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Immunolocalisation of beta-amyloid precursor protein to plaque-associated synaptic alterations in the early and late stages of Alzheimer's disease

Citation

Saunders, HL and Dickson, TC and Vickers, JC, Immunolocalisation of beta-amyloid precursor protein to plaque-associated synaptic alterations in the early and late stages of Alzheimer's disease, Alzheimer's Reports, 1, (2) pp. 111-118. ISSN 1461-6130 (1998) [Refereed Article]

Abstract

Extracellular deposition of insoluble β-amyloid protein into plaque-like structures is a key pathological feature of Alzheimer's disease (AD). A fundamental issue is the origin of the β-amyloid that comprises plaques and how this relates to the neuronal and synaptic alterations associated with this disease. Multiple labelling immunohistochemistry was utilised to localise β-amyloid precursor protein (APP), relative to β-amyloid, synaptic proteins and markers for the staging of cytoskeletal changes underlying neurofibrillary pathology. Clusters of APP labelled globular structures were present in a subset (3-45%) of neocortical β-amyloid plaques in both AD and preclinical AD cases. A higher proportion of plaques in layers V and VI were associated with APP labelled pathological structures than plaques in layers II and III. In contrast, virtually no plaques in layer I were associated with APP labelled structures. Double labelling verified that the clusters of APP immunoreactive elements did not occur in the absence of β-amyloid deposits. Furthermore, the APP labelled globular structures were localised to a subset of neuritic plaques. At a cellular level, APP immunoreactivity colocalised with a synaptic marker, chromogranin A, but not with the neuritic abnormalities labelled with antibodies to neurofilaments or tau. These data indicate that the clusters of APP immunoreactive material are unlikely to contribute towards the β-amyloid misprocessing that leads to the development of plaques in AD. Alternatively, APP labelling may be a marker for reactive synaptogenesis, possibly in response to the neuritic damage caused by plaque formation. © MSJ.

Item Details

Item Type:Refereed Article
Research Division:Medical and Health Sciences
Research Group:Neurosciences
Research Field:Neurology and Neuromuscular Diseases
Objective Division:Health
Objective Group:Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:Nervous System and Disorders
Author:Saunders, HL (Ms Helen Louise Saunders)
Author:Dickson, TC (Associate Professor Tracey Dickson)
Author:Vickers, JC (Professor James Vickers)
ID Code:14697
Year Published:1998
Web of Science® Times Cited:5
Deposited By:Pathology
Deposited On:1998-08-01
Last Modified:2011-08-09
Downloads:0

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