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Article Publish Status: FREE
Abstract Title:

Melatonin Prevents Brain Damage and Neurocognitive Impairment Induced byANKA Infection in Murine Model of Cerebral Malaria.

Abstract Source:

Front Cell Infect Microbiol. 2020 ;10:541624. Epub 2020 Sep 30. PMID: 33102250

Abstract Author(s):

Brenda Jaqueline de Azevedo Ataide, Nayara Kauffmann, Nívia de Souza Franco Mendes, Marjorie Lujan Marques Torres, Larissa Medeiros Dos Anjos, Adelaide da Conceição Fonseca Passos, Suellen Alessandra Soares de Moraes, Evander de Jesus Oliveira Batista, Anderson Manoel Herculano, Karen Renata Herculano Matos Oliveira

Article Affiliation:

Brenda Jaqueline de Azevedo Ataide

Abstract:

Cerebral malaria is characterized by permanent cognitive impairments in-infected children. Antimalarial therapies show little effectiveness to avoid neurological deficits and brain tissue alterations elicited by severe malaria. Melatonin is a well-recognized endogenous hormone involved in the control of brain functions and maintenance of blood-brain barrier integrity. The current study has evaluated the effect of melatonin on the histological alterations, blood-brain barrier leakage, and neurocognitive impairments in mice developing cerebral malaria. Swiss mice infected withANKA strain was used as cerebral malaria model. Melatonin treatment (5 and 10 mg/kg) was performed for four consecutive days after the infection, and data have shown an increased survival rate in infected mice treated with melatonin. It was also observed that melatonin treatment blocked brain edema and prevented the breakdown of blood-brain barrier induced by theinfection. Furthermore, hematoxylin and eosin staining revealed that melatonin mitigates the histological alterations in-infected animals. Melatonin was also able to prevent motor and cognitive impairments in infected mice. Taken together, these results show for the first time that melatonin treatment prevents histological brain damages and neurocognitive alterations induced by cerebral malaria.

Study Type : Animal Study

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