Microglial activation and the fight against Amyloid β in late-onset Alzheimer’s

Broeke, Jesse ten (2025) Microglial activation and the fight against Amyloid β in late-onset Alzheimer’s. Bachelor's Thesis, Biology.

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Abstract

Alzheimer’s disease is the leading cause of dementia, with late-onset Alzheimer’s disease (LOAD) accounting for the majority of cases. A key feature of the disease is the build-up of amyloid-β (Aβ) plaques in the brain, which contributes to cognitive decline. Microglia, the brain’s primary immune cells, play a central role in responding to these plaques. They work by identifying and clearing Aβ through a process called phagocytosis. Their function is guided by several surface receptors, including TLR2 (Toll-like receptor 2) and TAM (Gas6/Tyro3-Axl-Mer receptors) receptors (Axl and Mer), which help them recognize and remove harmful substances. However, when overactivated, these responses can become harmful, contributing to ongoing inflammation and damage. Recent research shows that microglia are more complex than once thought. Rather than falling neatly into “good” (anti-inflammatory) or “bad” (pro-inflammatory) categories, like previously believed, microglia show a wide range of states that change depending on the environment and disease stage. One important discovery is the presence of disease-associated microglia (DAMs), which become activated in response to Aβ plaques. This shift in state is regulated by genes such as TREM2 and APOE, which are known to influence the risk of developing Alzheimer’s. These genetic risk factors can affect how well microglia respond to damage and clear plaques, making them important targets for future research and therapy. Ultimately, the thesi

Item Type:	Thesis (Bachelor's Thesis)
Supervisor name:	Eisel, U.L.M.
Degree programme:	Biology
Thesis type:	Bachelor's Thesis
Language:	English
Date Deposited:	26 Jun 2025 07:35
Last Modified:	26 Jun 2025 07:35
URI:	https://fse.studenttheses.ub.rug.nl/id/eprint/35542

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