Jeney Ramírez-Sánchez

Centro de Aplicaciones Tecnológicas y Desarrollo Nuclear

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Yanier Núñez-Figueredo

Centro de Aplicaciones Tecnológicas y Desarrollo Nuclear

Gilberto L. Pardo‐Andreu

University of Havana

Diogo O. Souza

Universidade Federal do Rio Grande do Sul

René Delgado

Universitat de Barcelona

Estael Ochoa

University of Havana

Yamila Verdecia-Reyes

University of Havana

Maylin Wong-Guerra

Universidad de Santiago de Chile

Luis Arturo Fonseca-Fonseca

Centro de Aplicaciones Tecnológicas y Desarrollo Nuclear

Yanay Montano-Peguero

Centro de Aplicaciones Tecnológicas y Desarrollo Nuclear

Alejandro Saúl Padrón-Yaquis

Centro de Aplicaciones Tecnológicas y Desarrollo Nuclear

Cooperative Institutions

Centro de Investigación y Desarrollo de medicamentos

Centro de Aplicaciones Tecnológicas y Desarrollo Nuclear

Universidade Católica de Pelotas

Universidade Federal do Rio Grande do Sul

University of Havana

Centro de Investigación y Desarrollo

Centre d'Innovació i Desenvolupament Empresarial

Centro de Información y Desarrollo de la Mujer

Universidade Federal de Santa Maria

Universidade Federal da Bahia

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Effect of JM-20 on Age-related cognitive impairment in mice

Research Square (Research Square) (2024)

Maylin Wong-Guerra Yanay Montano-Peguero Jeney Ramírez-Sánchez Enrique García Alfonso Daniela Hernández-Enseñat

Abstract The decline in cognitive function associated with aging significantly impacts the well-being of elderly individuals and their families. This decline is a major recognized risk factor for neurodegenerative diseases, notably Alzheimer's disease. Animal models of aging provide a platform for evaluating drugs concerning aspects like memory and oxidative stress. JM-20 has demonstrated protective effects on short-term memory acquisition and consolidation, along with antioxidant properties and modulation of Acetylcholinesterase activity. This study assesses the potential protective JM-20 against cognitive decline and age-related memory loss. For the study, aged mice exhibiting aging-associated damage were initially selected. Experimental groups were then formed, and the effect of 8 mg/kg of JM-20 was evaluated for 40 days on aging-related behavior, such as spatial memory, novelty recognition memory, ambulatory activity, and anxiety. Subsequently, animals were sacrificed, and the hippocampal region was extracted for redox studies and to assess acetylcholinesterase activity. Results indicated that JM-20 at 8 mg/kg reversed damage to spatial working and reference memory, exhibiting performance comparable to untreated young adult animals. Furthermore, JM-20 preserved the enzymatic activity of superoxide dismutase, catalase, and total sulfhydryl levels in age-related cognitive impairment in mice, indicating a potent protective effect against oxidative events at the brain level. However, only young, healthy animals showed decreased acetylcholinesterase enzyme activity. These findings provide preclinical pharmacological evidence supporting the neuroprotective activity of JM-20, positioning it as a promising therapeutic candidate for treating memory disorders associated with aging.

Memory Impairment

Cognitive Decline

10.21203/rs.3.rs-4863448/v1

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Citations (0)

Corrigendum to “JM-20 treatment prevents neuronal damage and memory impairment induced by aluminum chloride in rats” [Neurotoxicology 87 (2021) 70–85]

NeuroToxicology (2023)

Maylin Wong-Guerra Yanay Montano-Peguero Jeney Ramírez-Sánchez Javier Jiménez-Martín Luis Arturo Fonseca-Fonseca

Memory Impairment

Neuronal damage

10.1016/j.neuro.2023.09.003

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Citations (0)

JM-20 Treatment After MCAO Reduced Astrocyte Reactivity and Neuronal Death on Peri-infarct Regions of the Rat Brain

Molecular Neurobiology (2018)

Jeney Ramírez-Sánchez Elisa Nicoloso Simões Pires André Meneghetti Gisele Hansel Yanier Núñez-Figueredo

Astrogliosis

NeuN

Stroke

10.1007/s12035-018-1087-8

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Citations (29)

Multi-targeting effects of a new synthetic molecule (JM-20) in experimental models of cerebral ischemia

Pharmacological Reports (2018)

Yanier Núñez-Figueredo Jeney Ramírez-Sánchez Gilberto L. Pardo‐Andreu Estael Ochoa Yamila Verdecia-Reyes

Stroke

Neurochemical

Penumbra

Excitotoxicity

Brain ischemia

10.1016/j.pharep.2018.02.013

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Citations (12)

Effect of JM-20 on Age-Related Cognitive Impairment in Mice

Neurochemical Research (2024)

Maylin Wong-Guerra Yanay Montano-Peguero Jeney Ramírez-Sánchez Enrique García Alfonso Daniela Hernández-Enseñat

Neurochemistry

10.1007/s11064-024-04254-1

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Citations (1)

A novel multi-target ligand (JM-20) protects mitochondrial integrity, inhibits brain excitatory amino acid release and reduces cerebral ischemia injury in vitro and in vivo

Neuropharmacology (2014)

Yanier Núñez-Figueredo Jeney Ramírez-Sánchez Gisele Hansel Elisa Nicoloso Simões Pires Nelsón Merino

Brain ischemia

10.1016/j.neuropharm.2014.06.009

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Citations (50)

JM-20 administration to animals with lesion of the nigrostriatal dopamine pathway induced by 6-hydroxydopamine, partially reverses motor damage and oxidative stress

bioRxiv (Cold Spring Harbor Laboratory) (2024)

Luis Arturo Fonseca-Fonseca Laura Reina Taño Portuondo Jeney Ramírez-Sánchez Nancy Pavón Fuentes Abel Mondelo Rodríguez

Abstract Previous studies have shown that JM-20, a new chemical hybrid molecule, protects against rotenone and 6-hydroxydopamine neurotoxicity. Also, we demonstrated that JM-20 blocks the formation of toxic alpha-synuclein aggregated species and aminochrome cytotoxicity. The present study sought to determine the neuroprotective property of JM-20 in animals with a partial lesion of the nigrostriatal dopamine pathway induced by 6-hydroxydopamine (6-OHDA). For in vivo studies, adult male Wistar rats were lesioned in the right substantia nigra pars compacta (SNpc) with 6-OHDA administration. Fifteen days after surgery, the animals asymmetry levels were assessed. Those with asymmetry values higher than 50% were divided into two groups: animals that did not receive any treatment and those that were administered with JM-20 (40 mg/kg, intragastric via gavage) for 27 days. Every seven days, the asymmetry values of the animals were analyzed until day 42 after the surgery. At the end of the experiment, the animals were euthanized and the SNpc and striatum were taken out for the analysis of oxidative stress. Our results reveal a behavioral function progressively recovered in the JM-20-treated animals, diminishing the percentage of motor asymmetry. Also, it improves some oxidative stress markers in the SNpc and the striatum of these animals. Our study provides the preclinical evidence to support the long-term neuroprotective potential of JM-20 in 6-OHDA hemiparkinson rat model, pointing out to its possible use as a disease-modifying agent in PD.

Pars compacta

Hydroxydopamine

Oxidopamine

Nigrostriatal pathway

MPTP

Neurotoxicity

Rotenone

10.1101/2024.07.30.605870

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Citations (0)

Neuroprotective Action and Free Radical Scavenging Activity of Guttiferone-A, a Naturally Occurring Prenylated Benzophenone

Arzneimittelforschung (2012)

Yanier Núñez-Figueredo Laura García-Pupo Jeney Ramírez-Sánchez Y. Alcántara-Isaac Osmany Cuesta‐Rubio

Reactive oxygen species (ROS) are important mediators in a number of neurodegenerative diseases and molecules capable of scavenging ROS may be a feasible strategy for protecting neuronal cells. We previously demonstrated a powerful iron-chelating action of Guttiferone-A (GA), a naturally occurring polyphenol, on oxidative stress injuries initiated by iron overload. Here we addressed the neuroprotective potential of GA in hydrogen peroxide and glutamate-induced injury on rat’s primary culture of cortical neurons and PC12 cells, respectively, and antioxidant properties concerning scavenging and anti-lipoperoxidative activities in cell-free models. The decrease in cell viability induced by each of the toxins, assessed by [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] (MTT) assay, was significantly attenuated by GA. In addition, GA was found to be a potent antioxidant, as shown by (i) inhibition of 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical reduction (EC₅₀=20.0 μM), (ii) prevention against chemically or electrochemically generated superoxide radicals, (iii) inhibition of spontaneous brain lipid peroxidation and (iv) interference with the Fenton reaction. These results indicate that GA exerts neuroprotective effects against H₂O₂ or glutamate toxicity and its antioxidant activity, demonstrated in vitro, could be at least partly involved. They also suggest a promising potential for GA as a therapeutic agent against neurodegenerative diseases involving ROS and oxidative damage.

Viability assay

10.1055/s-0032-1327612

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Citations (6)

KM-34, a Novel Antioxidant Compound, Protects against 6-Hydroxydopamine-Induced Mitochondrial Damage and Neurotoxicity

Neurotoxicity Research (2018)

Luis Arturo Fonseca-Fonseca Yanier Núñez-Figueredo Jeney Ramírez-Sánchez Maylin Wong Guerra Estael Ochoa

Hydroxydopamine

Neurotoxicity

Neurochemistry

Neuronal damage

10.1007/s12640-017-9851-5

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Citations (10)

JM-20 protects memory acquisition and consolidation on scopolamine model of cognitive impairment

Neurological Research (2019)

Maylin Wong-Guerra Javier Jiménez-Martín Luis Arturo Fonseca-Fonseca Jeney Ramírez-Sánchez Yanay Montano-Peguero

JM-20, a novel hybrid synthetic molecule, has been reported to have antioxidant, mitoprotective, anti-excitotoxic, anti-apoptotic and anti-inflammatory properties. However, the neuroprotective effect of JM-20 against memory impairment in preclinical AD-like models has not been analyzed. The aim of this study was to evaluate the potential neuroprotection of JM-20 that preserves essential memory process from cholinergic dysfunction and other molecular damages.The effects of JM-20 on scopolamine (1 mg/kg)-induced cognitive disorders were studied. Male Wistar rats (220-230 g) were treated with JM-20 and/or scopolamine, and behavioral tasks were performed. The AChE activity, superoxide dismutase activity, catalase activity, MDA and T-SH level on brain tissue were determined by spectrophotometric methods. Mitochondrial functionality parameters were measured after behavioral tests. Histological analyses on hippocampus and prefrontal cortex were processed with hematoxylin and eosin, and neuronal and axonal damage were determined.The behavioral, biochemical and histopathological studies revealed that oral pre-treatment with JM-20 (8 mg/kg) significantly attenuated the scopolamine-induced memory deficits, mitochondrial malfunction, oxidative stress, and prevented AChE hyperactivity probably due to specific inhibition of AChE enzyme. It was also observed marked histological protection on hippocampal and prefrontal-cortex regions.The multimodal action of this molecule could mediate the memory protection here observed and suggest that it may modulate different pathological aspects of memory deﬁcits associated with AD in humans.

Memory Impairment

10.1080/01616412.2019.1573285

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Citations (23)