The dark chocolate story again: Very good for grossly mistreated mice

Dark chocolate can reduce brain damage following a stroke, a study suggests. Scientists have discovered that a compound called epicatechin, commonly found in dark chocolate, protects the brain against strokes by shielding nerve cells.

They based their findings on tests in mice and hope the effects can be replicated in humans. The U.S. researchers gave the mice a dose of epicatechin - a flavanol - and then 90 minutes later induced a stroke in the animals by cutting off the blood supply to their brains.

They found that the mice that had taken the epicatechin had 'significantly less' brain damage than those that had not.

The researchers, from Johns Hopkins University in Baltimore, Maryland, also discovered that epicatechin had a protective effect when given to mice after they had a stroke....

Researchers from America's Johns Hopkins University say the findings could be important in the possible treatment of strokes.

Associate Professor Sylvain Doré said: 'Animals that had preventively ingested the epicatechin suffered significantly less brain damage than the ones that had not been given the compound.

'While most treatments against stroke in humans have to be given within a two- to three-hour time window to be effective, epicatechin appeared to limit further neuronal damage when given to mice 3.5 hours after a stroke.

'Given six hours after a stroke, however, the compound offered no protection to brain cells.'

Professor Doré said the finding could a step forward in our understanding of strokes. 'I hope this research into these pathways could lead to insights into limiting acute stroke damage and possibly protecting against chronic neurological degenerative conditions, such as Alzheimer's disease and other age-related cognitive disorders.

'The amount of dark chocolate people would need to consume to benefit from its protective effects remains unclear, because we have not studied it in clinical trials. 'People shouldn't take this research as a free pass to go out and consume large amounts of chocolate, which is high in calories and fat.

The study has been published in the Journal of Cerebral Blood Flow and Metabolism.

Professor Doré said scientists have been intrigued by the potential health benefits of epicatechin by studying the Kuna Indians, a remote population living on islands off the coast of Panama.

He added: 'The islands' residents had a low incidence of cardiovascular disease. Scientists who studied them found nothing striking in the genes and realized that when they moved away from Kuna, they were no longer protected from heart problems.

'Researchers soon discovered the residents of Kuna regularly drank a very bitter cocoa drink, with a consistency like molasses, instead of coffee or soda. The drink was high in the compound epicatechin.'

But Professor Doré said the amount of epicatechin needed could end up being quite small because the suspected beneficial mechanism was indirect.

He explained: 'Epicatechin itself may not be shielding brain cells from free radical damage directly, but instead, epicatechin, and its metabolites, may be prompting the cells to defend themselves.'

SOURCE






Powerful new drugs that could 'switch on' memory in the brain giving hope to Alzheimer's sufferers

A memory 'masterswitch' has been identified in the brain, raising hopes of powerful new drugs to treat Alzheimer's and other diseases.

When the switch is turned off by ageing and illness, memories fade. But when a drug is used to flick the switch back on, the brain's ability to store information dramatically improves.

Triggering the switch in mice led to elderly creatures regaining the memory power of their youth, the journal Science reports.

The researchers are confident that a similar switch exists in the human brain - and say that drugs that capitalise on their discovery could be in use in ten years. The drug used on the mice, Vorinostat, is already used to treat a rare blood cancer but is too destructive for use in the human brain.

There is an urgent need for new Alzheimer's treatments because the number of Britons affected by the disease is forecast to double from the current 400,000 within a generation.

Current drugs can halt the progression of the disease but do not work for everyone and their effects wear off over time.

Researcher André Fischer said: 'This is a very important development. It will not cure Alzheimer's alone - that will require many different approaches - but it could certainly help.'

Dr Fischer, of the European Neuroscience Institute in Goettingen, Germany, pinpointed a tiny protein called H4K12 that controls genes key to memory and learning in the mouse brain. He said: 'The drug companies need to know what they need to specifically target for Alzheimer's disease. 'I am pretty optimistic that in at least the next ten years we are going to have some good stuff we can actually use.'

In an accompanying article, Professor David Sweatt , a U.S. neurobiologist, said that turning on H4K12 was likely to help with both Alzheimer's and age-related memory loss. He said the German results 'provide important proof of principle that this might be a viable approach to therapeutic interventions in ageing'.

'These studies will hopefully lead to more effective prevention strategies to improve quality of life in the aged, as well as contribute to a better understanding of memory function,' he added.

The treatment of other brain conditions, such as schizophrenia and Parkinson's disease, could be improved by finding other switches that act in a similar way.

Dr Marie Janson, of the Alzheimer's Research Trust, said: 'Although in mice, this research gives us clues about how memories are formed and function in the brain. 'We now need to find out if the same processes happen in the human brain. 'This understanding is vital if we are to develop ways to protect the ageing brain from cognitive decline.

'Alzheimer's and other dementias are complex, with many things happening in the brain, so it's likely that we'll need several drugs to treat them effectively. 'We hope that these findings will stimulate further research towards developing new dementia treatments that are so urgently needed.'

Professor Clive Ballard, of the Alzheimer's Society, said: 'A lot more work is needed to see how this links to later life diseases such as Alzheimer's disease.' He added: 'One in three people will die with dementia yet dementia research is desperately under-funded.'

SOURCE