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Abstract
We have examined the various diverse morphologies of catecholamine axons in the brains
of patients with Alzheimer's disease. Alzheimer's disease and aged control brain tissue
were obtained by a rapid autopsy protocol (mean postmortem delay < 1 h). Tissue blocks
from the superior frontal cortex (Brodmann area 9), the hippocampal gyrus, and the
calcarine cortex (Brodmann area 17) were processed for identification of catecholamine
axons using tyrosine hydroxylase immunocytochemistry. A total of 1275 tyrosine hydroxylase
immunoreactive axons were randomly sampled from coded sections and classified into
one of six distinct axon-type categories. The axon classification from patients with
Alzheimer's disease significantly differed from those of an age-matched control population
in the hippocampus. The Alzheimer's disease brains were decreased in the frequency
of very long, thin, tyrosine hydroxylase immunoreactive axons (type 1) and had an
increased frequency of shorter, tortuous, axons (type 3). These selective quantitative
shifts in hippocampal catecholaminergic axon morphology are consistent with the hypothesis
that sympathetic noradrenergic axons invade the hippocampus of patients with Alzheimer's
disease. Multivariate modeling of the frequency sampling data found that the axon
type classification scheme successfully predicted the presence of Alzheimer's disease.
In particular, the use of quantitative neuroanatomical measures of the catecholaminergic
system in human brain tissue was found to have errorless predictive ability with respect
to late onset (> 75 years) Alzheimer's disease. In summary, the use of quantitative
neuroanatomical measures of catecholamine axonal morphologies in Alzheimer's disease
brain tissue identified a specific frequency shift which may represent hippocampal
sympathetic ingrowth and this unique measure was found to have predictive utility
with respect to Alzheimer's disease.
Keywords
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Article info
Publication history
Accepted:
April 18,
1993
Received in revised form:
April 13,
1993
Received:
October 15,
1992
Identification
Copyright
© 1993 Published by Elsevier Inc.