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Article ; Online: Nanolithium, a New Treatment Approach to Alzheimer's Disease: A Review of Existing Evidence and Clinical Perspectives.

Guilliot, S / Wilson, E N / Touchon, J / Soto, M E

The journal of prevention of Alzheimer's disease

2024 Volume 11, Issue 2, Page(s) 428–434

Abstract: Lithium has been approved and used for several decades in the treatment of psychiatric disorders, and its potential effect in neurodegenerative diseases has been subject to increasing research interest in recent years. Nanolithium is a new experimental ... ...

Abstract	Lithium has been approved and used for several decades in the treatment of psychiatric disorders, and its potential effect in neurodegenerative diseases has been subject to increasing research interest in recent years. Nanolithium is a new experimental product using a novel drug-delivery technology (Aonys®), which optimizes its bioavailability while reducing its toxicity profile. Therapeutic doses of lithium used in Nanolithium are more than 50 times lower than the minimal dose of classical lithium salts. In this review we report data from non-clinical pharmacology studies supporting Nanolithium efficacy and the mechanism of action in Alzheimer's disease. GSK-3β inhibition is thought to be central to Nanolithium's mechanism of action, triggering a reduction of the production of toxic amyloid plaques and decrease in tau hyperphosphorylation, which could potentially benefit both neuropsychiatric symptoms and cognitive decline. We then summarize outcomes from non-clinical proof-of-concept studies. These data supported the initiation of a currently ongoing phase II proof-of-concept study to evaluate the safety and efficacy of Nanolithium in patients with mild-to-severe Alzheimer's disease. We highlight key aspects of the study design. We finish this review with a discussion on the potential place of Nanolithium in the current and future Alzheimer's disease treatment landscape.
MeSH term(s)	Humans ; Alzheimer Disease/diagnosis ; Lithium/therapeutic use ; Glycogen Synthase Kinase 3 beta ; Cognitive Dysfunction ; Cognition
Chemical Substances	Lithium (9FN79X2M3F) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1)
Language	English
Publishing date	2024-02-19
Publishing country	Switzerland
Document type	Review ; Journal Article
ZDB-ID	2782183-3
ISSN	2426-0266 ; 2274-5807
ISSN (online)	2426-0266
ISSN	2274-5807
DOI	10.14283/jpad.2024.26
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Article ; Online: In health and illness: does taste remain consistent? Exploring the influence of inflammation on taste perception through a systematic review and meta-analysis.

López-Salido, S C / Espinoza-Gutiérrez, H A / Housni, F E / Flores-Soto, M E / Viveros-Paredes, J M

European review for medical and pharmacological sciences

2024 Volume 28, Issue 8, Page(s) 3085–3098

Abstract: Objective: Dysgeusia is characterized by a loss of taste perception, leading to malnutrition. This situation affects inflammatory conditions such as respiratory and neurological conditions, obesity, cancer, chemotherapy, aging, and many others. To date, ...

Abstract	Objective: Dysgeusia is characterized by a loss of taste perception, leading to malnutrition. This situation affects inflammatory conditions such as respiratory and neurological conditions, obesity, cancer, chemotherapy, aging, and many others. To date, there is not much information on the prevalence and risk of dysgeusia in an inflammatory condition; also, it is unclear which flavor is altered. Materials and methods: We systematically searched three databases from January 2018 to January 2023. Participants were children, adults, or elderly persons with an inflammatory condition and evaluated taste loss. A random effects model was used for statistical analysis to calculate the pooled odds ratio with its corresponding 95.0% confidence interval to estimate the probability of taste alteration (dysgeusia) in an inflammatory condition. Results: The data allowed us to conduct a systematic review, including 63 original articles and 15 studies to perform the meta-analysis. The meta-analysis indicated a heterogenicity of 84.7% with an odds ratio of 3.25 (2.66-3.96), indicating a significant risk of Alzheimer's disease, SARS-CoV-2, chemotherapy, and rhinosinusitis. Conclusions: Inflammatory conditions and taste alterations are linked. Dysgeusia is associated with a higher risk of malnutrition and poorer general health status, especially in vulnerable populations.
MeSH term(s)	Humans ; Inflammation ; Dysgeusia/epidemiology ; Taste Perception ; COVID-19/epidemiology ; Alzheimer Disease/epidemiology ; Taste/physiology ; Malnutrition/epidemiology ; SARS-CoV-2
Language	English
Publishing date	2024-05-03
Publishing country	Italy
Document type	Journal Article ; Systematic Review ; Meta-Analysis
ZDB-ID	605550-3
ISSN	2284-0729 ; 1128-3602 ; 0392-291X
ISSN (online)	2284-0729
ISSN	1128-3602 ; 0392-291X
DOI	10.26355/eurrev_202404_36024
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Article ; Online: Oxidative, Reductive, and Nitrosative Stress Effects on Epigenetics and on Posttranslational Modification of Enzymes in Cardiometabolic Diseases.

Pérez-Torres, I / Soto, M E / Castrejón-Tellez, V / Rubio-Ruiz, M E / Manzano Pech, L / Guarner-Lans, V

Oxidative medicine and cellular longevity

2020 Volume 2020, Page(s) 8819719

Abstract: Oxidative (OS), reductive (RS), and nitrosative (NSS) stresses produce carbonylation, glycation, glutathionylation, sulfhydration, nitration, and nitrosylation reactions. OS, RS, and NSS are interrelated since RS results from an overactivation of ... ...

Abstract	Oxidative (OS), reductive (RS), and nitrosative (NSS) stresses produce carbonylation, glycation, glutathionylation, sulfhydration, nitration, and nitrosylation reactions. OS, RS, and NSS are interrelated since RS results from an overactivation of antioxidant systems and NSS is the result of the overactivation of the oxidation of nitric oxide (NO). Here, we discuss the general characteristics of the three types of stress and the way by which the reactions they induce (a) damage the DNA structure causing strand breaks or inducing the formation of 8-oxo-d guanosine; (b) modify histones; (c) modify the activities of the enzymes that determine the establishment of epigenetic cues such as DNA methyl transferases, histone methyl transferases, acetyltransferases, and deacetylases; (d) alter DNA reparation enzymes by posttranslational mechanisms; and (e) regulate the activities of intracellular enzymes participating in metabolic reactions and in signaling pathways through posttranslational modifications. Furthermore, the three types of stress may establish new epigenetic marks through these reactions. The development of cardiometabolic disorders in adult life may be programed since early stages of development by epigenetic cues which may be established or modified by OS, RS, and NSS. Therefore, the three types of stress participate importantly in mediating the impact of the early life environment on later health and heritability. Here, we discuss their impact on cardiometabolic diseases. The epigenetic modifications induced by these stresses depend on union and release of chemical residues on a DNA sequence and/or on amino acid residues in proteins, and therefore, they are reversible and potentially treatable.
MeSH term(s)	Animals ; Cardiovascular Diseases/enzymology ; Cardiovascular Diseases/genetics ; Cardiovascular Diseases/metabolism ; Cardiovascular Diseases/pathology ; Epigenesis, Genetic ; Humans ; Metabolic Diseases/enzymology ; Metabolic Diseases/genetics ; Metabolic Diseases/metabolism ; Metabolic Diseases/pathology ; Nitrosative Stress/physiology ; Oxidative Stress/physiology ; Protein Processing, Post-Translational ; Signal Transduction
Language	English
Publishing date	2020-10-30
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2455981-7
ISSN	1942-0994 ; 1942-0994
ISSN (online)	1942-0994
ISSN	1942-0994
DOI	10.1155/2020/8819719
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Article ; Online: Response to Chen

Chávez-Hurtado, P / González-Castañeda, R E / Beas-Zarate, C / Flores-Soto, M E / Viveros-Paredes, J M

Journal of medicinal food

2020 Volume 23, Issue 6, Page(s) 687–688

MeSH term(s)	Animals ; DNA ; Galactose ; Glial Fibrillary Acidic Protein ; Hippocampus ; Mice ; Mice, Inbred BALB C ; Polycyclic Sesquiterpenes ; Prefrontal Cortex
Chemical Substances	Glial Fibrillary Acidic Protein ; Polycyclic Sesquiterpenes ; DNA (9007-49-2) ; caryophyllene (BHW853AU9H) ; Galactose (X2RN3Q8DNE)
Language	English
Publishing date	2020-04-27
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	1427365-2
ISSN	1557-7600 ; 1096-620X
ISSN (online)	1557-7600
ISSN	1096-620X
DOI	10.1089/jmf.2020.0057
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Article ; Online: Chronic Inhibition of FAAH Reduces Depressive-Like Behavior and Improves Dentate Gyrus Proliferation after Chronic Unpredictable Stress Exposure.

Tejeda-Martínez, A R / Viveros-Paredes, J M / Hidalgo-Franco, G V / Pardo-González, E / Chaparro-Huerta, V / González-Castañeda, R E / Flores-Soto, M E

Behavioural neurology

2021 Volume 2021, Page(s) 6651492

Abstract: Symptoms of depressive disorders such as anhedonia and despair can be a product of an aberrant adaptation to stress conditions. Chronic unpredictable stress model (CUS) can generate an increase in the activity of the hypothalamic-pituitary-adrenal axis ( ... ...

Abstract	Symptoms of depressive disorders such as anhedonia and despair can be a product of an aberrant adaptation to stress conditions. Chronic unpredictable stress model (CUS) can generate an increase in the activity of the hypothalamic-pituitary-adrenal axis (HPA) and induce a reduction of neurotrophin signaling and the proliferation of neural progenitors in the adult dentate gyrus, together with increased oxidative stress. Levels of the endocannabinoid anandamide (AEA) seem to affect these depression-by-stress-related features and could be modulated by fatty acid amide hydrolase (FAAH). We aimed to evaluate the effects of FAAH inhibitor, URB597, on depressive-like behavior and neural proliferation of mice subjected to a model of CUS. URB597 was administered intraperitoneally at a dose of 0.2 mg/kg for 14 days after CUS. Depressive-like behaviors, anhedonia, and despair were evaluated in the splash and forced swimming tests, respectively. Alterations at the HPA axis level were analyzed using the relative weight of adrenal glands and serum corticosterone levels. Oxidative stress and brain-derived neurotrophic factor (BDNF) were also evaluated. Fluorescence immunohistochemistry tests were performed for the immunoreactivity of BrdU and Sox2 colabeling for comparison of neural precursors. The administration of URB597 was able to reverse the depressive-like behavior generated in mice after the model. Likewise, other physiological responses associated with CUS were reduced in the treated group, among them, increase in the relative weight of the adrenal glands, increased oxidative stress, and decreased BDNF and number of neural precursors. Most of these auspicious responses to enzyme inhibitor administration were blocked by employing a cannabinoid receptor antagonist. In conclusion, the chronic inhibition of FAAH generated an antidepressant effect, promoting neural progenitor proliferation and BDNF expression, while reducing adrenal gland weight and oxidative stress in mice under the CUS model.
MeSH term(s)	Amidohydrolases ; Animals ; Cell Proliferation ; Corticosterone ; Dentate Gyrus ; Disease Models, Animal ; Hypothalamo-Hypophyseal System ; Mice ; Pituitary-Adrenal System ; Stress, Psychological/drug therapy
Chemical Substances	Amidohydrolases (EC 3.5.-) ; fatty-acid amide hydrolase (EC 3.5.1.-) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2021-03-24
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1001896-7
ISSN	1875-8584 ; 0953-4180
ISSN (online)	1875-8584
ISSN	0953-4180
DOI	10.1155/2021/6651492
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Article ; Online: Using Digital Tools to Advance Alzheimer's Drug Trials During a Pandemic: The EU/US CTAD Task Force.

Kaye, J / Aisen, P / Amariglio, R / Au, R / Ballard, C / Carrillo, M / Fillit, H / Iwatsubo, T / Jimenez-Maggiora, G / Lovestone, S / Natanegara, F / Papp, K / Soto, M E / Weiner, M / Vellas, B

The journal of prevention of Alzheimer's disease

2021 Volume 8, Issue 4, Page(s) 513–519

Abstract: The 2020 COVID-19 pandemic has disrupted Alzheimer's disease (AD) clinical studies worldwide. Digital technologies may help minimize disruptions by enabling remote assessment of subtle cognitive and functional changes over the course of the disease. The ... ...

Abstract	The 2020 COVID-19 pandemic has disrupted Alzheimer's disease (AD) clinical studies worldwide. Digital technologies may help minimize disruptions by enabling remote assessment of subtle cognitive and functional changes over the course of the disease. The EU/US Clinical Trials in Alzheimer's Disease (CTAD) Task Force met virtually in November 2020 to explore the opportunities and challenges associated with the use of digital technologies in AD clinical research. While recognizing the potential of digital tools to accelerate clinical trials, improve the engagement of diverse populations, capture clinically meaningful data, and lower costs, questions remain regarding the stability, validity, generalizability, and reproducibility of digital data. Substantial concerns also exist regarding regulatory acceptance and privacy. Nonetheless, the Task Force supported further exploration of digital technologies through collaboration and data sharing, noting the need for standardization of digital readouts. They also concluded that while it may be premature to employ remote assessments for trials of novel experimental medications, remote studies of non-invasive, multi-domain approaches may be feasible at this time.
MeSH term(s)	Advisory Committees ; Alzheimer Disease/drug therapy ; Biomedical Research/organization & administration ; COVID-19 ; Clinical Trials as Topic/organization & administration ; Digital Technology ; European Union ; Humans ; United States
Language	English
Publishing date	2021-09-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2782183-3
ISSN	2426-0266 ; 2274-5807
ISSN (online)	2426-0266
ISSN	2274-5807
DOI	10.14283/jpad.2021.36
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Article: Chitosan/copper nanocomposites: Correlation between electrical and antibacterial properties

Prokhorov, E / Cruz-Soto, M-E / Elizalde-Peña, E.A / España-Sánchez, B.L / Kovalenko, Y / Luna-Bárcenas, G / Padilla-Vaca, F / Vázquez-Lepe, M.O

Colloids and surfaces. 2019 Aug. 01, v. 180

2019

Abstract: Correlation between electrical and antibacterial properties of chitosan/copper nanocomposites (CS/CuNPs) is investigated. We aim at achieving the minimum CuNPs concentration in a CS-matrix while keeping high antibacterial activity. UV–vis, TEM and XRD ... ...

Abstract	Correlation between electrical and antibacterial properties of chitosan/copper nanocomposites (CS/CuNPs) is investigated. We aim at achieving the minimum CuNPs concentration in a CS-matrix while keeping high antibacterial activity. UV–vis, TEM and XRD measurements confirms the formation of polygonal metallic CuNPs (ca. 30–50 nm). Interactions between NH2/OH groups of CS and CuNPs were determined by FTIR and XPS suggesting Cu chelation-induced mechanism during the CuNPs formation. DC electrical conductivity measurements reveals a percolation threshold at CuNPs volumetric concentration of ca. 0.143%. Antibacterial assays against Gram-positive bacteria and DC measurements helps correlate the antibacterial potency to the electron transfer between the negatively charged bacteria and CuNPs. Our study suggests that nanocomposite’s maximum antibacterial activity is obtained below the electrical percolation threshold at extremely low CuNPs concentrations; this fact may prove useful in the design of nontoxic nanocomposites for biomedical applications.
Keywords	antibacterial properties ; chitosan ; copper ; copper nanoparticles ; electrical conductivity ; electron transfer ; Fourier transform infrared spectroscopy ; Gram-positive bacteria ; nanocomposites ; transmission electron microscopy ; ultraviolet-visible spectroscopy ; X-ray diffraction ; X-ray photoelectron spectroscopy
Language	English
Dates of publication	2019-0801
Size	p. 186-192.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	1500523-9
ISSN	1873-4367 ; 0927-7765
ISSN (online)	1873-4367
ISSN	0927-7765
DOI	10.1016/j.colsurfb.2019.04.047
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Article ; Online: Effects of bupropion on the ejaculatory response of male rats.

Hueletl-Soto, M E / Carro-Juárez, M / Rodríguez-Manzo, G

International journal of impotence research

2014 Volume 26, Issue 6, Page(s) 205–212

Abstract: Chronic antidepressant treatment is associated with sexual side effects, particularly affecting the ejaculatory response. Bupropion (BP), an antidepressant inhibiting dopamine/noradrenaline reuptake, seems to have a low impact upon male sexual function. ... ...

Abstract	Chronic antidepressant treatment is associated with sexual side effects, particularly affecting the ejaculatory response. Bupropion (BP), an antidepressant inhibiting dopamine/noradrenaline reuptake, seems to have a low impact upon male sexual function. Ejaculation is regulated both at the brain and spinal cord by the spinal generator for ejaculation (SGE). We investigated the effects of chronic BP treatment on ejaculatory behavior and on SGE functioning. Sexually experienced male rats were intraperitoneally (i.p.) injected with BP (7.5 or 15 mg kg(-1)) during 14 days and tested for sexual behavior on days 1, 7 and 14 of treatment; these same males were used to evaluate the functioning of the SGE by recording the genital motor pattern for ejaculation (GMPE). Acute and chronic BP administration did not importantly modify copulatory behavior of male rats. Chronic treatment with the low dose of BP produced deficits in the functioning of the SGE that were restored by activation of the SGE through afferent stimulation. Conversely, chronic treatment with the high-dose of BP disrupted the functioning of the SGE, as the deficits were not compensated by activating the SGE through sensory stimulation. It is concluded that chronic BP at high doses alters the functioning of the SGE.
MeSH term(s)	Animals ; Bupropion/pharmacology ; Dopamine Uptake Inhibitors/pharmacology ; Ejaculation/drug effects ; Male ; Motor Activity ; Rats ; Sexual Behavior, Animal/drug effects
Chemical Substances	Dopamine Uptake Inhibitors ; Bupropion (01ZG3TPX31)
Language	English
Publishing date	2014-05-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1034295-3
ISSN	1476-5489 ; 0955-9930
ISSN (online)	1476-5489
ISSN	0955-9930
DOI	10.1038/ijir.2014.12
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Zs.A 2910: Show issues

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Article ; Online: β-Caryophyllene exerts protective antioxidant effects through the activation of NQO1 in the MPTP model of Parkinson's disease.

Flores-Soto, M E / Corona-Angeles, J A / Tejeda-Martinez, A R / Flores-Guzman, P A / Luna-Mujica, I / Chaparro-Huerta, V / Viveros-Paredes, J M

Neuroscience letters

2020 Volume 742, Page(s) 135534

Abstract: Parkinson's disease (PD) is a neurodegenerative disorder, caused by the selective death of dopaminergic neurons in the substantia nigra pars compacta. β-caryophyllene (BCP) is a phytocannabinoid with several pharmacological properties, producing anti- ... ...

Abstract	Parkinson's disease (PD) is a neurodegenerative disorder, caused by the selective death of dopaminergic neurons in the substantia nigra pars compacta. β-caryophyllene (BCP) is a phytocannabinoid with several pharmacological properties, producing anti-inflammatory and antihypertensive effects. In addition, BCP protects dopaminergic neurons from neuronal death induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), yet it remains unclear if this effect is due to its antioxidant activity. To assess whether this is the case, the effect of BCP on the expression and activity of NAD(P)H quinone oxidoreductase (NQO1) was evaluated in mice after the administration of MPTP. Male C57BL/6 J mice were divided into four groups, the first of which received saline solution i.p. in equivalent volume and served as a control group. The second group received MPTP. The second group received MPTP hydrochloride (5 mg/kg, i.p.) daily for seven consecutive days. The third group received BCP (10 mg/kg) for seven days, administered orally and finally, the fourth group received MPTP as described above and BCP for 7 days from the fourth day of MPTP administration. The results showed that BCP inhibits oxidative stress-induced cell death of dopaminergic neurons exposed to MPTP at the same time as it enhances the expression and enzymatic activity of NQO1. Also, the BCP treatment ameliorated motor dysfunction and protected the dopaminergic cells of the SNpc from damage induced by MPTP. Hence, BCP appears to achieve at least some of its antioxidant effects by augmenting NQO1 activity, which protects cells from MPTP toxicity. Accordingly, this phytocannabinoid may represent a promising pharmacological option to safeguard dopaminergic neurons and prevent the progression of PD.
MeSH term(s)	Animals ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; MPTP Poisoning/metabolism ; MPTP Poisoning/pathology ; MPTP Poisoning/prevention & control ; Male ; Mice ; Mice, Inbred C57BL ; NAD(P)H Dehydrogenase (Quinone)/biosynthesis ; Pars Compacta/drug effects ; Pars Compacta/metabolism ; Pars Compacta/pathology ; Polycyclic Sesquiterpenes/pharmacology ; Polycyclic Sesquiterpenes/therapeutic use ; Random Allocation
Chemical Substances	Antioxidants ; Polycyclic Sesquiterpenes ; caryophyllene (BHW853AU9H) ; NAD(P)H Dehydrogenase (Quinone) (EC 1.6.5.2) ; Nqo1 protein, mouse (EC 1.6.5.2)
Language	English
Publishing date	2020-11-30
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2020.135534
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Article ; Online: Effect of inhibition of fatty acid amide hydrolase on MPTP-induced dopaminergic neuronal damage.

Viveros-Paredes, J M / Gonzalez-Castañeda, R E / Escalante-Castañeda, A / Tejeda-Martínez, A R / Castañeda-Achutiguí, F / Flores-Soto, M E

Neurologia (Barcelona, Spain)

2017 Volume 34, Issue 3, Page(s) 143–152

Abstract: Introduction: Parkinson's disease (PD) is a neurodegenerative disorder characterised by balance problems, muscle rigidity, and slow movement due to low dopamine levels and loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). The ... ...

Title translation	Efecto del inhibidor de amida hidrolasa de ácidos grasos en el daño neuronal dopaminérgico inducido por MPTP.
Abstract	Introduction: Parkinson's disease (PD) is a neurodegenerative disorder characterised by balance problems, muscle rigidity, and slow movement due to low dopamine levels and loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). The endocannabinoid system is known to modulate the nigrostriatal pathway through endogenous ligands such as anandamide (AEA), which is hydrolysed by fatty acid amide hydrolase (FAAH). The purpose of this study was to increase AEA levels using FAAH inhibitor URB597 to evaluate the modulatory effect of AEA on dopaminergic neuronal death induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Methods: Our study included 4 experimental groups (n = 6 mice per group): a control group receiving no treatment, a group receiving URB597 (0.2mg/kg) every 3 days for 30 days, a group treated with MPTP (30mg/kg) for 5 days, and a group receiving URB597 and subsequently MPTP injections. Three days after the last dose, we conducted a series of behavioural tests (beam test, pole test, and stride length test) to compare motor coordination between groups. We subsequently analysed immunoreactivity of dopaminergic cells and microglia in the SNpc and striatum. Results: Mice treated with URB597 plus MPTP were found to perform better on behavioural tests than mice receiving MPTP only. According to the immunohistochemistry study, mice receiving MPTP showed fewer dopaminergic cells and fibres in the SNpc and striatum. Animals treated with URB597 plus MPTP displayed increased tyrosine hydroxylase immunoreactivity compared to those treated with MPTP only. Regarding microglial immunoreactivity, the group receiving MPTP showed higher Iba1 immunoreactivity in the striatum and SNpc than did the group treated with URB597 plus MPTP. Conclusion: Our results show that URB597 exerts a protective effect since it inhibits dopaminergic neuronal death, decreases microglial immunoreactivity, and improves MPTP-induced motor alterations.
MeSH term(s)	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/pharmacology ; Amidohydrolases/metabolism ; Animals ; Benzamides ; Carbamates ; Disease Models, Animal ; Dopaminergic Neurons/drug effects ; Dopaminergic Neurons/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Motor Skills/drug effects ; Neuroprotective Agents/therapeutic use ; Parkinson Disease ; Substantia Nigra/drug effects ; Substantia Nigra/metabolism ; Tyrosine 3-Monooxygenase
Chemical Substances	Benzamides ; Carbamates ; Neuroprotective Agents ; cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester ; 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (9P21XSP91P) ; Tyrosine 3-Monooxygenase (EC 1.14.16.2) ; Amidohydrolases (EC 3.5.-) ; fatty-acid amide hydrolase (EC 3.5.1.-)
Language	Spanish
Publishing date	2017-01-16
Document type	Journal Article
ISSN	2173-5808
ISSN (online)	2173-5808
DOI	10.1016/j.nrl.2016.11.008
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