Abstract
AD (Alzheimer's disease) is a neurodegenerative disorder characterized by the abnormal hyperphosphorylation and aggregation of the microtubule-associated protein tau and the misfolding and deposition of Abeta peptide. The mechanisms by which tau and Abeta become abnormal is not clearly understood, neither is it known what role either protein plays in the neurodegenerative process underlying AD. We have modelled aspects of AD in Drosophila melanogaster to shed light on these processes and to further our understanding of the relationship between tau and amyloid in this disease.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Alzheimer Disease / genetics
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Alzheimer Disease / pathology*
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Amyloid beta-Peptides / metabolism
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Amyloid beta-Peptides / physiology
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Animals
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Disease Models, Animal*
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Drosophila melanogaster* / genetics
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Drosophila melanogaster* / physiology
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Humans
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Models, Biological
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Nerve Degeneration / metabolism
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Nerve Degeneration / pathology
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Peptide Hydrolases / metabolism
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Phosphorylation
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Synaptic Transmission / physiology
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tau Proteins / metabolism
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tau Proteins / physiology
Substances
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Amyloid beta-Peptides
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tau Proteins
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Peptide Hydrolases