Therapist Unlimited Blog

Here is a piece of good news to those persons suffering from dementia and Alzheimer’s disease.
A recent study has shown that a group of chemicals found in many fruits and vegetables, as well as tea, cocoa and red wine could protect the brain from Alzheimer’s disease.
Alzheimer’s disease is a devastating, progressive disorder affecting an estimated 15-20 million people worldwide.
Over the past four decades, through worldwide research efforts, it is now known that in the brains of people with Alzheimer’s disease there are abnormal cellular processes which lead to neurodegeneration and dementia. Understanding these disease processes at the molecular level will allow the development of pharmacological agents to block these processes, and lead the way for effective therapies in Alzheimer’s disease.
Central to the development of Alzheimer’s disease is toxic beta-amyloid peptide, a substance that is normally produced in the brain but, in this disease, is deposited abnormally as amyloid plaques.
Dr. Robert Williams, a Biochemist working at Kings College London revealed that while much more research needs to be done, there is mounting evidence that certain flavonoids chemicals found in plants and food derived from plants - might provide therapeutic benefit for Alzheimer’s sufferers.
Williams told the media in a recent interview that there have been some intriguing epidemiological studies that the consumption of flavonoid-rich vegetables, fruit juices and red wine delays the onset of the disease.
He said these reports, while not as powerful as controlled, randomized clinical trials, have encouraged a number of research groups, including our own, to investigate the biology of flavonoids in more detail.
The medical expert revealed a lack of good research and clinical trial data meant this field of research had suffered from a lack of scientific credibility, not helped by early positive health claims for flavonoids that cannot access the brain or are broken down too rapidly by the body to be of any benefit.
The medical expert added skepticism also persists because flavonoids are known antioxidants and yet clinical trials with other antioxidants, such as vitamin E, showed no reported benefit on either symptoms or disease progression in dementia.
Williams said a new concept is emerging that suggests flavonoids do not act simply as antioxidants but exert their biological effects through other mechanisms.

To all those persons suffering from dementia and Alzheimer’s disease it is time to consume tea, cocoa and red wine since they contain flavonoid which could treat your sickness.

He said a small number of recent studies carried out in models of Alzheimer’s disease have found that oral administration of green tea flavonoids or grape flavonoids reduces brain pathology and, in some cases, improves cognition. Dr Williams and colleagues have focused their own cellular studies on a flavonoid called epicatechin, which is abundant in a number of foodstuffs, including cocoa.
Furthermore, Williams said he and his team found that epicatechin protects brain cells from damage but through a mechanism unrelated to its antioxidant activity and shown in laboratory tests that it can also reduce some aspects of Alzheimer’s disease pathology.
Williams said their findings is very interesting because epicatechin and its breakdown products are measurable in the bloodstream of humans for a number of hours after ingestion and it is one of the relatively few flavonoids known to access the brain suggesting it has the potential to be bioactive in humans.
He said flavonoids can protect brain cells against the toxic actions of beta-amyloid.
He adds: "Although our findings support the general concept that dietary intake of flavonoid-rich foods or supplements could impact on the development and progression of dementia, they are clearly insufficient to make any sort of nutritional recommendations at this stage.
Williams said the challenge now is to identify the single flavonoid or combination of flavonoids that exert the most positive effects and to define the mechanisms of action and optimal quantity required before embarking on clinical trials to treat their effectiveness in dementia.