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Folic acid prevented cognitive impairment in experimental pneumococcal meningitis
Tatiana Barichello1, Jaqueline S Generoso, Lutiana R Simões
1Laboratório de Microbiologia Experimental, Programa de Pós-Graduação em Ciências da Saúde (PPGCS), Unidade Acadêmica de Ciências da Saúde (UNASAU), Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil, tba@unesc.net.
Abstract:
Streptococcus pneumoniae is a common cause of bacterial meningitis, with a high mortality rate and neurological sequelae. In contrast, folic acid plays an important role in neuroplasticity and the preservation of neuronal integrity. In the present study, we evaluated the influence of folic acid on memory, oxidative damage, enzymatic defence, and brain-derived neurotrophic factor (BDNF) expression in experimental pneumococcal meningitis. In animals that received folic acid at a dose of 10 or 50 mg, there was a reduction in both crossing and rearing during an open-field task compared with the training session, demonstrating habituation memory. During a step-down inhibitory avoidance task, there was a difference between the training and the test sessions, demonstrating aversive memory. In the hippocampus, BDNF expression decreased in the meningitis group; however, adjuvant treatment with 10 mg of folic acid increased BDNF expression, decreased lipid peroxidation, protein carbonylation, nitrate/nitrite levels, and myeloperoxidase activity and increased superoxide dismutase activity. In frontal cortex adjuvant treatment with 10 mg of folic acid decreased lipid peroxidation and protein carbonylation. There is substantial interest in the role of folic acid and related pathways in nervous system function and in folic acid's potential therapeutic effects. Here, adjuvant treatment with vitamin B9 prevented memory impairment in experimental pneumococcal meningitis.
Insights
Folic acid (vitamin B9) supplementation prevented memory deficits in experimental pneumococcal meningitis. This neuroprotective effect was linked to reduced oxidative stress and increased brain-derived neurotrophic factor (BDNF).
Area of Science:
- Neuroscience
- Pharmacology
- Infectious Diseases
Background:
- Streptococcus pneumoniae causes bacterial meningitis with high mortality and neurological damage.
- Folic acid is crucial for neuroplasticity and maintaining neuronal health.
- Pneumococcal meningitis leads to memory impairment and oxidative stress in the brain.
Purpose of the Study:
- To investigate folic acid's impact on memory, oxidative damage, and neurotrophic factors in experimental pneumococcal meningitis.
- To assess the therapeutic potential of folic acid (vitamin B9) as an adjuvant treatment.
Main Methods:
- Experimental pneumococcal meningitis model in animals.
- Behavioral tests (open-field, step-down inhibitory avoidance) to assess memory.
- Biochemical analysis of oxidative stress markers (lipid peroxidation, protein carbonylation, nitrate/nitrite) and enzymatic activity (superoxide dismutase, myeloperoxidase) in brain tissues.
- Measurement of brain-derived neurotrophic factor (BDNF) expression.
Main Results:
- Meningitis induced memory impairment, decreased BDNF expression, and increased oxidative damage.
- Folic acid treatment (10 mg/kg) reversed memory deficits.
- Folic acid administration increased BDNF levels and antioxidant enzyme activity (superoxide dismutase).
- Folic acid reduced markers of oxidative stress (lipid peroxidation, protein carbonylation, nitrate/nitrite) and inflammation (myeloperoxidase) in the hippocampus and frontal cortex.
Conclusions:
- Adjuvant folic acid treatment effectively prevented memory impairment in experimental pneumococcal meningitis.
- Folic acid demonstrates neuroprotective effects by mitigating oxidative stress and enhancing BDNF expression.
- Vitamin B9 holds therapeutic promise for managing neurological complications associated with bacterial meningitis.
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