Alzheimer's disease: Are cellular neurofibrillary tangles linked to beta/A4 formation at the projection sites?

Richard A. Armstrong

Research output: Contribution to journalArticle

Abstract

The density of senile plaques (SP) and cellular neurofibrillary tabgles (NFT) revealed by the Glees and Gallyas stains; and beta/A4 deposits revealed by immunocytochemical staining, was estimated in the hippocampus and adjacent gyri in Alzheimer's disease (AD). Stepwise multiple regression was used to detemine whether the density of cellular NFT was related to the density of SP or beta/A4 deposits totalled over the projection sites. Cellular NFT density was only weakly correlated with the density of Glees SP and beta/A4 deposits at some of the projection sites. However, beta/A4 deposit density in a tissue was strongly correlated with the density of beta/A4 deposits at the projection sites suggesting that the lesions could spread through the brain. Hence, although there is a strong correlation between the density of beta/A4 deposits in different parts of the hippocampal formation there is little association between SP or beta/A4 and cellular NFT. These results do not provide strong evidence that beta/A4 protein is the cause of the neuritc changes in AD.
Original languageEnglish
Pages (from-to)171-178
Number of pages8
JournalNeuroscience Research Communications
Volume11
Issue number3
Publication statusPublished - 1992

Fingerprint

Neurofibrillary Tangles
Amyloid Plaques
Alzheimer Disease
Parahippocampal Gyrus
Hippocampus
Coloring Agents
Staining and Labeling
Brain
Proteins

Keywords

  • Alzheimer's disease
  • beta/A4 deposits
  • senile plaques
  • neurofibrillary tangles
  • hippocampus
  • projection sites

Cite this

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title = "Alzheimer's disease: Are cellular neurofibrillary tangles linked to beta/A4 formation at the projection sites?",
abstract = "The density of senile plaques (SP) and cellular neurofibrillary tabgles (NFT) revealed by the Glees and Gallyas stains; and beta/A4 deposits revealed by immunocytochemical staining, was estimated in the hippocampus and adjacent gyri in Alzheimer's disease (AD). Stepwise multiple regression was used to detemine whether the density of cellular NFT was related to the density of SP or beta/A4 deposits totalled over the projection sites. Cellular NFT density was only weakly correlated with the density of Glees SP and beta/A4 deposits at some of the projection sites. However, beta/A4 deposit density in a tissue was strongly correlated with the density of beta/A4 deposits at the projection sites suggesting that the lesions could spread through the brain. Hence, although there is a strong correlation between the density of beta/A4 deposits in different parts of the hippocampal formation there is little association between SP or beta/A4 and cellular NFT. These results do not provide strong evidence that beta/A4 protein is the cause of the neuritc changes in AD.",
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Alzheimer's disease: Are cellular neurofibrillary tangles linked to beta/A4 formation at the projection sites? / Armstrong, Richard A.

In: Neuroscience Research Communications, Vol. 11, No. 3, 1992, p. 171-178.

Research output: Contribution to journalArticle

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T1 - Alzheimer's disease: Are cellular neurofibrillary tangles linked to beta/A4 formation at the projection sites?

AU - Armstrong, Richard A.

PY - 1992

Y1 - 1992

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AB - The density of senile plaques (SP) and cellular neurofibrillary tabgles (NFT) revealed by the Glees and Gallyas stains; and beta/A4 deposits revealed by immunocytochemical staining, was estimated in the hippocampus and adjacent gyri in Alzheimer's disease (AD). Stepwise multiple regression was used to detemine whether the density of cellular NFT was related to the density of SP or beta/A4 deposits totalled over the projection sites. Cellular NFT density was only weakly correlated with the density of Glees SP and beta/A4 deposits at some of the projection sites. However, beta/A4 deposit density in a tissue was strongly correlated with the density of beta/A4 deposits at the projection sites suggesting that the lesions could spread through the brain. Hence, although there is a strong correlation between the density of beta/A4 deposits in different parts of the hippocampal formation there is little association between SP or beta/A4 and cellular NFT. These results do not provide strong evidence that beta/A4 protein is the cause of the neuritc changes in AD.

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