Sesame seed extract shows promise for Parkinson’s
Around 1 million people in the United States and 10 million people worldwide have Parkinson’s. It's the second most usual neurodegenerative disorder after Alzheimer’s disease.
Parkinson’s disease is a progressive brain disorder that influences dopamine-producing neurons. It causes tremors, muscular stiffness or rigidity, and slowness of movements, among other symptoms.
Reduction and degeneration of dopamine-producing neurons in a specific region of the mind called the substantia nigra triggers the movement-related, or “motor,” symptoms that can characterize Parkinson’s.
There is no cure for Parkinson’s disease, though several prescription drugs can help alleviate the symptoms. The mostly prescribed medication for this purpose is levodopa (Sinemet), which replenishes dopamine levels.
“Currently, there is no preventive medicine for Parkinson’s disease,” notes Dr. Akiko Kojima-Yuasa, an associate professor at the Graduate School of Individuals Life Technology at Osaka City University, in Japan, “we just have coping treatments.”
One reason behind cell damage in the substantia nigra is oxidative stress. This led Dr. Kojima-Yuasa and colleagues to research whether sesaminol, a robust antioxidant, could prevent nerve cell fatality in a model of Parkinson’s.
Sesaminol is situated in abundance in sesame seed husks, which are a waste material product from the professional extraction of sesame oil.
Oxidative damage
The researchers used a toxic chemical called 6-hydroxydopamine to model the oxidative damage occurring in Parkinson’s.
If they applied the chemical to individuals nerve skin cells growing in lab cultures, the concentration of damaging reactive oxygen species increased, and the skin cells began to pass away off.
Adding sesaminol to the cultures significantly reduced the concentration of reactive oxygen species and prevented cell death. Sesaminol appeared to shield the cells from oxidative destruction by increasing their development of two protective proteins: Nrf2 and NQO1.
Next, the researchers turned to a typical animal style of Parkinson’s disease, that involves dosing mice with the neurotoxin rotenone.
The toxin reduces dopamine creation in the animals’ brains. This impairs their motor capabilities and reduces their gut motility, that are both basic symptoms of Parkinson’s in humans. Actually, people with the disease might experience constipation decades before problems with movement become visible.
Mice that ate an eating plan containing sesaminol for 36 days had higher dopamine levels and performed better on a standard test of motor abilities than control-group mice that ate a standard diet. The gut motility of the mice in the test group was also normal.
Furthermore, the mice that ate sesaminol had lower degrees of alpha-synuclein in their substantia nigras. Alpha-synuclein is a protein that clumps alongside one another to form greater set ups called Lewy bodies, which are a quality feature of neurodegeneration in Parkinson’s.
Source: www.medicalnewstoday.com
