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

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

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Facultad de Cs de la Salud, Universidad San Sebastian, Lientur 1457, Concepcion, 4030000, Chile.
Research and Development, Bay Pines VA Healthcare System, Bay Pines, FL, USA.
Departamento de Nutricion y Bioquimica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogota D.C., Colombia.
Center for Biomedical Research, Universidad Autonoma de Chile, Carlos Antunez 1920, Providencia, Santiago, Chile.
Institute of Pharmacy and Translational Medicine, Sechenov First Moscow State Medical University, 2-4 Bolshaya Pirogovskaya St., 119991 Moscow, Russia.
GALLY International Biomedical Research Consulting LLC San Antonio, TX, USA.
School of Health Science and Healthcare Administration, University of Atlanta, Johns Creek, Georgia, 30097, USA.
Institute of Physiologically Active Compounds Russian Academy of Sciences, Chernogolovka, 142432, Russia.



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.


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.


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

[Indexed for MEDLINE]

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