Monday’s medical myth: alcohol kills brain cells

Do you ever wake up with a raging hangover and picture the row of brain cells that you suspect have have started to decay? Or wonder whether that final glass of wine was too much for those tiny cells, and pushed you over the line?

Well, it’s true that alcohol can indeed harm the brain in many ways. But directly killing off brain cells isn’t one of them.

The brain is made up of nerve cells (neurons) and glial cells. These cells communicate with each other, sending signals from one part of the brain to the other, telling your body what to do. Brain cells enable us to learn, imagine, experience sensation, feel emotion and control our body’s movement.

Alcohol’s effects can be seen on our brain even after a few drinks, causing us to feel tipsy. But these symptoms are temporary and reversible. The available evidence suggests alcohol doesn’t kill brain cells directly.

There is some evidence that moderate drinking is linked to improved mental function. A 2005 Australian study of 7,500 people in three age cohorts (early 20s, early 40s and early 60s) found moderate drinkers (up to 14 drinks for men and seven drinks for women per week) had better cognitive functioning than non-drinkers, occasional drinkers and heavy drinkers.

But there is also evidence that even moderate drinking may impair brain plasticity and cell production. Researchers in the United States gave rats alcohol over a two-week period, to raise their alcohol blood concentration to about 0.08. While this level did not impair the rats’ motor skills or short-term learning, it impacted the brain’s ability to produce and retain new cells, reducing new brain cell production by almost 40%. Therefore, we need to protect our brains as best we can.

Excessive alcohol undoubtedly damages brain cells and brain function. Heavy consumption over long periods can damage the connections between brain cells, even if the cells are not killed. It can also affect the way your body functions. Long-term drinking can cause brain atrophy or shrinkage, as seen in brain diseases such as stroke and Alzheimer’s disease.

There is debate about whether permanent brain damage is caused directly or indirectly.

We know, for example, that severe alcoholic liver disease has an indirect effect on the brain. When the liver is damaged, it’s no longer effective at processing toxins to make them harmless. As a result, poisonous toxins reach the brain, and may cause hepatic encephalopathy (decline in brain function). This can result in changes to cognition and personality, sleep disruption and even coma and death.

Alcoholism is also associated with nutritional and absorptive deficiencies. A lack of Vitamin B1 (thiamine) causes brain disorders called Wernicke’s ncephalopathy (which manifests in confusion, unsteadiness, paralysis of eye movements) and Korsakoff’s syndrome (where patients lose their short-term memory and coordination).

So, how much alcohol is okay?

To reduce the lifetime risk of harm from alcohol-related disease or injury, the National Health and Medical Research Council recommends healthy adults drink no more than two standard drinks on any day. Drinking less frequently (such as weekly rather than daily) and drinking less on each occasion will reduce your lifetime risk.

To avoid alcohol-related injuries, adults shouldn’t drink more than four standard drinks on a single occasion. This applies to both sexes because while women become intoxicated with less alcohol, men tend to take more risks and experience more harmful effects.

For pregnant women and young people under the age of 18, the guidelines say not drinking is the safest option.

So while alcohol may not kill brain cells, if this myth encourages us to rethink that third beer or glass of wine, I won’t mind if it hangs around.

Computer Model May Help Athletes and Soldiers Avoid Brain Damage and Concussions

Concussions can occur in sports and in combat, but health experts do not know precisely which jolts, collisions and awkward head movements during these activities pose the greatest risks to the brain. To find out, Johns Hopkins engineers have developed a powerful new computer-based process that helps identify the dangerous conditions that lead to concussion-related brain injuries. This approach could lead to new medical treatment options and some sports rule changes to reduce brain trauma among players.

The research comes at a time when greater attention is being paid to assessing and preventing the head injuries sustained by both soldiers and athletes. Some kinds of head injuries are difficult to see with standard diagnostic imaging but can have serious long-term consequences. Concussions, once dismissed as a short-term nuisance, have more recently been linked to serious brain disorders.

“Concussion-related injuries can develop even when nothing has physically touched the head, and no damage is apparent on the skin,” said K. T. Ramesh, the Alonzo G. Decker Jr. Professor of Science and Engineering who led the research at Johns Hopkins. “Think about a soldier who is knocked down by the blast wave of an explosion, or a football player reeling after a major collision. The person may show some loss of cognitive function, but you may not immediately see anything in a CT-scan or MRI that tells you exactly where and how much damage has been done to the brain. You don’t know what happened to the brain, so how do you figure out how to treat the patient?”

To help doctors answer this question, Ramesh led a team that used a powerful technique called diffusion tensor imaging, together with a computer model of the head, to identify injured axons, which are tiny but important fibers that carry information from one brain cell to another. These axons are concentrated in a kind of brain tissue known as “white matter,” and they appear to be injured during the so-called mild traumatic brain injury associated with concussions. Ramesh’s team has shown that the axons are injured most easily by strong rotations of the head, and the researchers’ process can calculate which parts of the brain are most likely to be injured during a specific event.

The team described its new technique in the Jan. 8 edition of the Journal of Neurotrauma. The lead author, Rika M. Wright, played a major role in the research while completing her doctoral studies in Johns Hopkins’ Whiting School of Engineering, supervised by Ramesh. Wright is now a postdoctoral research fellow at Carnegie Mellon University. Ramesh is continuing to conduct research using the technique at Johns Hopkins with support from the National Institutes of Health.

Beyond its use in evaluating combat and sports-related injuries, the work could have wider applications, such as detecting axonal damage among patients who have received head injuries in vehicle accidents or serious falls. “This is the kind of injury that may take weeks to manifest,” Ramesh said. “By the time you assess the symptoms, it may be too late for some kinds of treatment to be helpful. But if you can tell right away what happened to the brain and where the injury is likely to have occurred, you may be able to get a crucial head-start on the treatment.”

Cooling may prevent trauma-induced epilepsy

In the weeks, months and years after a severe head injury, patients often experience epileptic seizures that are difficult to control. A new study in rats suggests that gently cooling the brain after injury may prevent these seizures.

“Traumatic head injury is the leading cause of acquired epilepsy in young adults, and in many cases the seizures can’t be controlled with medication,” says senior author Matthew Smyth, MD, associate professor of neurological surgery and of pediatrics at Washington University School of Medicine in St. Louis. “If we can confirm cooling’s effectiveness in human trials, this approach may give us a safe and relatively simple way to prevent epilepsy in these patients.”

The researchers reported their findings in Annals of Neurology.

Cooling the brain to protect it from injury is not a new concept. Cooling slows down the metabolic activity of nerve cells, and scientists think this may make it easier for brain cells to survive the stresses of an injury. 

Doctors currently cool infants whose brains may have had inadequate access to blood or oxygen during birth. They also cool some heart attack patients to reduce peripheral brain damage when the heart stops beating.

Smyth has been exploring the possibility of using cooling to prevent seizures or reduce their severity.

“Warmer brain cells seem to be more electrically active, and that may increase the likelihood of abnormal electrical discharges that can coalesce to form a seizure,” Smyth says. “Cooling should have the opposite effect.”

Smyth and colleagues at the University of Washington and the University of Minnesota test potential therapies in a rat model of brain injury. These rats develop chronic seizures weeks after the injury.

Researchers devised a headset that cools the rat brain. They were originally testing its ability to stop seizures when they noticed that cooling seemed to be not only stopping but also preventing seizures.

Scientists redesigned the study to focus on prevention. Under the new protocols, they put headsets on some of the rats that cooled their brains by less than 4 degrees Fahrenheit. Another group of rats wore headsets that did nothing. Scientists who were unaware of which rats they were observing monitored them for seizures during treatment and after the headsets were removed.

Rats that wore the inactive headset had progressively longer and more severe seizures weeks after the injury, but rats whose brains had been cooled only experienced a few very brief seizures as long as four months after injury.

Brain injury also tends to reduce cell activity at the site of the trauma, but the cooling headsets restored the normal activity levels of these cells.

The study is the first to reduce injury-related seizures without drugs, according to Smyth, who is director of the Pediatric Epilepsy Surgery program at St. Louis Children’s Hospital.

“Our results show that the brain changes that cause this type of epilepsy happen in the days and weeks after injury, not at the moment of injury or when the symptoms of epilepsy begin,” says Smyth. “If clinical trials confirm that cooling has similar effects in humans, it could change the way we treat patients with head injuries, and for the first time reduce the chance of developing epilepsy after brain injury.”

Smyth and his colleagues have been testing cooling devices in humans in the operating room, and are planning a multi-institutional trial of an implanted focal brain cooling device to evaluate the efficacy of cooling on established seizures.

When Brain Damage Unlocks The Genius Within

Brain damage has unleashed extraordinary talents in a small group of otherwise ordinary individuals. Will science find a way for everyone to tap their inner virtuoso?

Full article

Training speech networks to treat aphasia

About 80,000 people develop aphasia each year in the United States alone. Nearly all of these individuals have difficulty speaking. For example, some patients (nonfluent aphasics) have trouble producing sounds clearly, making it frustrating for them to speak and difficult for them to be understood. Other patients (fluent aphasics) may select the wrong sound in a word or mix up the order of the sounds. In the latter case, “kitchen” can become “chicken.” Blumstein’s idea is to use guided speech to help people who have suffered stroke-related brain damage to rebuild their neural speech infrastructure.

Blumstein has been studying aphasia and the neural basis of language her whole career. She uses brain imaging, acoustic analysis, and other lab-based techniques to study how the brain maps sound to meaning and meaning to sound.

What Blumstein and other scientists believe is that the brain organizes words into networks, linked both by similarity of meaning and similarity of sound. To say “pear,” a speaker will also activate other competing words like “apple” (which competes in meaning) and “bear”(which competes in sound). Despite this competition, normal speakers are able to select the correct word.

In a study published in the Journal of Cognitive Neuroscience in 2010, for example, she and her co-authors used functional magnetic resonance imaging to track neural activation patterns in the brains of 18 healthy volunteers as they spoke English words that had similar sounding “competitors” (“cape” and “gape” differ subtly in the first consonant by voicing, i.e. the timing of the onset of vocal cord vibration). Volunteers also spoke words without similar sounding competitors (“cake” has no voiced competitor in English; gake is not a word). What the researchers found is that neural activation within a network of brain regions was modulated differently when subjects said words that had competitors versus words that did not.

One way this competition-mediated difference is apparent in speech production is that words with competitors are produced differently from words that do not have competitors. For example, the voicing of the “t” in “tot” (with a voiced competitor ‘dot’) is produced with more voicing than the “t” in “top” (there is no ‘dop’ in English). Through acoustic analysis of the speech of people with aphasia, Blumstein has shown that this difference persists, suggesting that their word networks are still largely intact.

Blood May Hold Clues to Risk of Memory Problems After Menopause

New Mayo Clinic research suggests that blood may hold clues to whether post-menopausal women may be at an increased risk for areas of brain damage that can lead to memory problems and possibly increased risk of stroke. The study shows that blood’s tendency to clot may contribute to areas of brain damage called white matter hyperintensities. The findings are published in the Feb. 13 online issue of Neurology, the medical journal of the American Academy of Neurology.

The study involved 95 women with an average age of 53 who recently went through menopause. The women had magnetic resonance imaging, or MRIs, taken of their brains at the start of the study. They then received a placebo, oral hormone therapy or the hormone skin patch. They had MRIs periodically over the next four years.

During the study, women with higher levels of thrombogenic microvesicles, the platelets more likely to cause blood to clot, were likelier to have higher increases in the amount of white matter hyperintensities (shown as concentrated white areas on an MRI scan), which may lead to memory loss.

"This study suggests that the tendency of the blood to clot may contribute to a cascade of events leading to the development of brain damage in women who have recently gone through menopause," says study author Kejal Kantarci, M.D., of Mayo Clinic. "Preventing the platelets from developing these microvesicles could be a way to stop the progression of white matter hyperintensities in the brain."

All of the women had white matter hyperintensities at the start of the study. The amount increased by an average volume of 63 cubic millimeters at 18 months, 122 cubic millimeters at three years and 155 cubic millimeters at four years.

(Image: Shutterstock)

Chemical reaction keeps stroke-damaged brain from repairing itself

Nitric oxide, a gaseous molecule produced in the brain, can damage neurons. When the brain produces too much nitric oxide, it contributes to the severity and progression of stroke and neurodegenerative diseases such as Alzheimer’s. Researchers at Sanford-Burnham Medical Research Institute recently discovered that nitric oxide not only damages neurons, it also shuts down the brain’s repair mechanisms. Their study was published by the Proceedings of the National Academy of Sciences the week of February 4.

“In this study, we’ve uncovered new clues as to how natural chemical reactions in the brain can contribute to brain damage—loss of memory and cognitive function—in a number of diseases,” said Stuart A. Lipton, M.D., Ph.D., director of Sanford-Burnham’s Del E. Webb Neuroscience, Aging, and Stem Cell Research Center and a clinical neurologist.

Lipton led the study, along with Sanford-Burnham’s Tomohiro Nakamura, Ph.D., who added that these new molecular clues are important because “we might be able to develop a new strategy for treating stroke and other disorders if we can find a way to reverse nitric oxide’s effect on a particular enzyme in nerve cells.”

Nitric oxide inhibits the neuroprotective ERK1/2 signaling pathway

Learning and memory are in part controlled by NMDA-type glutamate receptors in the brain. These receptors are linked to pores in the nerve cell membrane that regulate the flow of calcium and sodium in and out of the nerve cells. When these NMDA receptors get over-activated, they trigger the production of nitric oxide. In turn, nitric oxide attaches to other proteins via a reaction called S-nitrosylation, which was first discovered by Lipton and colleagues. When those S-nitrosylated proteins are involved in cell survival and lifespan, nitric oxide can cause brain cells to die prematurely—a hallmark of neurodegenerative disease.

In their latest study, Lipton, Nakamura and colleagues used cultured neurons as well as a living mouse model of stroke to explore nitric oxide’s relationship with proteins that help repair neuronal damage. They found that nitric oxide reacts with the enzyme SHP-2 to inhibit a protective cascade of molecular events known as the ERK1/2 signaling pathway. Thus, nitric oxide not only damages neurons, it also blocks the brain’s ability to self-repair.