Investigating the role that astrocytes play in mediating changes in synaptic health in Alzheimer's disease
Başlık çevirisi mevcut değil.
- Tez No: 721621
- Danışmanlar: Belirtilmemiş.
- Tez Türü: Yüksek Lisans
- Konular: Nöroloji, Psikiyatri, Psikoloji, Neurology, Psychiatry, Psychology
- Anahtar Kelimeler: Belirtilmemiş.
- Yıl: 2020
- Dil: İngilizce
- Üniversite: King's College London
- Enstitü: Yurtdışı Enstitü
- Ana Bilim Dalı: Belirtilmemiş.
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: 64
Özet
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Özet (Çeviri)
Alzheimer's Disease (AD), the leading cause of dementia, is pathologically characterised by amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs), which are composed of extracellular amyloidal protein deposits and abnormally phosphorylated tau protein, respectively. Furthermore, reactive astrocytes have been demonstrated near Aβ plaques, and their presence is concordant with neuroinflammation. Reactive astrocytes respond to chronic neuroinflammation by releasing a number of inflammatory cytokines and chemotactic cytokines (chemokines), including CXCL1, which is a ligand for the receptor CXCR2, both of which are overly expressed in AD brain. More recently, it has been shown that CXCL1 is involved in tau phosphorylation in AD. Phosphorylated tau is found in the somatodendritic parts of neurons in AD brain in contrast to its axonal location in healthy brain and it's highly correlated with the pre-and postsynaptic dysregulations. Previous research in our lab showed that CXCL1 reduced the spine density in primary mice neuronal cultures via the receptor CXCR2. In this study, we further examined whether CXCL1 has any specific synaptotoxic impacts on the density of mushroom, stubby, and thin spines in AD through its receptor CXCR2 and we investigated if such effects are through the missorting of tau protein into somatodendritic compartments via the receptor CXCR2. Here we report that a decreasing trend was found in the density of mushroom, stubby, and thin spines following CXCL1 exposure. However, in contrast to our hypothesis, CXCL1 reduced tau mislocalisation in the dendritic compartments. Moreover, antagonising the receptor CXCR2 eliminated the effects of CXCL1 on both tau mislocalisation and given spine densities, suggesting that CXCL1 implemented its effects through the interaction with the receptor CXCR2. However, the precise mechanisms underlying the effects of ligand CXCL1 pairing with the receptor CXCR2 on tau pathology, spine loss and neuronal health remain elusive.
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