Relationship of neurofibrillary pathology to cerebral amyloid angiopathy in Alzheimer's disease

Over 90% of patients with Alzheimer's disease (AD) develop cerebral amyloid angiopathy (CAA). Severe dyshoric CAA, in which amyloid extends into the surrounding brain parenchyma, may be associated with adjacent clustering of tau‐immunopositive neurites but the relationship of CAA to neurofibril...

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Bibliographic Details
Published in:Neuropathology and applied neurobiology 2005-08, Vol.31 (4), p.414-421
Main Authors: Williams, S., Chalmers, K., Wilcock, G. K., Love, S.
Format: Article
Language:English
Subjects:
Aged
Aged, 80 and over
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Alzheimer's disease
Amyloid beta-Peptides - metabolism
apolipoprotein E
Apolipoproteins E - genetics
Arteries - metabolism
Arteries - pathology
Arterioles - metabolism
Arterioles - pathology
Biological and medical sciences
Brain - blood supply
Brain - pathology
cerebral amyloid angiopathy
Cerebral Amyloid Angiopathy - metabolism
Cerebral Amyloid Angiopathy - pathology
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Female
Genotype
Human viral diseases
Humans
Image Processing, Computer-Assisted
Immunohistochemistry
Infectious diseases
Male
Medical sciences
Middle Aged
neurofibrillary tangles
Neurofibrillary Tangles - metabolism
Neurofibrillary Tangles - pathology
Neurology
Phosphorylation
tau
tau Proteins - metabolism
Viral diseases
Viral diseases of the nervous system
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Summary:Over 90% of patients with Alzheimer's disease (AD) develop cerebral amyloid angiopathy (CAA). Severe dyshoric CAA, in which amyloid extends into the surrounding brain parenchyma, may be associated with adjacent clustering of tau‐immunopositive neurites but the relationship of CAA to neurofibrillary pathology has not been systematically investigated. In the present study this relationship was examined in sections of frontal, temporal and parietal cortex from 25 AD patients with moderate to severe CAA and 26 with mild or absent CAA. We measured immunolabelling of abnormally phosphorylated tau adjacent to Aβ‐laden and non‐Aβ‐laden arteries and arterioles, and in cortex away from arteries and arterioles. We also analysed the possible influence of APOE genotype on these measurements. There were no significant differences between the lobes in measurements of tau labelling, either around blood vessels or elsewhere in the cortex. However, tau labelling around Aβ‐laden arteries and arterioles significantly exceeded that around non‐Aβ‐laden blood vessels (P 
ISSN:0305-1846
1365-2990
DOI:10.1111/j.1365-2990.2005.00663.x