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  JM-20 treatment prevents neuronal damage and memory impairment induced by aluminum chloride in rats

Wong-Guerra, M., Montano-Peguero, Y., Ramírez-Sánchez, J., Jiménez-Martin, J., Fonseca-Fonseca, L. A., Hernández-Enseñat, D., et al. (2021). JM-20 treatment prevents neuronal damage and memory impairment induced by aluminum chloride in rats. NeuroToxicology, 87, 70-85. doi:10.1016/j.neuro.2021.08.017.

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10 September 2023
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 Creators:
Wong-Guerra, Maylin, Author
Montano-Peguero, Yanay, Author
Ramírez-Sánchez, Jeney, Author
Jiménez-Martin, Javier, Author
Fonseca-Fonseca, Luis Arturo, Author
Hernández-Enseñat, Daniela, Author
Nonose, Yasmine, Author
Valdés, Odalys, Author
Mondelo-Rodriguez, Abel, Author
Ortiz-Miranda, Yaquelin, Author
Bergado, Gretchen, Author
Carmenate, Tania, Author
Soto del Valle, Roberto Menéndez, Author
Pardo-Andreu, Gilberto, Author
Outeiro, Tiago Fleming1, Author           
Padrón-Yaquis, Alejandro Saúl, Author
Martimbianco de Assis, Adriano, Author
O Souza, Diogo, Author
Nuñez-Figueredo, Yanier, Author
Affiliations:
1Experimental Neurodegeneration, Max Planck Institute of Experimental Medicine, Max Planck Society, ou_3398149              

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 Abstract: The number of people with dementia worldwide is estimated at 50 million by 2018 and continues to rise mainly due to increasing aging and population growth. Clinical impact of current interventions remains modest and all efforts aimed at the identification of new therapeutic approaches are therefore critical. Previously, we showed that JM-20, a dihydropyridine-benzodiazepine hybrid molecule, protected memory processes against scopolamine-induced cholinergic dysfunction. In order to gain further insight into the therapeutic potential of JM-20 on cognitive decline and Alzheimer's disease (AD) pathology, here we evaluated its neuroprotective effects after chronic aluminum chloride (AlCl3) administration to rats and assessed possible alterations in several types of episodic memory and associated pathological mechanisms. Oral administration of aluminum to rodents recapitulates several neuropathological alterations and cognitive impairment, being considered a convenient tool for testing the efficacy of new therapies for dementia. We used behavioral tasks to test spatial, emotional- associative and novel object recognition memory, as well as molecular, enzymatic and histological assays to evaluate selected biochemical parameters. Our study revealed that JM-20 prevented memory decline alongside the inhibition of AlCl3 -induced oxidative stress, increased AChE activity, TNF-α and pro-apoptotic proteins (like Bax, caspase-3, and 8) levels. JM-20 also protected against neuronal damage in the hippocampus and prefrontal cortex. Our findings expanded our understanding of the ability of JM-20 to preserve memory in rats under neurotoxic conditions and confirm its potential capacity to counteract cognitive impairment and etiological factors of AD by breaking the progression of key steps associated with neurodegeneration.

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Language(s): eng - English
 Dates: 2021
 Publication Status: Issued
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 Rev. Type: Peer
 Identifiers: DOI: 10.1016/j.neuro.2021.08.017
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Title: NeuroToxicology
Source Genre: Journal
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Publ. Info: Amsterdam : Elsevier
Pages: - Volume / Issue: 87 Sequence Number: - Start / End Page: 70 - 85 Identifier: ISSN: 0161813X