Is VEGF a Key Target of Cotinine and Other Potential Therapies Against Alzheimer Disease?

Curr Alzheimer Res. 2017;14(11):1155-1163. doi: 10.2174/1567205014666170329113007.

Abstract

Background: The vascular endothelial growth factor (VEGF) is a neuroprotective cytokine that promotes neurogenesis and angiogenesis in the brain. In animal models, it has been shown that environmental enrichment and exercise, two non-pharmacological interventions that are beneficial decreasing the progression of Alzheimer disease (AD) and depressive-like behavior, enhance hippocampal VEGF expression and neurogenesis. Furthermore, the stimulation of VEGF expression promotes neurotransmission and synaptic plasticity processes such as neurogenesis. It is thought that these VEGF actions in the brain, may underly its beneficial therapeutic effects against psychiatric and other neurological conditions.

Conclusion: In this review, evidence linking VEGF deficit with the development of AD as well as the potential role of VEGF signaling as a therapeutic target for cotinine and other interventions in neurodegenerative conditions are discussed.

Keywords: Alzheimer disease; VEGF; amyotrophic lateral sclerosis; angiogenesis; cotinine; dementia; depression; neurodegeneration; nicotinic receptors; tobacco.

Publication types

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

MeSH terms

  • Alzheimer Disease / drug therapy*
  • Alzheimer Disease / metabolism*
  • Animals
  • Cotinine / pharmacology
  • Cotinine / therapeutic use*
  • Humans
  • Neuroprotective Agents / pharmacology
  • Neuroprotective Agents / therapeutic use*
  • Vascular Endothelial Growth Factor A / metabolism*

Substances

  • Neuroprotective Agents
  • Vascular Endothelial Growth Factor A
  • Cotinine