat model, as indicated by the restoration of dopaminergic neurons in the SN and striatum reduction in the behavioural defcit in the rat [12]. Paraquat is [24]. Additionally, the ginsenoside Rb1 exhibited a strong a pesticide that has been linked to PD, and it has been demon- ability to disaggregate fbrils and to inhibit the polymerisation strated that EGb761 protects against paraquat-induced apop- of �-synuclein [25]. Rg1 treatment inhibited the activation of tosis of PC12 cells by increasing bcl-2 activation, maintaining microglia and reduced the infltration of CD3+ and T cells of mitochondrial membrane potential (û Ψm)anddecreasing and also protected TH-positive cells in the SN and reduced caspase-3 activation through the mitochondria-dependent the serum concentrations of proinfammatory cytokines pathway [13]. Te neuroprotective efect of EGb761 against TNF�,IFN�,IL-1�,andIL-6inMPTPmousemodels[26]. MPTP neurotoxicity is associated
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