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Journal of Neuroscience, Vol 15, 6213-6221, Copyright © 1995 by Society for Neuroscience
Nerve growth factor in Alzheimer's disease: increased levels throughout the brain coupled with declines in nucleus basalis
SA Scott, EJ Mufson, JA Weingartner, KA Skau and KA Crutcher
Department of Neurosurgery, University of Cincinnati, Ohio, USA.
The current study analyzed NGF protein levels in the brains of patients
with Alzheimer's disease (AD) as compared with aged neurologically normal
individuals. An established two-site ELISA was used to measure NGF-like
immunoreactivity in the hippocampus, superior temporal gyrus, superior
frontal gyrus, inferior parietal lobule, frontal and occipital cortical
poles, cerebellum, amygdala, putamen, and nucleus basalis of Meynert (nbM).
ChAT activity was assayed in adjacent tissue samples. NGF levels were also
evaluated in Parkinson's disease for comparison with both AD and
age-matched control cases. Regardless of the brain bank (University of
Cincinnati, Rush Presbyterian St. Luke's Medical Center in Chicago, or
University of Alabama at Birmingham), NGF-like activity was at least
moderately increased with AD in virtually every brain region examined
except for the nbM, in which significant declines were observed. NGF levels
were also increased when compared with age- matched Parkinson's cases
(frontal cortex). NGF-like activity was not related to age at onset or
disease duration in AD cases, nor did NGF levels correlate with age at
death in the control or AD groups. Correlations between ChAT and NGF-like
activity across brains varied considerably and were generally not
significant. The present findings indicate that AD is characterized by a
widespread increase in cortical and subcortical NGF. Although a correlation
with ChAT activity was not observed in cortex, the AD-related decline in
NGF found in nbM is consistent with the possibility of impaired retrograde
transport of NGF to this region.
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