Abstract
The phosphorylation of normal tau by mitogen activated protein (MAP) or extracellular signal related kinases (ERKs) induces tau to acquire biochemical properties of Alzheimer's disease (AD) paired helical filament (PHF) proteins in vitro. We show here that a monoclonal antibody to MAP kinases recognizes ERK2 in normal and AD cortex, but ERK2 levels are slightly reduced in the AD brain. Since ERK2 was detected in neurofibrillary tangles and senile plaque neurites in the AD hippocampus, ERK2 is positioned to phosphorylate normal tau and could play a role in the generation of PHFs in AD.
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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Aged
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Aged, 80 and over
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Alzheimer Disease / enzymology*
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Alzheimer Disease / pathology
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Antibodies, Monoclonal / immunology
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Blotting, Western
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Enzyme Activation / drug effects
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Hippocampus / pathology
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Humans
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Middle Aged
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Mitogen-Activated Protein Kinase 1
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Mitogens / pharmacology
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Neurites / enzymology*
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Neurofibrillary Tangles / enzymology*
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Neurofibrillary Tangles / pathology
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Protein Serine-Threonine Kinases / immunology
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Protein Serine-Threonine Kinases / metabolism*
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tau Proteins / metabolism
Substances
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Antibodies, Monoclonal
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Mitogens
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tau Proteins
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Protein Serine-Threonine Kinases
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Mitogen-Activated Protein Kinase 1