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Journal ArticleDOI

Accumulation of abnormally phosphorylated τ precedes the formation of neurofibrillary tangles in Alzheimer's disease

TLDR
It is suggested that the accumulation of abnormally phosphorylated tau is one of the earliest cytoskeletal changes in the process of tangle formation and exposure of certain ubiquitin epitopes in the pathological fibers may reflect an unsuccessful attempt of proteolytic degradation.
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This article is published in Brain Research.The article was published on 1989-01-16. It has received 808 citations till now. The article focuses on the topics: Neurofibrillary tangle & Tau protein.

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Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry.

TL;DR: To better meet the demands of routine laboratories this procedure is revised here by adapting tissue selection and processing to the needs of paraffin-embedded sections and by introducing a robust immunoreaction (AT8) for hyperphosphorylated tau protein that can be processed on an automated basis.
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Staging of Alzheimer's disease-related neurofibrillary changes.

TL;DR: Specific immunocytochemical methods (AT8) permit evaluation of neuronal changes well before the actual formation of neurofibrillary tangles and neuropil threads, which facilitates recognition of even subtle pathologic changes throughout the entire extent of cortical territories such as the transentorhinal and entorHinal regions.
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Frequency of Stages of Alzheimer-Related Lesions in Different Age Categories

TL;DR: The arithmetic means of the stages of both the amyloid-depositing and the neurofibrillary pathology increase with age, and age is a risk factor for Alzheimer's disease.
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Life and Death of Neurons in the Aging Brain

TL;DR: The qualitative and quantitative differences between aging and Alzheimer's disease with respect to neuron loss are discussed, and age-related changes in functional and biochemical attributes of hippocampal circuits that might mediate functional decline in the absence of neuron death are explored.
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Inflammation as a central mechanism in Alzheimer's disease

TL;DR: An overview of inflammation in AD is provided and a detailed coverage of a number of microglia‐related signaling mechanisms that have been implicated in AD are reviewed.
References
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Journal ArticleDOI

Abnormal phosphorylation of the microtubule-associated protein tau (tau) in Alzheimer cytoskeletal pathology

TL;DR: It is suggested that tau in Alzheimer brain is an abnormally phosphorylated protein component of PHF, the two major locations of paired-helical filaments in Alzheimer disease brain.
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Fine structural localization of a blood-brain barrier to exogenous peroxidase

TL;DR: These findings localize, at a fine structural level, a "barrier" to the passage of peroxidase at the endothelium of vessels in the cerebral cortex in mice, particularly with reference to a recent study in which similar techniques were applied to capillaries in heart and skeletal muscle.
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Microtubule-associated protein tau. A component of Alzheimer paired helical filaments.

TL;DR: Human brain tau and paired helical filament polypeptides co-migrated on sodium dodecyl sulfate-polyacrylamide gels suggest that tau is a major component of Alzheimer paired helicals filaments.
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The distribution of tau in the mammalian central nervous system.

TL;DR: Observations indicate that tau may help define a subpopulation of microtubules that is restricted to axons, and the monoclonal antibody described in this report should prove very useful to investigators studying axonal sprouting and growth because it is an exclusive axonal marker.
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