Green tea has always been considered synonymous with health thanks to its anticancer, anti-diabetes, anti-obesity and anti-inflammatory properties. But green tea is also neuroprotective and it has been observed that its consumption is inversely proportional to the incidence of diseases such as Alzheimer's, Parkinson's and dementia. But what happens when these diseases are already present? Well, as evidenced by a scientific research published in The Journal of Nutrition by a team from Iowa State University, the active ingredient in green tea, epigallocatechin gallate, has shown the ability to help recover the functionality of neurons in the process of degeneration once Parkinson's disease was already present.
Parkinson's disease is a disease characterized by the degeneration of dopaminergic neurons in the substantia nigra. The reason why these neurons undergo degeneration seems to be due to three factors, namely oxidative stress, chronic inflammation and iron accumulation. Epigallocatechin gallate, the most abundant polyphenol in green tea, is an antioxidant, fights free radicals and inflammation and counteracts the accumulation of iron. The scientists then tried to understand what could happen in animals with the intake of epigallocatechin gallate in a situation where Parkinson's was already present. What emerged, compared to the control group that had not received the supplement, was that epigallocatechin gallate was able to restore the behavioral and neurochemical deficit, thus reversing the degeneration process, counteracting oxidative stress and regulating the transit of iron.
This study does not speak of cups of green tea but of supplements of the pure active ingredient, epigallocatechin gallate, which should always be taken under medical supervision. In addition, it is a preliminary study that requires further investigation. In any case, it is certainly useful to show that a so scented and tasty drink such as green tea can be included in one's daily diet to fight free radical damage and to protect the brain by trying to prevent neuron degeneration.
