One more shot of espresso, for memory’s sake

How much do Portlanders love their coffee? A lot. According to a 2011 poll by CNBC, Portland is the third most caffeinated city in the U.S., with almost 900 coffee shops and 30 local coffee roasters.

And does this love of coffee have any effect on brain health? A new study published in the journal Nature Neuroscience suggests that caffeine might actually be a good thing for how our brain stores and processes long-term memories.

Many studies have documented the positive effects of caffeine on attention and processing speed, which we are all probably familiar with from our own personal experiences. I’m usually happy with just one small cup of coffee with breakfast. But if I feel sleepy after a big lunch, sometimes I’ll indulge in a second cup to perk myself up for a busy afternoon or evening. Like most people, I usually think of caffeine as a little pick-me-up to give me the energy to tackle a task that I have to take on in the future.

In the new study by Daniel Borota and his colleagues, the researchers flipped the caffeine question around to ask: what if we give subjects caffeine after they perform a memory task? This is called a “post-study” design, and the researchers paired it with a randomized, double-blind, placebo-controlled experimental set-up. Randomized means that the 160 subjects were randomly assigned to the caffeine or non-caffeine (placebo) conditions. Double-blind means that in addition to the researchers not knowing which group each subject belonged to when they were collecting and analyzing the data, the test subjects did not even know they were going to be asked to perform a memory task. Experimental studies are designed with these features to reduce conscious and unconscious bias both in the test subjects and the researchers, so that the results and conclusions can be as biologically meaningful as possible.

There were two other important characteristics of the test subjects that allowed the researchers to conclude that changes in memory were associated with the caffeine given during the study. All the subjects consumed only small amounts of caffeine in their daily lives (even less then I drink!), and they were “caffeine-naïve,” meaning that they did not have any other sources of caffeine in their diet during the study.

The test subjects were shown a series of common, every day objects, and were asked to report on certain qualities of each object. After the test period, they were then given a moderate amount of caffeine or placebo. Twenty-four hours later, they were tested again, but this time they were asked to recall if the objects presented were different, similar, or exactly the same as the objects they saw the day before. Those who had received caffeine the day before were better at knowing the difference between objects that were exactly the same vs. objects that were similar to the previous day. The researchers concluded that caffeine given after the task had a significant impact on the subjects’ ability to consolidate and store long-term memories, specifically when it comes to distinguishing between similar but different objects.

Importantly, the researchers measured the amount of caffeine in the saliva of all subjects, and showed that there was no caffeine in their system on the second day, at the time of the memory task, indicating that caffeine did not affect the subjects’ ability to recall memories. Furthermore, when caffeine was given just before the memory task on the second day, there was no benefit, which shows that caffeine was not able to beef up memory retrieval.

Of course, we all have had the experience where too much coffee sends you into a jittery, counter-productive, can’t-sit-still-and-focus state. Along these lines, the researchers also report a dose effect in their study: 200 milligrams of caffeine produced the optimum effect, while 100 milligrams was not enough, and a higher dose of 300 milligrams did not significantly enhance the effect. To put that into perspective, a 16-ounce Starbucks drip coffee has about 330 milligrams of caffeine, while a 16-ounce latte has only 150 mg, and an espresso shot has about 75 milligrams.

As with most things, moderation is key. But perhaps a bit of caffeine right after your next big brain-demanding task will help you remember those important parts of your day.

Kateri Spinelli, Ph.D.
Post doctoral fellow, Dept. of Neurology
OHSU Brain Institute

The road to a healthy heart is the road to a healthy brain

What if we told you that you could live your life in simple ways that give you a very, very good chance of having a healthy heart and a sharp brain well into old age?

No special drugs, no special surgeries, no amazing scientific discoveries and no wonder cures.

Sounds pretty good, doesn’t it? And it’s simple. Science is beginning to understand that the route to a healthy brain and healthy heart might be pretty much on the same road. The important mileposts on that road: eating smartly, getting moderate exercise, controlling your weight, your blood pressure and your cholesterol levels and stopping smoking.

The two of us — one a brain expert, the other a heart expert — will talk about brains and hearts and health this Monday night, Feb. 24, as part of the OHSU Brain Institute’s Brain Awareness Season lecture series. Our lecture will begin at 7 p.m. at the Newmark Theater in downtown Portland.

We’ll talk about how science has known for years that following some of these “living healthy” principles can help your heart health. But we’re increasingly seeing that the same good practices that help your heart also seem to help your brain.

For example, science knows no absolute cure or prevention — yet — for dementia. But there are hints.

A long-term study of 678 Roman Catholic nuns (known, not surprisingly, as the Nun Study) has shown that in patients with an equivalent number of “plaques” and “tangles” in the brain associated with Alzheimer’s disease, only those who also had had small strokes showed signs of dementia. That could mean small strokes somehow “activated” the dementia in brains that had the plaques.

And that suggests that if you decrease your risk factors for stroke — by following those “living healthy” principles — you also decrease your risk of dementia.

We’re also increasingly understanding how important prenatal nutrition is to that baby’s health — heart health, brain health and overall health — as an adult. Lower birth weight from poor prenatal nutrition means a higher risk of stroke and heart disease. And many organs, including the heart and brain, grow abnormally when nutrition is poor before birth.

There’s a lot more to talk about, in terms of how lifestyle decisions you make every day have a long-term effect on your heart and brain. So join us Monday night — on the road to better heart and brain health.

And you don’t have to stop learning on Monday. You can learn much more by joining the OHSU Brain Institute’s just-launched Healthy Brain campaign. The campaign will offer monthly tips and a way to celebrate your progress and learn more from each other and OHSU experts in September.

Joe Quinn, M.D.

Director, OHSU Parkinson Center
Professor, Department of Neurology
OHSU Brain Institute

Kent L. Thornburg, Ph.D.
M. Lowell Edwards Chair,
 Professor of Medicine, OHSU School of Medicine
Director, Center for Developmental Health, Knight Cardiovascular Institute
Director, Bob and Charlee Moore Institute for Nutrition & Wellness

 

Your brain … in love

Neuroscientists have long wondered whether or not there’s a love locus in the brain; a spot where romance resides amidst the complex circuits and intricate chemicals that comprise our emotional nervous system. Recent studies have surprised us as neurologists; there is such a spot and, interestingly, it involves the nerve cells and neural circuits that drive us to crave food, water and even illicit drugs. And these are not the circuits that involve lust or sexual desire.

Recent studies support this love locus by demonstrating brain images in functional MRI scans. These specialized scans display pictures that capture the activity, not just the structure (as in regular MRI scans) of brain cells. Young, love-crazed college students were shown pictures of the objects of their affection while undergoing functional MRI scans. Behold, the parts of the brain that were activated when the students saw their love’s photograph were the areas that have a high concentration of dopamine, one of the brain’s key neurotransmitters.

Dopamine is a chemical that carries messages that influence reward, craving, and, also, drug addiction. So, in effect, these young lovers were truly “addicted” to one another, and, in fact, were found to have physically painful withdrawal symptoms when their fresh young love was thwarted.

But what about those of us long past the dizzying, delirious highs of a fevered, lovesick youngster? Actually, there is great news for those of us much farther into our relationships with the one we love. A recent study from Stony Brook University in New York demonstrated that some mature couples — who had been in love for years, even decades — still had the burst of frenzied activity in the dopamine pathways in the brain when they looked at pictures of their longtime lovers. Just as if they were college students. So no one can say that young love fades and passion wanes over time, at least not from a neurobiological standpoint!

Love does live on, but it also has many facets. I was particularly enthralled by a study from the University of Minnesota, whose researchers asked young men and women to make four lists: of their friends, the people they loved, the people they thought sexually attractive, and, lastly, those with whom they were “in love.”

The last list most often had just one name. But, consistently, that name was also on all the other lists. True love is a powerful force that embraces friendship, affection, sexual attraction and romantic impulse. It is as intoxicating as a drug. So this Valentine’s Day, I hope you appreciate the complex pathways in your brain that comprise those feelings you have of potent and enduring romantic love. Whatever your age, and however long you have been in love.

Tarvez Tucker, M.D.
Associate Professor of Neurology and Neurocritical Care
OHSU Brain Institute

 

Next OHSU brain awareness lecture: fighting traumatic brain injury

The impact of concussions and other traumatic brain injuries on society are staggering.

How staggering? Consider these numbers:

• Each year in the U.S., 3.4 million people suffer a traumatic brain injury, or TBI.

• TBI is one of the leading causes of death and disability in America. Each year, 53,000 Americans die due to TBI.

• Eight teenagers die every day in the U.S. from TBI.

• There are 5 million Americans living with TBI-related disabilities; direct and indirect costs of TBI in the U.S. is $76 billion per year.

The non-profit I work for — One Mind for Research — is led by retired U.S. Army General Peter Chiarelli, former commander of the multi-national corps in Iraq. He has seen first hand how TBI has affected America’s soldiers. And he is now helping to lead the fight to find ways to battle and prevent TBI.

One Mind for Research’s mission is to fund groundbreaking research and accelerate development of better diagnostics, better treatments, and ultimately, preventions and cures for a wide range of mental illnesses and brain injuries. One of our most important goals is to help science make advances in understanding, treating and, ultimately, preventing and curing TBI.

While TBI affects millions of people worldwide, it is a silent epidemic — its symptoms are frequently invisible, thus difficult to diagnose and treat. But while symptoms aren’t always easy to notice, TBI leads to motor, cognitive, and social impairments that interfere with an individual’s ability to be productive.

One Mind’s initial research project is called the “Gemini Program,” which will include 3,000 to 5,000 patients with traumatic brain injury and, in some cases, post traumatic stress. The patients will participate in a multi-year longitudinal study that will help researchers learn more about these devastating conditions.

Want to learn more about the fight against TBI? I am speaking this coming Tuesday evening — Feb. 18 — in Portland as part of the Brain Awareness Season lecture series sponsored by the OHSU Brain Institute. Gen. Chiarelli has prepared a video presentation that will also be shown at the lecture.

I hope you can join me. We need more people to understand TBI — and to join us in the fight against it.

Janet Carbary
Chief Financial Officer
One Mind for Research

 

Brain Insitute speaker: Mad Cow expert and neuroscience pioneer

Did you know that, according to the American Red Cross, you are forbidden from donating blood in the United States if you have spent a cumulative time of three months or more in the United Kingdom, from Jan. 1, 1980 through December 31, 1996?

The reason? It stems from the discovery that in some parts of the world, cattle can get an infectious, fatal brain disease called Mad Cow Disease. In these same locations, humans have started to get a new disease called variant Creutzfeld-Jacob Disease, also a fatal brain disease.

Jean Manson, Brain Awareness Lecture Series speaker

All of this relates to the first lecturer in the OHSU Brain Institute’s popular Brain Awareness Season lecture series. The lecture, at 7 p.m. on Monday Feb. 10 at the Newmark Theater in downtown Portland, will be presented by Jean Manson, one of the world’s leading experts on the group of diseases that include Mad Cow Disease.

But first, a few more details on what Mad Cow Disease has to do with humans.

Scientists believe that variant Creutzfeld-Jacob Diseases is Mad Cow Disease that has somehow transferred to humans, possibly through the food chain. There is now evidence from a small number of case reports involving patients and laboratory animal studies that vCJD — as it’s sometimes called — can be transmitted through blood transfusion. There is no test for vCJD in humans that could be used to screen blood donors and to protect the blood supply. This means that blood programs — like the American Red Cross’s — must take special precautions to keep vCJD out of the blood supply by avoiding collections from those who have been where this disease is found.

Which means that the OHSU Brain Institute’s first lecturer — a world renowned expert on this group of diseases — is not allowed to give blood in the United States.

Manson is head of the neurobiology division of the Roslin Institute in Edinburgh, Scotland. (The Roslin Institute is where the world’s most famous sheep, Dolly, was cloned.) She is also chair of Neurodegenerative Disease at the University of Edinburgh.

Professor Manson is an internationally recognized research scientist in what are called transmissible spongiform encephalopathies, or TSEs, a group of fatal diseases that affect the brain and nervous system of many animals, including humans. They’re also called prion diseases. Mad Cow Disease and Creutzfeld-Jacob Disease are within this group of diseases.

Research into the prion diseases not only tries to advance scientific knowledge into these mysterious diseases. It also has led to research advances in conditions such as Alzheimer’s disease.

Professor Manson will be talking about all of that during her lecture. She’ll also talk about the differences in how neuroscientists in the United Kingdom and the United States investigate brain disease.

Although I don’t study prion diseases specifically, my own research focuses on the aging brain and neuroendocrine changes that lead to cognitive impairment in the elderly. So as a neuroscientist, I’m very interested in her work.  (We also share the blood-giving problem; like Manson, I can’t give blood in the United States, since I’m originally from the U.K.)

I’m going to be there to listen. It promises to be fascinating.

Henryk Urbanski, Ph.D., D.Sc.
Professor and senior scientist, divisions of Neuroscience and Reproductive & Developmental Sciences, Oregon National Primate Research Center
Professor, Departments of Behavioral Neuroscience and Physiology & Pharmacology, OHSU Brain Institute

Vitamin D, mood and memory in persons with Parkinson’s disease

Vitamin D has become a hot topic in recent years. For many years, vitamin D has been known to play a role in bone health. More recent research suggests it may have a much broader role in multiple body systems.

In regard to the brain, we know that there are receptors for vitamin D in most parts of the human brain. In persons without Parkinson’s disease, some research suggests vitamin D may be related to mood and cognitive function. These data are somewhat limited, however, and a definitive conclusion has not been drawn.

To look more closely at mood, memory and their relationship with vitamin D in persons with Parkinson’s, some colleagues and I conducted an observational study of 286 people with Parkinson’s. We did testing of cognitive function and mood and had blood drawn. When correcting for age, disease duration, and Parkinson’s disability, we found associations between vitamin D concentrations and several measures of language function. These included how many animals or vegetables a person could name in one minute, known as verbal fluency, and how good they were at remembering a list of words. This relationship — between higher vitamin D levels and better language function — was present in those persons with Parkinson’s who were not demented, but not present in those with dementia. In regard to mood, a self reported scale of depression showed an association with vitamin D concentrations — again, just in the non-demented subset of Parkinson’s patients.

It appears that there may be a relationship between vitamin D and cognition and mood in persons with Parkinson’s. Cause and effect cannot be determined from this type of study. It is possible, for example, that persons with Parkinson’s who are depressed are less likely to get outside and therefore have lower vitamin D concentrations.

To determine if a relationship truly exists, good intervention studies are needed to see what happens to cognition and mood when vitamin D concentrations are increased in persons with Parkinson’s. Currently we are pursuing a research project looking at this with a joint OHSU and Portland VA Medical Center study. We hope to have results in the next year or two.

Amie Peterson, M.D.
Assistant Professor of Neurology
OHSU Parkinson Center of Oregon
OHSU Brain Institute

A toast to your health

There’s possibly no better time to highlight this research story than on New Year’s eve: a drink or two a day — a glass of wine, a glass of beer — might also keep the doctor away.

That’s what colleagues and I found in a study published this month in the journal Vaccine. We studied the drinking behaviors of rhesus macaque monkeys, who were given 22-hour-a-day access to a mixture of alcohol and water — and allowed to drink or not drink it. What we found after 14 months of study: the immune system of the monkeys that drank “moderate” amounts of alcohol were actually bolstered — more than the monkeys who drank more heavily and more than a control group of monkeys who drank a low-calorie sugar solution. We defined “moderate” drinking as monkeys who had a blood alcohol level of 0.02 to 0.04 percent (A blood alcohol level of 0.08 percent is the limit for humans to be able to legally drive a vehicle.).

The media coverage of our work — which has been extensive, in USA Today, Time, The Daily Beast and elsewhere — has focused on the happy news that drinking in moderation might help boost our immune system and help us fight off infection. But my colleague, Ilhem Messaoudi Powers (formerly at OHSU, now at the University of California-Riverside), and I want our research to go beyond that. We want to better understand how our body is reacting to moderate alcohol to actually have this effect. The goal would be to then find new, alcohol-free ways — maybe new medications — to boost the immune system, in generally healthy people and in people with immunodeficiency.

Of course, based on what we’ve found, it looks like people might be able to get that boost by enjoying their New Year’s Eve with that glass of wine, as well.  But remember — it’s all about moderation.

Kathy Grant, Ph.D.
Professor of Behavioral Neuroscience
OHSU Brain Institute

 

Ask our expert: Aging & declining mental ability

Q: Does getting older always mean losing mental ability?

A: Part of normal brain aging may mean a slowing of mental processing, especially in your memory. Although many patients ask, it’s difficult to prescribe any particular type of mental exercise for your brain, though learning things that get you out of your normal routine can help, such as learning a new language or trying a different type of puzzle.

But your best option is physical activity: Research has shown that aerobic exercise — such as walking, swimming, biking or hiking — for about 30 minutes a day, five times a week can promote the release of growth factors in the brain that create new cells.

Joseph Quinn, M.D.
Professor of Neurology
Layton Aging & Alzheimer’s Disease Center
OHSU Brain Institute

Do you have a question you’d like one of our expert to answer? Share it with us in the comments section below.

How our brains wash away the gunk during sleep

You wake on Saturday morning, drag your body out of bed and survey your home. You had entertained houseguests the night before, and it shows. Friends and family had filled your home, loud voices and much conversation echoed within your walls and everyone went home much later than you had planned. And now it is time to pay the piper. A full Saturday’s worth of dishwashing, floor scrubbing and shelf wiping stares you back in the face.

Such is our common experience, something each of us can likely relate to. New research, however, suggests that your brain may feel the same way at the end of a long day of thinking.

The brain is just like any other organ in the body in that the spaces in between its cells must be regularly swept clean to keep things running smoothly. Yet it has remained a bit of mystery how the brain accomplishes this task.

See, in the rest of the body, the lymphatic system takes care of most of this cleaning of the spaces between cells. The brain, however, has no lymphatic system.

In the summer of 2012, our research team reported in the journal Science Translational Medicine the discovery of a clever anatomical pathway by which the brain accomplishes this task of cleaning out the spaces between cells. Basically, it uses spaces on the outside of blood vessels as a dedicated set of plumbing that allows cerebrospinal fluid, or CSF, that surrounds the brain to wash through the brain, essentially flushing debris and waste out. This washing depended on water movement through support cells in the brain called “glial cells.” Thus we termed this brain-wide clearance pathway the “glymphatic system.”

Anyone who has every pulled an all nighter, or has had young children, knows that after a night with little or no sleep, not only do you feel more tired, but your mind is foggier. Why a good night’s sleep leaves the mind clear and crisp, and indeed why we would need sleep at all (since it represents “wasted” time not doing something more productive), has been one of the persistent mysteries in neuroscience.

In a study published last week in the journal Science, our team reported findings that may shed light on this question. By imaging the flushing of fluid through the brains of live mice that were awake or naturally asleep using a technique called 2-photon microscopy, we found that the rate of cleaning in the brain differed dramatically between the waking brain and the sleeping brain.

When the brain is asleep, we found that its cells shrink in order to open up the spaces between them, which allows CSF to flush through the sleeping brain at about 20 times the rate seen in the waking brain. This translated to a doubling in the efficiency of waste clearance from the sleeping versus waking brain. These findings suggest that part of the function of sleep is restorative – that it provides the brain an opportunity to tidy up and clean out the day’s accumulated waste when the activities of waking life aren’t getting in the way. It’s like cleaning up on a Saturday after Friday night’s houseguests have left.

These new findings do not simply illuminate a potential purpose of sleep, but may inform our understanding of the role of sleep disturbances in the setting of neurodegenerative diseases like Alzheimer’s disease. Alzheimer’s disease is believed to be caused by the buildup of plaques made up of a protein called amyloid beta in the aging brain. Two recent studies published in the journal JAMA Neurology have shown that in human patients that haven’t yet developed Alzheimer’s disease, poorer sleep quality is associated with greater buildup of amyloid beta plaques. Whether this is because bad sleep promotes amyloid beta accumulation, or whether low-level brain damage caused by amyloid beat promotes sleep disturbance has not been clear. However, our study suggests that one of the functions of sleep is the clearance of amyloid beta, and supports the idea that the inability to get proper sleep could promote the development of neurodegeneration.

While this most recent study was led by Dr. Maiken Nedergaard at the University of Rochester Medical Center in New York, follow-on studies are currently underway here at OHSU. In January of this year, I was recruited from the University of Rochester to come to OHSU and establish a research program based in part upon my work in this brain-wide, waste-clearance pathway. Bringing this research here to OHSU was made possible in large part by the generous gift from Phil and Penny Knight establishing the Knight Cardiovascular Institute at OHSU, of which I am now a part.

Using 2-photon microscopy and other approaches, we are working to define how this waste-clearance system becomes impaired in the aging brain and the contribution that damaged, aging blood vessels in the brain make to this process. The goal is to find key steps in this degenerative process that could be targeted with drugs to stop the failure of amyloid beta clearance and the accumulation of amyloid beta plaques in the brain.
With a lot of smart people working together, we hope that the discoveries that we’ve made so far in mice will translate to new opportunities to change the course of Alzheimer’s disease in patients.

Jeffrey Iliff
Assistant Professor of Anesthesiology and Peri-Operative Medicine
Knight Cardiovascular Institute

OHSU Brain Institute

 

Lewy body dementia — a less-known cause of cognitive problems

Not all people with cognitive problems have Alzheimer’s disease. While Alzheimer’s is the most common reason for memory problems as people get older, there are other types of dementia.

Lewy body dementia or Lewy body disease is a much less common cause of cognitive problems and is seen in about seven in a thousand people over the age of 65. People with LBD tend to have trouble with visual spatial function and executive function. Executive function involves the ability to carry out complex tasks that have multiple steps, such as baking a cake. Early in the course of the disease, persons with LBD often have a fairly good memory. For example, remembering a list of words told to them five minutes before.

People with LBD may also have hallucinations or delusions. They may see people who are not present or have false beliefs such as thinking their house belongs to someone else. They often fluctuate in their degree of cognitive problems, having some days when they seem to do very well and others when they really struggle.

On a physical exam, the doctor may see some features similar to Parkinson’s disease such as slowed walking, smaller movements and handwriting, and stiffness. It is also common that people with LBD have a history of a disorder of sleep called REM sleep behavior disorder, or RBD. RBD often starts many years before cognitive problems develop. In RBD, people act out their dreams (which occur during REM sleep) and can injure themselves and their bed partner.

Unfortunately, there are not perfect treatments for LBD. But medications called cholinesterase inhibitors can help some patients. Rivastigmine is the one that has been studied the most extensively. Memantine is a different type of medication that may help some patients as well.

One of the most important things to be aware of is that people with LBD can respond very poorly to many typical antipsychotic medications, such as haloperidol and chlorpromazine. These medications are often used to treat delusions and are also given frequently for agitation. The typical ones should be avoided in LBD. There are two antipsychotics — quetiapine and clozapine — that can be used if delusions and hallucinations are problematic. If the parkinsonian features are prominent, a medication used to treat Parkinson’s disease, levodopa, may also be tried.

People with cognitive problems as well as RBD or hallucinations may have Lewy body dementia — not Alzheimer’s Disease. In this type of dementia, a neurological consultation is often particularly helpful.

Amie Peterson, M.D.
Assistant Professor of Neurology
OHSU Parkinson Center of Oregon
OHSU Brain Institute

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