Astaxanthin Helps Cognition, Parkinson’s, Alzheimer’s
Several recent studies are suggesting that a natural nutrient called Astaxanthin may well be part of the solution for cognitive impairment. This means helping conditions relating to neuron damage such as Parkinson’s disease and Alzheimer’s disease.
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Clinical research on Astaxanthin
Clinical research has supported this finding and more. Last year, researchers from the Graduate School of Medicine at Japan’s Juntendo University tested Astaxanthin using 96 elderly adult volunteers. In this randomized, double-blind and placebo-controlled study, the researchers gave the subjects either a capsule with Astaxanthin extract or a placebo for three months.
Before, after and every four weeks during the study, the researchers tested the subjects’ cognition, and found that those who took both dosages of Astaxanthin extract – 12 milligrams or 6 milligrams – scored significantly higher on learning and cognition testing than the placebo group.
The researchers concluded that, “the results suggested that astaxanthin-rich Haematococcus pluvialis extract improves cognitive function in the healthy aged individuals.”
Another study from Japan – this from the Life Science Institute – found among ten healthy adults that 12 milligrams a day of Astaxanthin significantly improves cognitive function and psychomotor functions.
Other clinical studies have found that Astaxanthin treatment significantly raises blood levels of carotene, and improves the health of circulating red blood cells – reducing free radical related damage that can eventually produce nerve and brain cell damage. Even low dosages of one and three milligrams a day have shown a strengthening effect among red blood cells.
Research headed up by Dr. Mark Tso from the University of Illinois determined that the antioxidant Astaxanthin concentrations in the blood stream effectively cross the blood-brain barrier, allowing its protective factors to become available directly to brain cells and central nervous system cells.
Astaxanthin deters nerve damage
Researchers from China’s Fujian Medical University tested a nutrient called Astaxanthin with nerve cells and found that the nutrient blocked the type of oxidative stress that has been identified as the primary cause of neuron damage that result in brain and nerve damage.
The researchers found that Astaxanthin blocked the MPP+ related Heme oxygenase process implicated in nerve and brain cell damage. This type of oxidative damage has been linked to Parkinson’s disease, Huntington’s disease and Alzheimer’s disease.
Other research has found that Astaxanthin comes with antioxidant properties from an estimated one hundred to one thousand times the antioxidant level of vitamin E. One of the richest natural sources of Astaxanthin is the algae Haematococcus pluvialis.
The Fujian Medical University researchers’ conclusion:
“ATX suppresses MPP+-induced oxidative stress in PC12 cells via the HO-1/NOX2 axis. ATX should be strongly considered as a potential neuroprotectant and adjuvant therapy for patients with Parkinson’s disease.”
Astaxanthin inhibits Parkinson’s process
Parkinson’s disease has been linked to damage to the brain’s dopaminergic nerve cells located in the motor region of the brain, called the substantia nigra pars compacta. Research has increasingly unfolded the process of oxidative stress related to radical damage.
Research from the Tokyo Metropolitan Institute of Gerontology found that Astaxanthin inhibited this oxidative process, concluding that Astaxanthin “markedly abolished 6-OHDA-induced reactive oxygen species generation.”
This oxidative stress process is related to the same process that damages brain cells in the hypothalamus – causing the beta-amyloid peptide (Abeta) oxidative process linked with the memory loss associated with Alzheimer’s disease.
A 2009 study from Taiwan’s Hungkuang University using brain cells, found that Astaxanthin suppressed about 75% of the reactive oxygen species production along with other parts of the oxidative process involved in the beta-amyloid production process found in Alzheimer’s disease.
REFERENCES:
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