[Genetic expression of nerve growth factor in the central nervous system. Evaluation of an experimental model for Alzheimer's dementia].
OBJECTIVE
Several authors have suggested that loss of neuronal trophic support may be an important element in the physiopathology of degenerative conditions of the central nervous system such as Alzheimer's dementia, Parkinson's disease or amyotrophic lateral sclerosis amongst others. In the light of present knowledge, the survival of cholinergic populations of the anterior basal cerebrum, closely involved with cognitive processes of memory and learning, is associated with adequate function of the neural growth factor (NGF). These populations are markedly damaged in Alzheimer's disease, and this has been correlated with the progressive loss of memory and intellectual involvement seen in this disorder. The model used in this study was based on section of the septohippocampal connecting pathways, so that transport of regulatory impulses from the hippocampus to the medial septum was interrupted. This has lethal results for the cholinergic neurons of the latter. We have developed a study designed to characterize the expression of the gene of NGF in different regions of the brain, involved in cholinergic neurotransmission in healthy and in damaged tissue.


METHODS
We used a molecular hybridization technique with a cDNA catheter complementary to the radio-isotope marked NGF human gene.


CONCLUSIONS
The highest levels of expression were found in the healthy cortex and hippocampus. The reduction in the levels of mRNA of NGF in the damaged hippocampus supports the current thesis which considers synaptic activity to be a major regulator of the synthesis of this molecule in the brain.
González-Hoyuela
M
M
Departamento de Biología Molecular, Centro Internacional de Restauración Neurológica (CIREN), Ciudad de la Habana, Cuba. cineuro@neuro.slod.cu
Soto
J
J
García-Milian
R
R
Ubieta
R
R
Francis
L
L
Conde-Vázquez
R
R
D000544:Alzheimer Disease; D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism*; D002799:Cholinergic Fibers / Q000378:metabolism; D018076:DNA, Complementary / Q000235:genetics; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D006624:Hippocampus / Q000293:injuries / Q000378:metabolism*; D006801:Humans; D008297:Male; D009414:Nerve Growth Factors / Q000096:biosynthesis* / Q000235:genetics; D009419:Nerve Tissue Proteins / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017207:Rats, Sprague-Dawley; D012688:Septum Pellucidum / Q000293:injuries
D018076:DNA, Complementary; D009414:Nerve Growth Factors; D009419:Nerve Tissue Proteins; D012333:RNA, Messenger