Abstract
Neurofibrillary tangles are composed of insoluble aggregates of the microtubule-associated protein tau. In Alzheimer's disease the accumulation of neurofibrillary tangles occurs in the absence of tau mutations. Here we present mice that develop pathology from non-mutant human tau, in the absence of other exogenous factors, including beta-amyloid. The pathology in these mice is Alzheimer-like, with hyperphosphorylated tau accumulating as aggregated paired helical filaments. This pathologic tau accumulates in the cell bodies and dendrites of neurons in a spatiotemporally relevant distribution.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Age Factors
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Alternative Splicing
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Alzheimer Disease / genetics
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Alzheimer Disease / metabolism*
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Alzheimer Disease / pathology
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Animals
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Brain / metabolism
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Brain / pathology
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Brain Chemistry
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Dendrites / metabolism
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Dendrites / pathology
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Disease Models, Animal
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Humans
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Macromolecular Substances
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Mice
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Mice, Transgenic
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Neurofibrillary Tangles / chemistry
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Neurofibrillary Tangles / metabolism
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Neurofibrillary Tangles / pathology
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Neurons / metabolism
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Neurons / pathology
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Phosphorylation
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Protein Isoforms / genetics
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Protein Isoforms / metabolism
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Reverse Transcriptase Polymerase Chain Reaction
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tau Proteins / genetics*
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tau Proteins / metabolism*
Substances
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Macromolecular Substances
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Protein Isoforms
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tau Proteins