Munteanu, Mihai (2025) IL-1β, TNF-α, and C1q as Drivers of A1 Astrocyte Transformation in Alzheimer’s Disease. Bachelor's Thesis, Biology.
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Abstract
Alzheimer’s disease (AD) is the most common form of dementia, characterised by gradual cognitive decline and neurodegeneration. Traditionally, the research field has focused on amyloid-beta (Aβ) plaques and tau tangles as the primary pathological hallmarks of AD. However, growing evidence suggests that chronic neuroinflammation due to glial cell dysfunction plays a critical role in disease onset and progression. Among these glial cells, microglia and astrocytes are recognised as the main contributors to this neurotoxicity. Thus, this thesis focuses on the communication between microglia and astrocytes, particularly the microglia-derived cytokines IL-1β, TNF-α and C1q and how they contribute to astrocyte dysfunction to induce the neurotoxic A1 astrocyte phenotype in AD. Overall, this review concludes that the microglia transitioning to a chronically activated state while astrocytes transform into the A1 phenotype due to the secretion of microglial cytokines. The role of AD-risk genes, more specifically TREM2, APOE, and CD33 is also discussed. Overall, this review concludes that the microglia-astrocyte communication axis via IL-1β, TNF-α, and C1q is a critical mechanism driving neurodegeneration in AD. Understanding the glial crosstalk offers potential in AD therapies, but targeting these pathways requires precision to avoid disrupting essential immune functions.
| Item Type: | Thesis (Bachelor's Thesis) |
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| Supervisor name: | Eisel, U.L.M. and Kortholt, A. |
| Degree programme: | Biology |
| Thesis type: | Bachelor's Thesis |
| Language: | English |
| Date Deposited: | 05 Aug 2025 05:58 |
| Last Modified: | 05 Aug 2025 05:58 |
| URI: | https://fse.studenttheses.ub.rug.nl/id/eprint/36643 |
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