AI Article Synopsis
- Parkinson's disease (PD) and Alzheimer's disease (AD) involve neurodegeneration in specific brain areas, with angiotensin II (Ang II) contributing to neuron loss through oxidative stress.
- Captopril, an ACE inhibitor, was tested on Drosophila melanogaster expressing neurodegenerative peptides to assess its neuroprotective effects through various assays measuring motility and overall fitness.
- Results showed that captopril improved motility and climbing ability in Drosophila with neurodegeneration but did not significantly affect lifespan, supporting its potential as a neuroprotective agent.
Article Abstract
Background: Parkinson disease (PD) and Alzheimer's disease (AD) are progressive neurodegenerative disorders characterized by loss of selective neurons in discreet part of the brain. The peptide angiotensin II (Ang II) plays significant role in hippocampal and striatal neurons degeneration through the generation of reactive oxygen species. Blockade of the angiotensin converting enzyme or ATI receptors provides protection in animal models of neurodegenerative diseases. In the present study, the neuroprotective effect of captopril was investigated in Drosophila melanogaster model using the UAS-GAL4 system to express the synuclein and Aβ42 peptide in the flies' neurons.
Methods: The disease causing human Aβ42 peptide or α-syn was expressed pan-neuronally (elav-GAL4) or dopamine neuron (DDC-GAL4) using the UAS-GAL4 system. Flies were either grown in food media with or without captopril (1, 5, or 10µM). This was followed by fecundity, larva motility, negative geotaxis assay (climbing) and lifespan as a measure of neurodegeneration.
Results: Elav-Gal4
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http://dx.doi.org/10.54548/njps.v37i1.3 DOI Listing Publication Analysis
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