NERVE GROWTH-FACTOR IN ALZHEIMERS-DISEASE - INCREASED LEVELS THROUGHOUT THE BRAIN COUPLED WITH DECLINES IN NUCLEUS BASALIS

Citation
Sa. Scott et al., NERVE GROWTH-FACTOR IN ALZHEIMERS-DISEASE - INCREASED LEVELS THROUGHOUT THE BRAIN COUPLED WITH DECLINES IN NUCLEUS BASALIS, The Journal of neuroscience, 15(9), 1995, pp. 6213-6221
Citations number
63
Categorie Soggetti
Neurosciences,Neurosciences
Journal title
ISSN journal
02706474
Volume
15
Issue
9
Year of publication
1995
Pages
6213 - 6221
Database
ISI
SICI code
0270-6474(1995)15:9<6213:NGIA-I>2.0.ZU;2-E
Abstract
The current study analyzed NGF protein levels in the brains of patient s with Alzheimer's disease (AD) as compared with aged neurologically n ormal individuals. An established two-site ELISA was used to measure N GF-like immuno-reactivity in the hippocampus, superior temporal gyrus, superior frontal gyrus, inferior parietal lobule, frontal and occipit al 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 b ank (University of Cincinnati, Rush Presbyterian St, Luke's Medical Ce nter in Chicago, or University of Alabama at Birmingham), NGF-like act ivity was at least moderately increased with AD in virtually every bra in region examined except for the nbM, in which significant declines w ere observed. NGF levels were also increased when compared with age-ma tched Parkinson's cases (frontal cortex). NGF-like activity was not re lated to age at onset or disease duration in AD cases, nor did NGF lev els correlate with age at death in the control or AD groups. Correlati ons between ChAT and NGF-like activity across brains Varied considerab ly and were generally not significant. The present findings indicate t hat AD is characterized by a widespread increase in cortical and subco rtical NGF. Although a correlation with ChAT activity was not observed in cortex, the AD-related decline in NGF found in nbM is consistent w ith the possibility of impaired retrograde transport of NGF to this re gion.