Proteostasis denotes a cellular state in which protein synthesis,folding,and degradation are maintained at a homeostatic state such that an intact yet dynamic proteome is preserved.Cellular capacity to preserve proteo...Proteostasis denotes a cellular state in which protein synthesis,folding,and degradation are maintained at a homeostatic state such that an intact yet dynamic proteome is preserved.Cellular capacity to preserve proteostasis declines with age,which is assumed to contribute to the pathogenesis of age-related diseases.Proteostasis failure manifested as the formation of aberrant protein aggregates,including the amyloid plaques in Alzheimer’s disease(AD),Lewy bodies in Parkinson’s disease,and TAR DNA binging protein 43 inclusions in amyotrophic lateral sclerosis(ALS),is a defining feature of neurodegenerative diseases.展开更多
Background: Alzheimer’s disease (AD) is an increasingly prevalent neurodegenerative disease characterized by protein aggregation in the form of amyloid plaques containing beta-amyloid peptides and neurofibrillary tan...Background: Alzheimer’s disease (AD) is an increasingly prevalent neurodegenerative disease characterized by protein aggregation in the form of amyloid plaques containing beta-amyloid peptides and neurofibrillary tangles containing hyperphosphorylated tau protein. The central molecular events underlying AD pathogenesis remain controversial and poorly defined. Drosophila melanogaster has emerged as an important genetic resource for studying the pathology of AD. Many AD models have been created using Drosophila, taking advantage of its short generation times, sophisticated genetic tools, and abundance of homologs to human genes. Purpose: This review summarizes different models for studying AD in Drosophila melanogaster, including the full-length APP, C99, Aβ42 and Tau models, explaining how the models were built and what we have learned from them. Conclusion: Four main AD Drosophila models are introduced in this review, which can serve as a future method to investigate genes and drugs that can modify symptoms.展开更多
文摘Proteostasis denotes a cellular state in which protein synthesis,folding,and degradation are maintained at a homeostatic state such that an intact yet dynamic proteome is preserved.Cellular capacity to preserve proteostasis declines with age,which is assumed to contribute to the pathogenesis of age-related diseases.Proteostasis failure manifested as the formation of aberrant protein aggregates,including the amyloid plaques in Alzheimer’s disease(AD),Lewy bodies in Parkinson’s disease,and TAR DNA binging protein 43 inclusions in amyotrophic lateral sclerosis(ALS),is a defining feature of neurodegenerative diseases.
文摘Background: Alzheimer’s disease (AD) is an increasingly prevalent neurodegenerative disease characterized by protein aggregation in the form of amyloid plaques containing beta-amyloid peptides and neurofibrillary tangles containing hyperphosphorylated tau protein. The central molecular events underlying AD pathogenesis remain controversial and poorly defined. Drosophila melanogaster has emerged as an important genetic resource for studying the pathology of AD. Many AD models have been created using Drosophila, taking advantage of its short generation times, sophisticated genetic tools, and abundance of homologs to human genes. Purpose: This review summarizes different models for studying AD in Drosophila melanogaster, including the full-length APP, C99, Aβ42 and Tau models, explaining how the models were built and what we have learned from them. Conclusion: Four main AD Drosophila models are introduced in this review, which can serve as a future method to investigate genes and drugs that can modify symptoms.
