STAR 2019: The Misregulation of Tip60 in the Tau Drosophila Alzheimer’s Disease Model
Alzheimer’s Disease (AD) is a prevalent neurodegenerative disorder. A common feature of AD in the brain is neurofibrillary tangles, which block axonal transport of neurons due to hyperphosphorylation of the Tau protein. Through the examination of the Tau fly line, a Drosophila AD model, it is possible to see if there are cognitive defects resulting from decreased levels of the histone acetyltransferase Tip60. Histone acetylation is an important epigenetic regulatory mechanism, so the misregulation of Tip60 is thought to play a role in AD. This project investigated whether the Tau fly model exhibits a neurodegenerative phenotype and whether this phenotype is due to misregulation of Tip60 and its target genes. Behavioral assays including learning and memory, gustatory, and olfactory were conducted to test the cognitive defects of the Tau model. qPCR was used to determine expression levels of Tip60 and its target genes. Our results show that the Tau model has decreased cognitive abilities in comparison to the wild type, and this is likely due to misregulation of Tip60. Further work should investigate if overexpression of Tip60 can rescue the disease phenotype in the Tau model.
Alzheimer’s Disease (AD) is a prevalent neurodegenerative disorder. A common feature of AD in the brain is neurofibrillary tangles, which block axonal transport of neurons due to hyperphosphorylation of the Tau protein. Through the examination of the Tau fly line, a Drosophila AD model, it is possible to see if there are cognitive defects resulting from decreased levels of the histone acetyltransferase Tip60. Histone acetylation is an important epigenetic regulatory mechanism, so the misregulation of Tip60 is thought to play a role in AD. This project investigated whether the Tau fly model exhibits a neurodegenerative phenotype and whether this phenotype is due to misregulation of Tip60 and its target genes. Behavioral assays including learning and memory, gustatory, and olfactory were conducted to test the cognitive defects of the Tau model. qPCR was used to determine expression levels of Tip60 and its target genes. Our results show that the Tau model has decreased cognitive abilities in comparison to the wild type, and this is likely due to misregulation of Tip60. Further work should investigate if overexpression of Tip60 can rescue the disease phenotype in the Tau model.