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2000
Volume 22, Issue 6
  • ISSN: 1567-2050
  • E-ISSN: 1875-5828

Abstract

Introduction

Currently, there is no information on changes in the (), ), and () genes in the frontal cortex after brain ischemia with animal survival for 2 years. Furthermore, it is not known whether the and genes possess any influence on neurons in the frontal cortex due to ischemia.

Aims

The goal of the investigation was to evaluate alterations in the behavior of , and genes in the frontal cortex following ischemia with survival of 2 years.

Materials and Methods

Gene expression was assessed using an RT-PCR protocol at 2-30 days and 6-24-months after ischemia.

Results

gene expression after ischemic injury was lower than the control group during 7-30- days and 18 months, whereas overexpression was noted after 2 days, 6-, 12- and 24 months. In the case of gene expression, it was lower than the control group for 2-7 days and higher than the control throughout the remaining time after ischemia. Increased expression of the gene was observed except on days 7-30 following ischemia when its expression was lower compared to control values.

Discussion

The data seem to indicate that the observed changes in gene expression may reflect the activation and inhibition of different mechanisms involved in the advancement of neurodegeneration after ischemia.

Conclusion

Overexpression of gene is likely to be associated with the induction of neuroprotective phenomena, whereas overexpression of and genes can cause harmful effects.

© 2025 Bentham Science Publishers
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/content/journals/car/10.2174/0115672050385480250619045022
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Alterations of Mitophagy (BNIP3), Apoptosis (CASP3), and Autophagy (BECN1) Genes in the Frontal Cortex in an Ischemic Model of Alzheimer's Disease with Long-Term Survival
Curr Alzheimer Res 22, 442 (2025); https://doi.org/10.2174/0115672050385480250619045022
/content/journals/car/10.2174/0115672050385480250619045022
/content/journals/car/10.2174/0115672050385480250619045022
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  • Article Type:     Research Article
Keyword(s): Alzheimer’s disease; apoptosis; autophagy; Brain ischemia; frontal cortex; genes; long-term survival; mitophagy; neurodegeneration

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