ISLAMABAD – Scientists now have an explanation for why green tea is good for the brain - it lies in the chemical properties that affect the production of brain cells, improving memory and spatial learning.

“Green tea is a popular beverage across the world,” said Yun Bai, professor from the Third Military Medical University, Chongqing, China.

“There has been plenty of scientific attention on its use in helping prevent cardiovascular diseases, but now there is emerging evidence that its chemical properties may impact cellular mechanisms in the brain.”

Yun’s team focused on the organic chemical EGCG, (epigallocatechin-3 gallate) a key property of green tea. While EGCG is a known antioxidant, the team believed it could also have a beneficial effect against age-related degenerative diseases, the journal Molecular Nutrition and Food Research reports.

“We proposed that EGCG can improve cognitive function by impacting the generation of neuron cells, a process known as neurogenesis,” said Yun.

“We focused our research on the hippocampus, the part of the brain which processes information from short-term to long-term memory.”

The team found that ECGC boosts the production of neural progenitor cells, which like stem cells can adapt, or differentiate, into various types of cells. The team then used lab mice to discover if this increased cell production gave an advantage to memory or spatial learning, according to a Medical University statement.

“We ran tests on two groups of mice, one which had imbibed ECGC and a control group (without ECGC),” said Yun.

“First the mice were trained for three days to find a visible platform in their maze. Then they were trained for seven days to find a hidden platform.”

The team found that the ECGC treated mice required less time to find the hidden platform. Overall the results revealed that EGCG enhances learning and memory by improving object recognition and spatial memory.

Sleep disorders early signs of Alzheimer’s disease

A pattern of disturbed sleep could be an early warning sign of Alzheimer’s disease, suggest scientists.

Working on a mouse model, researchers from the Washington University School of Medicine in St. Louis, found that when the first signs of Alzheimer’s plaques appear in the brain, the normal sleep-wake cycle is significantly disrupted.

“If sleep abnormalities begin this early in the course of human Alzheimer’s disease, those changes could provide us with an easily detectable sign of pathology,” said senior study author David M Holtzman, professor and head of neurology at Washington, the journal Science Translational Medicine reported. “As we start to treat Alzheimer’s patients before the onset of dementia, the presence or absence of sleep problems may be a rapid indicator of whether the new treatments are succeeding,” added the scientist. Holtzman’s lab was among the first to link sleep problems and Alzheimer’s through studies of sleep in mice genetically altered to develop Alzheimer’s plaques as they age, according to a university statement.

In a 2009 study, he showed that brain levels of a primary component of the plaques naturally rise when healthy young mice are awake and drop after they go to sleep. Depriving the mice of sleep disrupted this cycle and accelerated the development of brain plaques.

A similar rising and falling of the plaque component, a protein called amyloid beta, was later detected in the cerebrospinal fluid of healthy humans studied by co-author Randall Bateman, professor of neurology at Washington University.

The new research, led by Jee Hoon Roh, neurologist and postdoctoral fellow in Holtzman’s lab, shows that when the first indicators of brain plaques appear, the natural fluctuations in amyloid beta levels stop in both mice and humans.

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Mice are nocturnal animals and normally sleep for 40 minutes during every hour of daylight, but when Alzheimer’s plaques began forming in their brains, their average sleep times dropped to 30 minutes per hour.

Vitamin D supplement won’t help in short term

Taking vitamin D supplements to compensate for its deficiency did not lower LDL or bad cholesterol levels - not at least in the short term - suggests new research. Researchers from The Rockefeller University, New York, studied 151 people with vitamin D deficiency who received either a mega-dose (50,000 internationals units) of vitamin D3 or placebo (substance containing zero medication) weekly for eight weeks.

Their cholesterol levels were measured before and after treatment.

Correcting vitamin D deficiencies with high doses of oral vitamin D supplements did not change LDL levels.

This was despite effectively increasing vitamin D to recommended levels, the journal “Arteriosclerosis, Thrombosis and Vascular Biology,” reports.

High levels of bad cholesterol or LDL begin to build up on your artery walls, along with other fats and debris. This build up is called plaque. Over time, plaque can cause narrowing of the arteries or atherosclerosis, which is usually the precursor of heart disease.

Vitamin D levels were nearly tripled in the group that received actual supplements, but were unchanged in the placebo group, according to a Rockefeller statement.

“Our study challenges the notion that vitamin D repletion improves cholesterol levels,” said Manish Ponda, assistant professor of clinical investigation in Jan Breslow’s lab of biochemical genetics and metabolism at The Rockefeller.

“For example, participants receiving vitamin D who had an increase in calcium levels experienced a seven percent increase in LDL (bad) cholesterol, while those whose calcium levels fell or did not change had a five percent decrease in LDL cholesterol. These clinical trial results confirm those from a recent data mining study,” Ponda, who led the study, said.