TY - JOUR
T1 - NGF mRNA is not decreased in frontal cortex from Alzheimer's Disease patients
AU - Jetté, N.
AU - Cole, M. S.
AU - Fahnestock, M.
N1 - Funding Information:
We thank Rose Ann Bell and Lori t3. ]aylom' fo~ technical assistance. We also appreciate the generous gift of normal and Alzheimer's disease tissue from Drs. Dorothy G. Flood, Paul D. Coleman, and Robert ~. Hamill, University of Rochester Alzheimer's Disease Project and Rochester Alzheimer's Disease Center, University of Rochester, Rochester, NY., as well as normal frontal cortex tissue from Dr. Jan Borcich, VA Hospital, Martinez, CA. We thank Dr. D.(;. Flood and Dr. S. Scott for critical reading of the manuscript. This work was supported by grants to M.F. ft'om the National Institutes of Health (AG03644), from SRI International (870D32PUA and 665D32PUB,C), and from the Medical Research Council of Canada (MT116371. The Rochester Alzheimer's Disease Center is supported by National Institutes of Health ()rant AG08665.
PY - 1994/9
Y1 - 1994/9
N2 - Alzheimer's disease (AD) is characterized by neuronal dysfunction and degeneration in certain brain regions such as cortex, hippocampus and basal forebrain. Specific neurochemical defects such as decreases in cholinergic enzymes and in the amounts of mRNA in AD brain have also been reported. Nerve growth factor (NGF), a protein necessary for the development, regulation and survival of basal forebrain cholinergic neurons (BFCN), is synthesized in target areas of BFCN (cortex, hippocampus) and is supplied to BFCN by retrograde transport. Thus, NGF is under investigation both as a potential therapeutic agent and for its possible involvement in the pathogenesis of AD. In this study, postmortem brain tissues from both control and AD cases were investigated for amounts of poly (A)+ mRNA and NGF mRNA in the frontal cortex, a region rich in cholinergic afferents. Yields of poly(A)+ mRNA were similar from normal and AD tissues. Human NGF mRNA comigrated with murine NGF mRNA on Northern blots. Additionally, dot blot quantitation demonstrated that NGF mRNA levels do not differ in the inferior frontal gyrus of normal and AD patients. Thus, we conclude that levels of mRNA in general, and of NGF mRNA in particular, are unchanged in the frontal cortex of individuals affected by AD.
AB - Alzheimer's disease (AD) is characterized by neuronal dysfunction and degeneration in certain brain regions such as cortex, hippocampus and basal forebrain. Specific neurochemical defects such as decreases in cholinergic enzymes and in the amounts of mRNA in AD brain have also been reported. Nerve growth factor (NGF), a protein necessary for the development, regulation and survival of basal forebrain cholinergic neurons (BFCN), is synthesized in target areas of BFCN (cortex, hippocampus) and is supplied to BFCN by retrograde transport. Thus, NGF is under investigation both as a potential therapeutic agent and for its possible involvement in the pathogenesis of AD. In this study, postmortem brain tissues from both control and AD cases were investigated for amounts of poly (A)+ mRNA and NGF mRNA in the frontal cortex, a region rich in cholinergic afferents. Yields of poly(A)+ mRNA were similar from normal and AD tissues. Human NGF mRNA comigrated with murine NGF mRNA on Northern blots. Additionally, dot blot quantitation demonstrated that NGF mRNA levels do not differ in the inferior frontal gyrus of normal and AD patients. Thus, we conclude that levels of mRNA in general, and of NGF mRNA in particular, are unchanged in the frontal cortex of individuals affected by AD.
KW - Densitometry
KW - Dot blotting
KW - Inferior frontal gyrus
KW - Nerve growth factor
KW - Northern blotting
KW - Phosphorimage analysis
KW - Postmortem interval
KW - mRNA yields
UR - http://www.scopus.com/inward/record.url?scp=0028129444&partnerID=8YFLogxK
U2 - 10.1016/0169-328X(94)90159-7
DO - 10.1016/0169-328X(94)90159-7
M3 - Article
C2 - 7808223
AN - SCOPUS:0028129444
SN - 0169-328X
VL - 25
SP - 242
EP - 250
JO - Molecular Brain Research
JF - Molecular Brain Research
IS - 3-4
ER -