Scott S.A., Mufson E.J., Weingartner J.A., Skau K.A. and Crutcher K.A. (1995). Nerve growth factor in Alzheimer's disease: increased levels throughout the brain coupled with declines in nucleus basalis. Journal of Neuroscience15,(9), 6213-21.
Abstract
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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