Thesis
Effects of Coriander Leaves Extract on GABA Level and GABAA Receptor Gene Expression in Scopolamine-induced Memory-impaired Mice Model
Alzheimer’s disease (AD) is a chronic neurodegenerative disease affecting cognition and memory. The
exact cause of AD remains unclear, but two primary theories have been suggested to explain its
cause: the cholinergic and amyloid hypothesis. The extracellular deposition of amyloid-beta (Aβ) and
intracellular accumulation of phosphorylated tau protein called neurofibrillary tangles (NFTs) along
with neuronal and synaptic loss have been recognized as hallmarks of AD. Current treatments for AD
are largely ineffective and often have significant side effects, highlighting the need for novel
therapies. The GABAergic system has emerged as a potential target for AD treatment. Changes in the
GABAergic system in AD patients, including reduced GABA levels and altered GABAAR subunit
expression, have been documented. Coriander (Coriandrum sativum L.) leaf extract has shown
potential in improving memory in mice, potentially through interactions with GABAARs. This study
aimed to investigate whether coriander leaf extract exerts its neuroprotective effects by modulating
the GABAergic system. To achieve that aim, this study evaluated the effects of coriander leaf extract
on GABA levels using LC-MS/MS, and GABAAR subunit gene expression using qRT-PCR in
scopolamine-induced memory-impaired mice model. However, issues with the scopolamine model
prevented this assessment. The administered scopolamine dose was insufficient to produce the
significant molecular changes anticipated in AD. Future research should focus on optimizing the
scopolamine dose to induce appropriate molecular changes associated with AD.
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