Title:Chlorogenic Acid as a Neuroprotective Agent: Enhancing Plasticity and Promoting Brain Health and Functional Reserve
Volume: 25
Issue: 2
Author(s): Elizabeth Hernandez-Echeagaray*, Ruben Vazquez-Roque, Julio Cesar Morales-Medina, Francisco M. Torres-Cruz, Elibeth Monroy, Gumaro Galindo-Paredes, Gabriel Gutierrez-Ospina and Gonzalo Flores
Affiliation:
- Biomedicine Research Unit, Faculty of Higher Studies Iztacala, Universidad Nacional Autónoma de México, Av. De
Los Barrios, #1 Los Reyes Iztacala, C.P. 54090, Tlalnepantla de Baz, State of Mexico, México
Keywords:
Chlorogenic acid, neuroprotective, neurodegeneration nutraceutics, antioxidants, neurotrophins, polyphenols, plasticity, ProBDNF.
Abstract:
Introduction: Functional reserve, the process that warrants the brain to have resources to
maintain key functions and processes when facing neurodegeneration, may be strengthened in nominally
healthy subjects by measures that prompt neural plasticity throughout life.
Methods: In this work, we administered Chlorogenic Acid (CGA) to evaluate its ability to promote
functional morphological plasticity in the frontal cortical-striatal circuit of healthy mice, a pathway
exposed constantly to oxidative challenges, excitotoxicity, and neuroinflammation. The magnitude
of neural plasticity was estimated by assessing spontaneous motor behavior (open field), the relative
magnitude of neuronal activation (number of c-Fos positive neurons), dendritic remodeling (Golgi-
Cox impregnation), the availability of Brain-Derived Neurotrophic Factor (BDNF) (semiquantitative
Western blotting), and lipid peroxidation (TBARS assay) in CGA- or vehicle-administered
C57BL/6 male mice.
Results: CGA administration increased c-Fos in the Dorsal striatum (Ds), changed the availability
of BDNF and Pro-BDNF in the Frontal Cortex (FC) and Ds, induced dendritic remodeling in FC
and DS neurons, and reduced FC and DS lipid peroxidation without affecting motor performance or
the availability of TrkB receptor isoforms.
Conclusion: Our findings suggest that CGA increases functional reserve by promoting neuronal
plasticity in healthy male mice. Future research should determine whether these additional resources
indeed protect against neurodegeneration.
