Role of nerve growth factor in plasticity of forebrain cholinergic neurons

Neuronal plastic rearrangements during the development and functioning of neurons are largely regulated by trophic factors, including nerve growth factor (NGF). NGF is also involved in the pathogenesis of Alzheimer’s disease. In the brain, NGF is produced in structures innervated by basal forebrain...

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Bibliographic Details
Published in:Biochemistry (Moscow) 2017-03, Vol.82 (3), p.291-300
Main Authors: Isaev, N. K., Stelmashook, E. V., Genrikhs, E. E.
Format: Article
Language:English
Subjects:
Alzheimer's disease
Animals
Biochemistry
Biomedical and Life Sciences
Biomedicine
Bioorganic Chemistry
Blood-brain barrier
Blood-Brain Barrier - metabolism
Brain research
Cholinergic Neurons - metabolism
Growth factors
Humans
Immune response
Life Sciences
Microbiology
Nerve growth factor
Nerve Growth Factor - metabolism
Neuronal Plasticity - physiology
Neurons
Neuroplasticity
Observations
Physiological aspects
Prosencephalon
Prosencephalon - metabolism
Review
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Summary:Neuronal plastic rearrangements during the development and functioning of neurons are largely regulated by trophic factors, including nerve growth factor (NGF). NGF is also involved in the pathogenesis of Alzheimer’s disease. In the brain, NGF is produced in structures innervated by basal forebrain cholinergic neurons and retrogradely transported along the axons to the bodies of cholinergic neurons. NGF is essential for normal development and functioning of the basal forebrain; it affects formation of the dendritic tree and modulates the activities of choline acetyltransferase and acetylcholinesterase in basal forebrain neurons. The trophic effect of NGF is mediated through its interactions with TrkA and p75 receptors. Experimental and clinical studies have shown that brain levels of NGF are altered in various pathologies. However, the therapeutic use of NGF is limited by its poor ability to penetrate the blood–brain barrier, adverse side effects that are due to the pleiotropic action of this factor, and the possibility of immune response to NGF. For this reason, the development of gene therapy methods for treating NGF deficit-associated pathologies is of particular interest. Another approach is creation of low molecular weight NGF mimetics that would interact with the corresponding receptors and display high biological activity but be free of the unfavorable effects of NGF.
ISSN:0006-2979
1608-3040
DOI:10.1134/S0006297917030075