Uric Acid Boosts Brain Cell Growth and Function in Parkinson’s Disease

Published on June 2, 2022

Imagine your brain as a city, and the neurons are the bustling citizens. In Parkinson’s disease, this city experiences a slowdown in growth and development due to reduced neurogenesis, the process of creating new neurons. But fear not, for uric acid (UA) is here to save the day! UA, a natural antioxidant, has been found to have neuroprotective properties in PD patients. In a recent study, researchers investigated whether increasing levels of UA could enhance neurogenesis in PD.This study used both animal and cellular models to explore the effects of UA on neurogenesis. In a parkinsonian mouse model, elevating serum UA levels led to a significant increase in the number of newly generated neurons in an area called the subventricular zone (SVZ). Similarly, in a cellular model using rat neural precursor cells, UA treatment promoted cell proliferation against a PD-associated toxin called MPP+.The researchers also uncovered some fascinating insights into how UA works its magic. They discovered that UA influenced mitochondrial dynamics, which are like the powerhouses of our cells. By regulating the fusion machinery of mitochondria, UA was able to boost neurogenesis and inhibit processes that hindered neuronal growth.Ultimately, this study highlights the potential of UA as a therapeutic approach to enhance brain cell growth and function in Parkinson’s disease. So why not dive deeper into this exciting research and explore how uric acid could help unlock new treatments for PD?

BackgroundAdult neurogenesis is the process of generating new neurons to enter neural circuits and differentiate into functional neurons. However, it is significantly reduced in Parkinson’s disease (PD). Uric acid (UA), a natural antioxidant, has neuroprotective properties in patients with PD. This study aimed to investigate whether UA would enhance neurogenesis in PD.MethodsWe evaluated whether elevating serum UA levels in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonian mouse model would restore neurogenesis in the subventricular zone (SVZ). For a cellular model, we primary cultured neural precursor cells (NPCs) from post-natal day 1 rat and evaluated whether UA treatment promoted cell proliferation against 1-methyl-4-phenylpyridinium (MPP+).ResultsUric acid enhanced neurogenesis in both in vivo and in vitro parkinsonian model. UA-elevating therapy significantly increased the number of bromodeoxyuridine (BrdU)-positive cells in the SVZ of PD animals as compared to PD mice with normal UA levels. In a cellular model, UA treatment increased the expression of Ki-67. In the process of modulating neurogenesis, UA elevation up-regulated the expression of mitochondrial fusion markers.ConclusionIn MPTP-induced parkinsonian model, UA probably enhanced neurogenesis via regulating mitochondrial dynamics, promoting fusion machinery, and inhibiting fission process.

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