Nerve growth factor in metabolic complications and Alzheimer's disease: Physiology and therapeutic potential

Xiao-Wen Ding; Rongzi Li; Thangiah Geetha; Ya-Xiong Tao; Jeganathan Ramesh Babu

doi:10.1016/j.bbadis.2020.165858

Nerve growth factor in metabolic complications and Alzheimer's disease: Physiology and therapeutic potential

Biochim Biophys Acta Mol Basis Dis. 2020 Oct 1;1866(10):165858. doi: 10.1016/j.bbadis.2020.165858. Epub 2020 Jun 10.

Authors

Xiao-Wen Ding¹, Rongzi Li¹, Thangiah Geetha², Ya-Xiong Tao³, Jeganathan Ramesh Babu⁴

Affiliations

¹ Department of Nutrition, Dietetics, and Hospitality Management, Auburn University, Auburn, AL 36849, USA.
² Department of Nutrition, Dietetics, and Hospitality Management, Auburn University, Auburn, AL 36849, USA; Boshell Metabolic Diseases and Diabetes Program, Auburn University, Auburn, AL 36849, USA.
³ Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, AL 36849, USA. Electronic address: taoyaxi@auburn.edu.
⁴ Department of Nutrition, Dietetics, and Hospitality Management, Auburn University, Auburn, AL 36849, USA; Boshell Metabolic Diseases and Diabetes Program, Auburn University, Auburn, AL 36849, USA. Electronic address: jeganrb@auburn.edu.

PMID: 32531260
DOI: 10.1016/j.bbadis.2020.165858

Abstract

As the population ages, obesity and metabolic complications as well as neurological disorders are becoming more prevalent, with huge economic burdens on both societies and families. New therapeutics are urgently needed. Nerve growth factor (NGF), first discovered in 1950s, is a neurotrophic factor involved in regulating cell proliferation, growth, survival, and apoptosis in both central and peripheral nervous systems. NGF and its precursor, proNGF, bind to TrkA and p75 receptors and initiate protein phosphorylation cascades, resulting in changes of cellular functions, and are associated with obesity, diabetes and its complications, and Alzheimer's disease. In this article, we summarize changes in NGF levels in metabolic and neuronal disorders, the signal transduction initiated by NGF and proNGF, the physiological and pathophysiological relevance, and therapeutic potential in treating chronic metabolic diseases and cognitive decline.

Keywords: Alzheimer's disease; Diabetic neuropathy; Diabetic retinopathy; NGF; Obesity; proNGF.

Publication types

Research Support, Non-U.S. Gov't
Review

MeSH terms

Adipokines / metabolism
Alzheimer Disease / etiology
Alzheimer Disease / metabolism
Alzheimer Disease / pathology*
Alzheimer Disease / therapy
Animals
Brain / drug effects
Brain / pathology
Cell- and Tissue-Based Therapy / methods
Cognition / drug effects
Cognition / physiology
Dependovirus
Diabetic Neuropathies / etiology
Diabetic Neuropathies / metabolism
Diabetic Neuropathies / pathology*
Diabetic Neuropathies / therapy
Diabetic Retinopathy / etiology
Diabetic Retinopathy / metabolism
Diabetic Retinopathy / pathology*
Diabetic Retinopathy / therapy
Disease Models, Animal
Genetic Therapy / methods
Genetic Vectors / administration & dosage
Genetic Vectors / genetics
Humans
Mice
Nerve Growth Factor / administration & dosage
Nerve Growth Factor / genetics
Nerve Growth Factor / metabolism*
Nerve Growth Factors / metabolism
Neural Stem Cells / transplantation
Obesity / complications*
Obesity / metabolism
Obesity / pathology
Obesity / therapy
Ophthalmic Solutions / administration & dosage
Parvovirinae / genetics
Protein Precursors / administration & dosage
Protein Precursors / metabolism*
Rats
Receptor, trkA / metabolism
Signal Transduction

Substances

Adipokines
NGF protein, human
Nerve Growth Factors
Ngf protein, rat
Ophthalmic Solutions
Protein Precursors
pro-nerve growth factor, human
pro-nerve growth factor, mouse
pro-nerve growth factor, rat
Nerve Growth Factor
Receptor, trkA

Supplementary concepts

Adeno-associated virus-2