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10th Edition of International Conference on Neurology and Brain Disorders

October 21-23, 2024

October 21 -23, 2024 | Baltimore, Maryland, USA
INBC 2024

Temporal progression of inflammatory changes of microglia in the brain of rat model of alzheimer’s disease

Speaker at Neuroscience Conference - Kaneeka Chakraborty
Little Rock Central High School, United States
Title : Temporal progression of inflammatory changes of microglia in the brain of rat model of alzheimer’s disease

Abstract:

Background: Alzheimer’s Disease (AD) has been shown to lead to deposition of Amyloid Aβ plaques and neurofibrillary tangles (NFT) in the cerebral cortex and hippocampus of the brain. These have the potential to cause neurological damage and suggests a relationship to the neuropathology in an AD brain. To examine this, this study analyzes the characteristics of one of the key neurovascular units of the brain such as microglia in an AD brain. Microglia are macrophages in the brain that respond to pathogens and neurological damage, engaging in phagocytosis to regulate the brain environment. The Toll-like receptors (TLR) of the microglia recognize pathogens which leads to an ameboid shape and phagocytic response. The purpose of this study is to determine a causative relationship between the buildup of Amyloid Aβ plaques and the activation and proliferation of microglia.

Methods: Both transgenic AD and non-transgenic female rat brain sections 25 micron thin were used and stained with a microglial marker, IBA1. Brain sections were additionally stained with Congo Red (CR) which detects amyloid Aβ plaques. Microglia labeling was visualized under light microscope (Nikon), and the CR staining was visualized under the fluorescence microscope to determine whether the increase in amyloid Aβ plaques was related to the activation/proliferation of microglia. Further quantitative analysis was performed using Image J software.

Results: In transgenic rats, microglial size significantly increased over time in the hippocampal and cerebral cortex regions. On the contrary, in non-transgenic rats, microglial size increased in the hippocampus and cerebral cortex, but was not significant.

Conclusion: In AD brain sections, the hippocampus and cerebral cortex experienced a significant increase in microglial proliferation and inflammation over time. This was not seen in non-transgenic brain sections. This signifies a relationship between temporal changes of microglia during AD progression.

Biography:

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