May 13, 2013 — Human intelligence cannot be explained by the size of the brain's frontal lobes, say researchers. Research into the comparative size of the frontal lobes in humans and other species has determined that they are not -- as previously thought -- disproportionately enlarged relative to other areas of the brain, according to the most accurate and conclusive study of this area of the brain.
It concludes that the size of our frontal lobes cannot solely account for humans' superior cognitive abilities.
The study by Durham and Reading universities suggests that supposedly more 'primitive' areas, such as the cerebellum, were equally important in the expansion of the human brain. These areas may therefore play unexpectedly important roles in human cognition and its disorders, such as autism and dyslexia, say the researchers.
The study is published in the Proceedings of the National Academy of Sciences (PNAS) today.
The frontal lobes are an area in the brain of mammals located at the front of each cerebral hemisphere, and are thought to be critical for advanced intelligence.
Lead author Professor Robert Barton from the Department of Anthropology at Durham University, said: "Probably the most widespread assumption about how the human brain evolved is that size increase was concentrated in the frontal lobes.
"It has been thought that frontal lobe expansion was particularly crucial to the development of modern human behaviour, thought and language, and that it is our bulging frontal lobes that truly make us human. We show that this is untrue: human frontal lobes are exactly the size expected for a non-human brain scaled up to human size.
"This means that areas traditionally considered to be more primitive were just as important during our evolution. These other areas should now get more attention. In fact there is already some evidence that damage to the cerebellum, for example, is a factor in disorders such as autism and dyslexia."
The scientists argue that many of our high-level abilities are carried out by more extensive brain networks linking many different areas of the brain. They suggest it may be the structure of these extended networks more than the size of any isolated brain region that is critical for cognitive functioning.
Previously, various studies have been conducted to try and establish whether humans' frontal lobes are disproportionately enlarged compared to their size in other primates such as apes and monkeys. They have resulted in a confused picture with use of different methods and measurements leading to inconsistent findings
Tuesday, May 14, 2013
Wednesday, May 8, 2013
Using Anticholinergics for as Few as 60 Days Causes Memory Problems in Older Adults
May 7, 2013 — Research from the Regenstrief Institute, the Indiana University Center for Aging Research and Wishard-Eskenazi Health on medications commonly taken by older adults has found that drugs with strong anticholinergic effects cause cognitive impairment when taken continuously for as few as 60 days. A similar impact can be seen with 90 days of continuous use when taking multiple drugs with weak anticholinergic effect.
The study of 3,690 older adults is among the first to explore how length of use of this group of drugs affects the brain. The study is available online in advance of publication in a print issue of Alzheimer's & Dementia, the journal of the Alzheimer's Association. The research was funded by a grant (R24MH080827) from the National Institute on Aging.
Anticholinergic drugs block acetylcholine, a nervous system neurotransmitter. Drugs with anticholinergic effects are sold over the counter and by prescription. Older adults commonly use over-the-counter drugs with anticholinergic effects as sleep aids and to relieve bladder leakage. Drugs with anticholinergic effects are frequently prescribed for many chronic diseases including hypertension, cardiovascular disease and chronic obstructive pulmonary disease.
A list of drugs noting their anticholinergic burden can be found on the Aging Brain Care website.
The Regenstrief Institute, IU Center for Aging Research and Wishard-Eskenazi Health researchers reported that continuously taking strong anticholinergics, like many sleeping pills or antihistamines, for only 60 days caused memory problems and other indicators of mild cognitive impairment. Taking multiple drugs with weaker anticholinergic effects, such as many common over-the-counter digestive aids, had a negative impact on cognition in 90 days.
"We found that a high anticholinergic burden -- either from one or multiple drugs -- plus two to three months of continuous exposure to that high burden approximately doubled the risk of developing cognitive impairment," said Noll Campbell, Pharm.D., study co-author and Regenstrief Institute investigator. "Millions of older adults are taking sleeping pills or prescription drugs year after year that may be impacting their organizational abilities and memory."
Dr. Campbell is also an IU Center for Aging Research scientist, a research assistant professor in the Department of Pharmacy Practice, Purdue University College of Pharmacy, and a clinical pharmacy specialist in geriatrics with Wishard-Eskenazi Health Services.
"While the link between anticholinergics and cognitive impairment has been reported by our group and others, the cumulative burden of anticholinergics was rather unexpected, as was the lack of a clear association between anticholinergic burden and dementia," said Regenstrief Institute investigator Malaz Boustani, M.D., MPH. Dr. Boustani, the senior author of the study, who is also associate director of the IU Center for Aging Research and an associate professor of medicine at IU School of Medicine. He sees patients at the Healthy Aging Brain Center at Wishard-Eskenazi Health.
"The fact that taking anticholinergics is linked with mild cognitive impairment, involving memory loss without functional disability, but not with Alzheimer's disease and other dementing disorders, gives hope. Our research efforts will now focus on whether anticholinergic-induced cognitive impairment may be reversible," Dr. Boustani said.
The study of 3,690 older adults is among the first to explore how length of use of this group of drugs affects the brain. The study is available online in advance of publication in a print issue of Alzheimer's & Dementia, the journal of the Alzheimer's Association. The research was funded by a grant (R24MH080827) from the National Institute on Aging.
Anticholinergic drugs block acetylcholine, a nervous system neurotransmitter. Drugs with anticholinergic effects are sold over the counter and by prescription. Older adults commonly use over-the-counter drugs with anticholinergic effects as sleep aids and to relieve bladder leakage. Drugs with anticholinergic effects are frequently prescribed for many chronic diseases including hypertension, cardiovascular disease and chronic obstructive pulmonary disease.
A list of drugs noting their anticholinergic burden can be found on the Aging Brain Care website.
The Regenstrief Institute, IU Center for Aging Research and Wishard-Eskenazi Health researchers reported that continuously taking strong anticholinergics, like many sleeping pills or antihistamines, for only 60 days caused memory problems and other indicators of mild cognitive impairment. Taking multiple drugs with weaker anticholinergic effects, such as many common over-the-counter digestive aids, had a negative impact on cognition in 90 days.
"We found that a high anticholinergic burden -- either from one or multiple drugs -- plus two to three months of continuous exposure to that high burden approximately doubled the risk of developing cognitive impairment," said Noll Campbell, Pharm.D., study co-author and Regenstrief Institute investigator. "Millions of older adults are taking sleeping pills or prescription drugs year after year that may be impacting their organizational abilities and memory."
Dr. Campbell is also an IU Center for Aging Research scientist, a research assistant professor in the Department of Pharmacy Practice, Purdue University College of Pharmacy, and a clinical pharmacy specialist in geriatrics with Wishard-Eskenazi Health Services.
"While the link between anticholinergics and cognitive impairment has been reported by our group and others, the cumulative burden of anticholinergics was rather unexpected, as was the lack of a clear association between anticholinergic burden and dementia," said Regenstrief Institute investigator Malaz Boustani, M.D., MPH. Dr. Boustani, the senior author of the study, who is also associate director of the IU Center for Aging Research and an associate professor of medicine at IU School of Medicine. He sees patients at the Healthy Aging Brain Center at Wishard-Eskenazi Health.
"The fact that taking anticholinergics is linked with mild cognitive impairment, involving memory loss without functional disability, but not with Alzheimer's disease and other dementing disorders, gives hope. Our research efforts will now focus on whether anticholinergic-induced cognitive impairment may be reversible," Dr. Boustani said.
Alzheimer's Fuzzy Signals Into High Definition
May 7, 2013 — Scientists at the Virginia Tech Carilion Research Institute have discovered how the predominant class of Alzheimer's pharmaceuticals might sharpen the brain's performance
17One factor even more important than the size of a television screen is the quality of the signal it displays. Having a life-sized projection of Harry Potter dodging a Bludger in a Quidditch match is of little use if the details are lost to pixilation.
The importance of transmitting clear signals, however, is not relegated to the airwaves. The same creed applies to the electrical impulses navigating a human brain. Now, new research has shown that one of the few drugs approved for the treatment of Alzheimer's disease helps patients by clearing up the signals coming in from the outside world.
The discovery was made by a team of researchers led by Rosalyn Moran, an assistant professor at the Virginia Tech Carilion Research Institute. Her study indicates that cholinesterase inhibitors -- a class of drugs that stop the breakdown of the neurotransmitter acetylcholine -- allow signals to enter the brain with more precision and less background noise.
"Increasing the levels of acetylcholine appears to turn your fuzzy, old analog TV signal into a shiny, new, high-definition one," said Moran, who holds an appointment as an assistant professor in the Virginia Tech College of Engineering. "And the drug does this in the sensory cortices. These are the workhorses of the brain, the gatekeepers, not the more sophisticated processing regions -- such as the prefrontal cortex -- where one may have expected the drugs to have their most prominent effect."
Alzheimer's disease affects more than 35 million people worldwide -- a number expected to double every 20 years, leading to more than 115 million cases by 2050. Of the five pharmaceuticals approved to treat the disease by the U.S. Food and Drug Administration, four are cholinesterase inhibitors. Although it is clear that the drugs increase the amount of acetylcholine in the brain, why this improves Alzheimer's symptoms has been unknown. If scientists understood the mechanisms and pathways responsible for improvement, they might be able to tailor better drugs to combat the disease, which costs more than $200 billion annually in the United States alone.
In the new study, Moran recruited 13 healthy young adults and gave them doses of galantamine, one of the cholinesterase inhibitors commonly prescribed to Alzheimer's patients. Two electroencephalographs were taken -- one with the drugs and one without -- as the participants listened to a series of modulating tones while focusing on a simple concentration task.
The researchers were looking for differences in neural activity between the two drug states in response to surprising changes in the sound patterns that the participants were hearing.
The scientists compared the results with computer models built on a Bayesian brain theory, known as the Free Energy Principle, which is a leading theory that describes the basic rules of neuronal communication and explains the creation of complex networks.
The theory hypothesizes that neurons seek to reduce uncertainty, which can be modeled and calculated using free energy molecular dynamics. Connecting tens of thousands of neurons behaving in this manner produces the probability machine that we call a brain.
Moran and her colleagues compiled 10 computer simulations based on the different effects that the drugs could have on the brain. The model that best fit the results revealed that the low-level wheels of the brain early on in the neural networking process were the ones benefitting from the drugs and creating clearer, more precise signals.
"When people take these drugs you can imagine the brain bathed in them," Moran said. "But what we found is that the drugs don't have broad-stroke impacts on brain activity. Instead, they are working very specifically at the cortex's entry points, gating the signals coming into the network in the first place."
17One factor even more important than the size of a television screen is the quality of the signal it displays. Having a life-sized projection of Harry Potter dodging a Bludger in a Quidditch match is of little use if the details are lost to pixilation.
The importance of transmitting clear signals, however, is not relegated to the airwaves. The same creed applies to the electrical impulses navigating a human brain. Now, new research has shown that one of the few drugs approved for the treatment of Alzheimer's disease helps patients by clearing up the signals coming in from the outside world.
The discovery was made by a team of researchers led by Rosalyn Moran, an assistant professor at the Virginia Tech Carilion Research Institute. Her study indicates that cholinesterase inhibitors -- a class of drugs that stop the breakdown of the neurotransmitter acetylcholine -- allow signals to enter the brain with more precision and less background noise.
"Increasing the levels of acetylcholine appears to turn your fuzzy, old analog TV signal into a shiny, new, high-definition one," said Moran, who holds an appointment as an assistant professor in the Virginia Tech College of Engineering. "And the drug does this in the sensory cortices. These are the workhorses of the brain, the gatekeepers, not the more sophisticated processing regions -- such as the prefrontal cortex -- where one may have expected the drugs to have their most prominent effect."
Alzheimer's disease affects more than 35 million people worldwide -- a number expected to double every 20 years, leading to more than 115 million cases by 2050. Of the five pharmaceuticals approved to treat the disease by the U.S. Food and Drug Administration, four are cholinesterase inhibitors. Although it is clear that the drugs increase the amount of acetylcholine in the brain, why this improves Alzheimer's symptoms has been unknown. If scientists understood the mechanisms and pathways responsible for improvement, they might be able to tailor better drugs to combat the disease, which costs more than $200 billion annually in the United States alone.
In the new study, Moran recruited 13 healthy young adults and gave them doses of galantamine, one of the cholinesterase inhibitors commonly prescribed to Alzheimer's patients. Two electroencephalographs were taken -- one with the drugs and one without -- as the participants listened to a series of modulating tones while focusing on a simple concentration task.
The researchers were looking for differences in neural activity between the two drug states in response to surprising changes in the sound patterns that the participants were hearing.
The scientists compared the results with computer models built on a Bayesian brain theory, known as the Free Energy Principle, which is a leading theory that describes the basic rules of neuronal communication and explains the creation of complex networks.
The theory hypothesizes that neurons seek to reduce uncertainty, which can be modeled and calculated using free energy molecular dynamics. Connecting tens of thousands of neurons behaving in this manner produces the probability machine that we call a brain.
Moran and her colleagues compiled 10 computer simulations based on the different effects that the drugs could have on the brain. The model that best fit the results revealed that the low-level wheels of the brain early on in the neural networking process were the ones benefitting from the drugs and creating clearer, more precise signals.
"When people take these drugs you can imagine the brain bathed in them," Moran said. "But what we found is that the drugs don't have broad-stroke impacts on brain activity. Instead, they are working very specifically at the cortex's entry points, gating the signals coming into the network in the first place."
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