Nerve growth factor in metabolic complications and Alzheimer's disease: Physiology and therapeutic potential
Open accessAbstract
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.
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The accumulation of proNGF and downregulation of TrkA levels favor the predominance of pro-apoptotic signaling mediated by p75NTR, further promoting degeneration of basal forebrain cholinergic neurons.
“The accumulation of proNGF and downregulation of TrkA (pro-survival signal) levels favor the predominance of pro-apoptotic signaling mediated by p75NTR, further promoting the degeneration of basal forebrain cholinergic neurons.346,347”
From Recent advances in Alzheimer's disease: Mechanisms, clinical trials and new drug development strategies. (2024) · cites this paper as [347]
Section 5.3 says proNGF accumulates, TrkA expression is lower in AD and MCI, and reduced TrkA shifts proNGF binding toward p75 and apoptosis. Section 2.1 identifies basal forebrain cholinergic neurons as NGF-dependent, but the copy does not directly link this proNGF–p75 shift to their degeneration; that final, neuron-specific step is an inference. (LLM, conf=0.85)
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References 220 · Cited by 36
Research works printed but not linked: 1
- H. Thoenen, C. Bandtlow, R. Heumann, The Physiological Function of Nerve Growth Factor in the Central Nervous System: Comparison with the Periphery, in: Reviews of Physiology, Biochemistry and Pharmacology, 109 Springer, Berlin Heidelberg, 1987, pp. 145-178.
- Authors
- Ding, X.-W., Li, R., Geetha, T., Tao, Y.-X., & Babu, J. R.
- Affiliations
- Auburn University (US)
- Auburn University System (US)
- Corresponding author
- Tao, Ya-Xiong
- Babu, Jeganathan Ramesh
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2020-10
- Volume
- 1866
- Issue
- 10
- Pages
- 165858
- ISSN
- 0925-4439 (ISSN-L)
- OpenAlex
- W3034546606
- Cited by
- 36
- References
- 220
- Citations by year
- 2026: 6 · 2025: 6 · 2024: 8 · 2023: 7 · 2022: 7 · 2021: 2
- FWCI
- 0.55
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion, other-oa)
- PubMed (publishedVersion)
- Funders
- Alabama Agricultural Experiment Station
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- nerve growth factor, proNGF, TrkA, p75 neurotrophin receptor, neurotrophic signaling, obesity, diabetes complications, Alzheimer's disease, cognitive decline, metabolic disorders, neuroprotection, therapeutic potential
- MeSH terms
- Dependovirus, Alzheimer Disease, Animals, Brain, Cognition, Diabetic Neuropathies, Diabetic Retinopathy, Disease Models, Animal, Genetic Vectors, Humans, Nerve Growth Factors, Obesity, Ophthalmic Solutions, Protein Precursors, Genetic Therapy, Signal Transduction, Parvovirinae, Receptor, trkA, Nerve Growth Factor, Mice, Rats, Adipokines, Neural Stem Cells, Cell- and Tissue-Based Therapy
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