Taking Natural supplements containing:
Phosphatidylcholine (PC), Phosphatidylserine (PS), DHA, EPA, Acetyl-L-Carnitine (ALC), Vitamin B6, Iron, Magnesium, Zinc, Copper, chromium, Green Tea Extract, DMAE, , L- Tyrosine, Herb-of-Grace (Bacopa monnieri), DLPhenylalanine, Gatrodine (Gastrodia elata), Bioperine, Ginkgo Biloba, B-Complex, Eluthero (Siberian Ginseng) and Vinpocetine is a derivative of Vincamine, which is extracted from the periwinkle plant (Vinca Minor, Vinca Pervinca). .
Vinpocetine works in three remarkable ways:
It boosts blood circulation in your brain. It zeros in on your brain tiny blood vessels so they can deliver oxygen more efficiently. It even helps your brain use oxygen better.
Since it keeps your brain cells charged up with high oxygen levels, it increases the amount of time your brain can go without fresh oxygen. That means it can keep your brain cells healthy.
It helps your body preserve its energy for a robust brain and power for healthy living. It preserves something called adenosine triphosphate” or ATP the fuel every cell of your body needs to function.
Scientists are investigating several different dietary additions for people with dementia. Two of the most promising areas:
A clinical trial showed that vitamin E helps slow down mental impairment in people with Alzheimers. Vitamin E is an antioxidant, which helps protect cells against damage. It’s now being researched in conjunction with B vitamins.
A large 2005 study found that healthy people who consumed more than 400 micrograms (the recommended daily amount for adults) of folate, a B vitamin that occurs naturally in many foods, cut their risk of developing Alzheimer’s in half. This slowing of cognitive decline is being looked at to see if it’s also true once decline has started.
This herb, traditionally used in Chinese medicine, comes from the dried leaves of the gingko (maidenhair) tree. It is sometimes called the “memory herb,” after findings that it appears to help slow down cognitive decline for some people in the early stages of Alzheimers disease. To date, research studies making this claim have been criticized, however, and a randomized clinical trial sponsored in part by the National Institute on Aging confirmed this.
A long-term reduction in neuronal activity reduces amyloid plaques associated with Alzheimer’s disease, Yale University researchers have found. The study, using mouse models of Alzheimer’s, found the opposite is also true – triggering an increase in neuronal activity spurs creation of plaques and toxic amyloid beta peptides believed to trigger the disease.
Research in the news: Hyperactive neurons may be culprit in Alzheimer’sIn the accompanying image, amyloid plaques in blue are surrounded by damaged neuronal branches.
Neuroscientists Jaime Grutzendler and Peng Yuan used a new technology called chemogenetics to alternately inhibit or excite neuronal signaling in mice with Alzheimer’s. The goal was to test the theory that hyperactivity in neurons might contribute to the onset of Alzheimer’s. Such an increase in neuronal activity might trigger the production of excess amounts of amyloid beta peptides, which in turn may be toxic to brain cells and cause the symptoms of dementia, Grutzendler said.