The molecular biology of senile plaques and neurofibrillary tangles in Alzheimer’s disease

Research output: Contribution to journalArticle

View graph of relations Save citation

Open

Authors

  • Richard A. Armstrong

Research units

Abstract

Since the earliest descriptions of the disease, senile plaques (SP) and neurofibrillary tangles (NFT) have been regarded as the pathological 'hallmarks' of Alzheimer's disease (AD). Whether or not SP and NFT are sufficient cause to explain the neurodegeneration of AD is controversial. The major molecular constituents of these lesions, viz., beta-amyloid (Ass) and tau, have played a defining role both in the diagnosis of the disease and in studies of pathogenesis. The molecular biology of SP and NFT, however, is complex with many chemical constituents. An individual constituent could be the residue of a pathogenic gene mutation, result from cellular degeneration, or reflect the acquisition of new proteins by diffusion and molecular binding. This review proposes that the molecular composition of SP and NFT is largely a consequence of cell degeneration and the later acquisition of proteins. Such a conclusion has implications both for the diagnosis of AD and in studies of disease pathogenesis.

Documents

Details

Original languageEnglish
Pages (from-to)289-99
Number of pages11
JournalFolia Neuropathologica
Volume47
Issue number4
Publication statusPublished - 29 Dec 2009

Bibliographic note

Creative Commons Attribution Non-Commercial Share Alike International 4.0

    Keywords

  • Alzheimer’s disease, senile plaque, neurofibrillary tangle, ß-amyloid, molecular composition, gene mutation, disease pathogenesis

Download statistics

No data available

Employable Graduates; Exploitable Research

Copy the text from this field...