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Neurochemical Diversity of Dystrophic Neurites in the Early and late Stages of Alzheimer's Disease

Citation

Dickson, TC and King, CE and McCormack, GH and Vickers, JC, Neurochemical Diversity of Dystrophic Neurites in the Early and late Stages of Alzheimer's Disease, Experimental Neurology, 156, (1) pp. 100-110. ISSN 0014-4886 (1999) [Refereed Article]

DOI: doi:10.1006/exnr.1998.7010

Abstract

We examined the neurochemical and morphological diversity of abnormal neurites associated with β-amyloid plaque formation in the early and late stages of Alzheimer's disease. Preclinical Alzheimer's disease was characterised by the presence of abnormal neurites containing either neurofilament or chromogranin A immunoreactivity. All clustered dystrophic neurites in these cases were associated with β-amyloid plaques. Neurofilament immunoreactive dystrophic neurites in preclinical Alzheimer's disease could be further subclassified into bulb- and ring-like structures, and these abnormal neurites contained both phosphorylated and dephosphorylated neurofilament epitopes. Dystrophic neurites in Alzheimer's disease could be subdivided into predominantly neurofilament, tau, or chromogranin A immunolabeled forms. Some neurofilament immunoreactive neurites had a core region labeled for tau. The neurofilaments of the dystrophic neurites in Alzheimer's disease had the same complement of phosphorylation- and dephosphorylation-dependent epitopes as observed in preclinical cases. Therefore, an abnormal accumulation of variably phosphorylated neurofilaments represent the earliest cytoskeletal alteration associated with dystrophic neurite formation. Furthermore, these data indicate that dystrophic neurites may 'mature' through neurofilament-abundant forms to the neurites containing the profoundly altered filaments labeled for tau. The precise morphological and neurochemical changes associated with dystrophic neurite formation suggests that β-amyloid plaques are causing physical damage to surrounding axons. The resultant axonal sprouting and profound cytoskeletal alterations would follow the chronic stimulation of the stereotypical reaction to such physical trauma.

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:Dickson, TC (Professor Tracey Dickson)
Author:King, CE (Dr Carolyn King)
Author:McCormack, GH (Mr Graeme McCormack)
Author:Vickers, JC (Professor James Vickers)
ID Code:17592
Year Published:1999
Web of Science® Times Cited:81
Deposited By:Pathology
Deposited On:1999-08-01
Last Modified:2000-05-26
Downloads:0

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