Dr. G. Saravanan
Head
Department of biochemistry
Wednesday, 22 February 2017
Wednesday, 15 February 2017
Grapes May
Help Fight Early Memory Decline in Alzheimer’s Disease
- A grape-enriched diet protected against memory decline
in Alzheimer's disease.
- Participants who consumed the grape-enriched diet
showed beneficial changes in regional brain metabolism that correlated to
improvements in cognition and working memory performance.
- Grape polyphenols help promote antioxidant and
anti-inflammatory activities.
- Grapes reduces oxidative stress and promotes healthy
blood flow in the brain.
Consuming grapes regularly for six months protected against
significant metabolic decline in Alzheimers disease. The related areas of the
brain which indicate early memory decline showed improvement.
Low metabolic
activity in these areas of the brain is a hallmark of early stage Alzheimer's
disease. Study results showed a grape-enriched diet protected against the
decline of metabolic activity.
Consuming grapes
for six months preserved healthy metabolic activity in the regions of the brain
that are affected by the earliest stages of Alzheimer's disease, where
metabolic decline takes hold.’
Additionally,
those consuming a grape-enriched diet also exhibited increased metabolism in
other areas of the brain that correlated with individual improvements in
attention and working memory performance, compared to those on the non-grape
diet.
"The study examines the impact of grapes as a whole fruit versus isolated compounds and the results suggest that regular intake of grapes may provide a protective effect against early decline associated with Alzheimer's disease," said Dr. Daniel H. Silverman, lead investigator of the study.
"The study examines the impact of grapes as a whole fruit versus isolated compounds and the results suggest that regular intake of grapes may provide a protective effect against early decline associated with Alzheimer's disease," said Dr. Daniel H. Silverman, lead investigator of the study.
Alzheimer's
disease is a brain disease that results in a slow decline of memory and
cognitive skills. Currently 5.4 million Americans are living with Alzheimer's
disease and the numbers continue to grow. The cause of Alzheimer's disease is
not yet fully understood, but believed to be a combination of genetic,
environmental and lifestyle factors.
"This pilot study contributes to the growing evidence that supports a beneficial role for grapes in neurologic and cardiovascular health, however more clinical studies with larger groups of subjects are needed to confirm the effects observed here."
In the study,
subjects with early memory decline were randomly selected to receive either
whole grape powder - equivalent to just 2 ¼ cups of grapes per day - or a
polyphenol-free placebo powder matched for flavor and appearance.
Cognitive performance was measured at baseline and 6 months later. Changes in brain metabolism, assessed by brain PET scans, were also measured at baseline and 6 months later. PET scans provide valuable predictive and diagnostic value to clinicians evaluating patients with dementia symptoms.
Cognitive performance was measured at baseline and 6 months later. Changes in brain metabolism, assessed by brain PET scans, were also measured at baseline and 6 months later. PET scans provide valuable predictive and diagnostic value to clinicians evaluating patients with dementia symptoms.
The results
showed that consuming grapes preserved healthy metabolic activity in the
regions of the brain that are affected by the earliest stages of Alzheimer's
disease, where metabolic decline takes hold.
Subjects who didn't consume grapes exhibited significant metabolic decline in these critical regions. Additionally, those consuming the grape-enriched diet showed beneficial changes in regional brain metabolism that correlated to improvements in cognition and working memory performance.
Grape polyphenols help promote antioxidant and anti-inflammatory activities. Research suggests that grapes may help support brain health by working in multiple ways - from reducing oxidative stress in the brain to promoting healthy blood flow in the brain to helping maintain levels of a key brain chemical that promotes memory to exerting anti-inflammatory effects.
Subjects who didn't consume grapes exhibited significant metabolic decline in these critical regions. Additionally, those consuming the grape-enriched diet showed beneficial changes in regional brain metabolism that correlated to improvements in cognition and working memory performance.
Grape polyphenols help promote antioxidant and anti-inflammatory activities. Research suggests that grapes may help support brain health by working in multiple ways - from reducing oxidative stress in the brain to promoting healthy blood flow in the brain to helping maintain levels of a key brain chemical that promotes memory to exerting anti-inflammatory effects.
Reference
- Daniel H. Silverman et al., Pilot study highlights role
of grapes in preventing Alzheimer's disease, Experimental Gerontology (2017)
http://dx.doi.org/10.1016/jexger.2016.10.004.
Sleeping
Helps Refresh Brain To Store More Information, Memories
- Sleep deprivation, sleep disorders and sleeping pills
can interfere with learning and memory.
- Information is contained in synapses, the connections
among neurons through which they communicate.
- Synapses are restructured throughout the mouse brain
every 12 hours.
- Scientists believe memories are encoded through these
synaptic changes and constant firing of information may tend to weaken the
capacity to convey information.
Ever wondered why we are often told to get adequate sleep
the night before an exam? Researchers at the Johns Hopkins University School of
Medicine find that a key purpose of sleep is to recalibrate the brain cells
responsible for learning and memory so the animals can "solidify"
lessons learned and use them when they awaken.
‘Sleep need is
controlled by adenosine, a chemical that accumulates in the brain as an animal
stays awake, provoking sleepiness.’
Diering focused on the areas of the mouse brain responsible
for learning and memory: the hippocampus and the cortex. He purified proteins
from receiving synapses in sleeping and awake mice, looking for the same
changes seen in lab-grown cells during scaling down.
Results showed a 20 percent drop in receptor protein levels in sleeping mice, indicating an overall weakening of their synapses, compared to mice that were awake.
"That was the first evidence of homeostatic scaling down in live animals," says Richard Huganir, Ph.D., professor of neuroscience, director of the Department of Neuroscience and lead author of the study. "It suggests that synapses are restructured throughout the mouse brain every 12 hours or so, which is quite remarkable."To learn specifically which molecules were responsible for the phenomenon, the team turned to a protein called Homer1a, discovered in 1997 by Paul Worley, M.D., professor of neuroscience, who was also part of the team conducting the new study.
Studies showed that Homer1a -- named for the ancient Greek author and the scientific "odyssey" required to identify it -- is important for the regulation of sleep and wakefulness, and for homeostatic scaling down in lab-grown neurons. Repeating his previous analysis of synaptic proteins, Diering indeed found much higher levels of Homer1a -- 250 percent more -- in the synapses of sleeping mice than awake mice. And in genetically engineered mice missing Homer1a, the previous decrease of synaptic receptor proteins associated with sleep was no longer present. By blocking or enhancing noradrenaline levels, both in lab-grown neurons and in mice, the researchers confirmed that when noradrenaline levels were high, Homer1a stayed away from synapses; when it was low, it collected there.Levels of Homer1a in the receiving synapses were much higher in the sleep-deprived mice than in those that got recovery sleep. That suggests, says Diering, that Homer1a is sensitive to an animal's "sleep need," not just what time of day it is.
Diering emphasizes that sleep need is controlled by adenosine, a chemical that accumulates in the brain as an animal stays awake, provoking sleepiness. When mice were given a drug during sleep deprivation that blocks adenosine, Homer1a levels no longer increased in their synapses.
"We think that Homer1a is a traffic cop of sorts," says Huganir. "It evaluates the levels of noradrenaline and adenosine to determine when the brain is sufficiently quiet to begin scaling down."
As the final test of their hypothesis that scaling down during sleep is crucial for learning and memory, the researchers tested the mice's ability to learn without scaling down. Individual mice were placed in an unfamiliar arena and given a mild electrical shock, either as they woke up or right before they went to sleep. Some mice then received a drug known to prevent scaling down.
When an undrugged mouse received a shock just before sleep, its brain went through the scaling-down process and formed an association between that arena and the shock. When placed in that same arena, those mice spent about 25 percent of their time motionless, in fear of another shock.
When placed in a different unfamiliar arena, they froze sometimes, but only about 9 percent of their time there, probably because they were relatively good a telling the difference between the two unfamiliar arenas.
Expecting that drugged mice that couldn't scale down during sleep would have weaker memories and therefore freeze less than undrugged mice, Diering was surprised that they were motionless longer (40 percent of their time) when returned to the arena where they were shocked.
But the drugged mice were also motionless longer (13 percent of their time) when in a new arena. When the shock was given after the mice woke up, the drug made no difference in how long the mice froze in either arena, confirming that scaling down only occurs during sleep.
"We think that the memory of the shock was stronger in the drugged mice because their synapses couldn't undergo scaling down, but all kinds of other memories also remained strong, so the mice were confused and couldn't easily distinguish the two arenas," says Diering. "This demonstrates why 'sleeping on it' can actually clarify your ideas."
"The bottom line," he says, "is that sleep is not really downtime for the brain. It has important work to do then, and we in the developed world are shortchanging ourselves by skimping on it."
Huganir says that sleep is still a big mystery. "In this study, we only examined what goes on in two areas of the brain during sleep. There are probably equally important processes happening in other areas, and throughout the body, for that matter," he adds.
Among the events that require further exploration is how learning and memory are affected by sleep disorders and other diseases known to disrupt sleep in humans, like Alzheimer's disease and autism.
Huganir also says that benzodiazapines and other drugs that are commonly prescribed as sedatives, such as muscle relaxants and other sleep aids, are known to prevent homeostatic scaling down and are likely to interfere with learning and memory, though that idea has yet to be tested experimentally.
Reference
Results showed a 20 percent drop in receptor protein levels in sleeping mice, indicating an overall weakening of their synapses, compared to mice that were awake.
"That was the first evidence of homeostatic scaling down in live animals," says Richard Huganir, Ph.D., professor of neuroscience, director of the Department of Neuroscience and lead author of the study. "It suggests that synapses are restructured throughout the mouse brain every 12 hours or so, which is quite remarkable."To learn specifically which molecules were responsible for the phenomenon, the team turned to a protein called Homer1a, discovered in 1997 by Paul Worley, M.D., professor of neuroscience, who was also part of the team conducting the new study.
Studies showed that Homer1a -- named for the ancient Greek author and the scientific "odyssey" required to identify it -- is important for the regulation of sleep and wakefulness, and for homeostatic scaling down in lab-grown neurons. Repeating his previous analysis of synaptic proteins, Diering indeed found much higher levels of Homer1a -- 250 percent more -- in the synapses of sleeping mice than awake mice. And in genetically engineered mice missing Homer1a, the previous decrease of synaptic receptor proteins associated with sleep was no longer present. By blocking or enhancing noradrenaline levels, both in lab-grown neurons and in mice, the researchers confirmed that when noradrenaline levels were high, Homer1a stayed away from synapses; when it was low, it collected there.Levels of Homer1a in the receiving synapses were much higher in the sleep-deprived mice than in those that got recovery sleep. That suggests, says Diering, that Homer1a is sensitive to an animal's "sleep need," not just what time of day it is.
Diering emphasizes that sleep need is controlled by adenosine, a chemical that accumulates in the brain as an animal stays awake, provoking sleepiness. When mice were given a drug during sleep deprivation that blocks adenosine, Homer1a levels no longer increased in their synapses.
"We think that Homer1a is a traffic cop of sorts," says Huganir. "It evaluates the levels of noradrenaline and adenosine to determine when the brain is sufficiently quiet to begin scaling down."
As the final test of their hypothesis that scaling down during sleep is crucial for learning and memory, the researchers tested the mice's ability to learn without scaling down. Individual mice were placed in an unfamiliar arena and given a mild electrical shock, either as they woke up or right before they went to sleep. Some mice then received a drug known to prevent scaling down.
When an undrugged mouse received a shock just before sleep, its brain went through the scaling-down process and formed an association between that arena and the shock. When placed in that same arena, those mice spent about 25 percent of their time motionless, in fear of another shock.
When placed in a different unfamiliar arena, they froze sometimes, but only about 9 percent of their time there, probably because they were relatively good a telling the difference between the two unfamiliar arenas.
Expecting that drugged mice that couldn't scale down during sleep would have weaker memories and therefore freeze less than undrugged mice, Diering was surprised that they were motionless longer (40 percent of their time) when returned to the arena where they were shocked.
But the drugged mice were also motionless longer (13 percent of their time) when in a new arena. When the shock was given after the mice woke up, the drug made no difference in how long the mice froze in either arena, confirming that scaling down only occurs during sleep.
"We think that the memory of the shock was stronger in the drugged mice because their synapses couldn't undergo scaling down, but all kinds of other memories also remained strong, so the mice were confused and couldn't easily distinguish the two arenas," says Diering. "This demonstrates why 'sleeping on it' can actually clarify your ideas."
"The bottom line," he says, "is that sleep is not really downtime for the brain. It has important work to do then, and we in the developed world are shortchanging ourselves by skimping on it."
Huganir says that sleep is still a big mystery. "In this study, we only examined what goes on in two areas of the brain during sleep. There are probably equally important processes happening in other areas, and throughout the body, for that matter," he adds.
Among the events that require further exploration is how learning and memory are affected by sleep disorders and other diseases known to disrupt sleep in humans, like Alzheimer's disease and autism.
Huganir also says that benzodiazapines and other drugs that are commonly prescribed as sedatives, such as muscle relaxants and other sleep aids, are known to prevent homeostatic scaling down and are likely to interfere with learning and memory, though that idea has yet to be tested experimentally.
Reference
- Graham H. Diering et al., Homer1a drives homeostatic
scaling-down of excitatory synapses during sleep, Science (2017)
DOI: 10.1126/science.aai8355.
Pregnant
Women Should Avoid Liquorice
- Liquorice contains a natural sweetener, glycyrrhizin,
that can affect the development of the growing fetus if consumed during
pregnancy.
- It impairs the child's cognitive reasoning, memory and
increases their likelihood of developing attention deficit hyperactivity
disorder (ADHD).
- Among girls, it caused puberty to start earlier.
Women should avoid consuming large amounts of liquorice
during pregnancy.
The new Finnish study supports these food recommendations
for families with children.
According to the recommendations, occasional consumption of small amounts such as a portion of liquorice ice cream or a few liquorice sweets is not considered dangerous.
However, the safe limit for consumption is not known. The natural sweetener, glycyrrhizin found in liquorice is said to cause the problem. Previous studies had established that glycyrrhizin causes higher blood pressure and shorter pregnancies in humans. But its long-lasting effects on the growing fetus have not been proven before.
According to the recommendations, occasional consumption of small amounts such as a portion of liquorice ice cream or a few liquorice sweets is not considered dangerous.
However, the safe limit for consumption is not known. The natural sweetener, glycyrrhizin found in liquorice is said to cause the problem. Previous studies had established that glycyrrhizin causes higher blood pressure and shorter pregnancies in humans. But its long-lasting effects on the growing fetus have not been proven before.
Study
The Glaku study was carried out by the University of Helsinki, the National Institute for Health and Welfare and the Helsinki and Uusimaa hospital districts. It compared 378 youths of average age 13 years. Their mothers had consumed liquorice in "large amounts" or "little/no", during pregnancy. The large amount corresponded to over 500 mg glycyrrhizin per week and little/no as less than 249 mg glycyrrhizin per week. 500 mg glycyrrhizin equals an average of 250 g liquorice.
The researchers then carried out cognitive reasoning tests to measure their level of intelligence.
The findings showed that:
The Glaku study was carried out by the University of Helsinki, the National Institute for Health and Welfare and the Helsinki and Uusimaa hospital districts. It compared 378 youths of average age 13 years. Their mothers had consumed liquorice in "large amounts" or "little/no", during pregnancy. The large amount corresponded to over 500 mg glycyrrhizin per week and little/no as less than 249 mg glycyrrhizin per week. 500 mg glycyrrhizin equals an average of 250 g liquorice.
The researchers then carried out cognitive reasoning tests to measure their level of intelligence.
The findings showed that:
- youths that were exposed to large amounts of liquorice
in the womb performed less well than others in cognitive reasoning tests
- it impairs IQ by at least seven points
- it affected their memory
- increased their chances of developing attention deficit
hyperactivity disorder (ADHD)
- girls hit their puberty much earlier, putting them at a risk of diabetes, breast cancer and heart disease
By
Dr. A. Praveena
Assistant Professor
Department of Biochemistry
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