Exercise May Help Ward Off Memory Decline

Newswise, October 24, 2016– Exercise may be associated with a small benefit for elderly people who already have memory and thinking problems, according to new research published in the October 19, 2016, online issue of Neurology®, a medical journal of the American Academy of Neurology.

The research involved people with vascular cognitive impairment, which is the second most common cause of dementia after Alzheimer’s disease. In vascular cognitive impairment, problems with memory and thinking skills result from damage to large and small blood vessels in the brain.

“Studies have shown that exercise can help reduce the risk of developing memory problems, but few studies have looked at whether it can help people who already have these problems get better or keep from getting worse,” said study author Teresa Liu-Ambrose, PT, PhD, of the University of British Columbia in Vancouver, Canada.

The study involved 70 people with an average age of about 74 who had mild vascular cognitive impairment.

Half of the participants took part in one-hour exercise classes three times a week for six months. The other half received information each month about vascular cognitive impairment and a healthy diet, but no information on physical activity.

All of the participants were tested before the study started, at the end of the study and again six months later on their overall thinking skills, executive function skills such as planning and organizing and how well they could complete their daily activities.

Those who exercised had a small improvement on the test of overall thinking skills compared to those who did not exercise. The scores of those who exercised improved by 1.7 points compared to those who did not exercise.

“This result, while modest, was similar to that seen in previous studies testing the use of drugs for people with vascular cognitive impairment,” Liu-Ambrose said.

 “However, the difference was less than what is considered to be a the minimal clinically important difference of three points.”

Six months after the participants stopped the exercise program, their scores were no different than those who did not exercise. Also, there was no difference between the two groups at any point on the tests of executive function skills or daily activities.

Those who exercised also improved compared to the other group in their blood pressure and on a test of how far they could walk in six minutes, which measured overall cardiovascular capacity.

These findings are also important to note given that high blood pressure is a risk factor for developing vascular cognitive impairment.

Liu-Ambrose said more studies are needed to determine whether exercise can improve thinking abilities in people with mild vascular cognitive impairment.

Because the study sample size was based on detecting a difference on the overall thinking skills test, large samples might be needed to detect differences in specific thinking abilities, such as planning, and everyday skills, such as managing one’s finances.

The study was supported by the Canadian Stroke Network and the Heart and Stroke Foundation of Canada.

To learn more about brain health, visit www.aan.com/patients.

The American Academy of Neurology is the world’s largest association of neurologists and neuroscience professionals, with 30,000 members. The AAN is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer’s disease, stroke, migraine, multiple sclerosis, concussion, Parkinson’s disease and epilepsy.

For more information about the American Academy of Neurology, visit http://www.aan.com or find us on Facebook, Twitter, LinkedIn and YouTube.

MEMORY LOSS NOT ENOUGH TO DIAGNOSE ALZHEIMER’S

 Alzheimer’s disease can have symptoms other than memory loss

Newswise, September 14, 2016 --- Relying on clinical symptoms of memory loss to diagnose Alzheimer’s disease may miss other forms of dementia caused by Alzheimer’s that don’t initially affect memory, reports a new Northwestern Medicine study.

“These individuals are often overlooked in clinical trial designs and are missing out on opportunities to participate in clinical trials to treat Alzheimer’s,” said first study author Emily Rogalski, associate professor at Northwestern’s Cognitive Neurology and Alzheimer’s Disease Center.

There is more than one kind of Alzheimer's disease. Alzheimer’s can cause language problems, disrupt an individual’s behavior, personality and judgment or even affect someone’s concept of where objects are in space.

If it affects personality, it may cause lack of inhibition. “Someone who was very shy may go up to grocery store clerk -- who is a stranger -- and try to give her a hug or kiss,” Rogalski said.

This all depends on what part of the brain it attacks. A definitive diagnosis can only be achieved with an autopsy.

Emerging evidence suggests an amyloid PET scan, an imaging test that tracks the presence of amyloid -- an abnormal protein whose accumulation in the brain is a hallmark of Alzheimer’s -- may be used during life to determine the likelihood of Alzheimer’s disease pathology.

In the study, the authors identify the clinical features of individuals with primary progressive aphasia (PPA), a rare dementia that causes progressive declines in language abilities due to Alzheimer’s disease. Early on in PPA, memory and other thinking abilities are relatively intact.

PPA can be caused either by Alzheimer’s disease or another neurodegenerative disease family called frontotemporal lobar degeneration. The presence of Alzheimer’s disease was assessed in this study by amyloid PET imaging or confirmed by autopsy.

The study demonstrates that knowing an individual’s clinical symptoms isn’t sufficient to determine whether someone has PPA due to Alzheimer’s disease or another type of neurodegenerative disease.

Therefore, biomarkers, such as amyloid PET imaging, are necessary to identify the neuropathological cause, the authors said.

Northwestern scientists looked at individuals in mild stages of language loss caused by Alzheimer’s disease and described their brain atrophy based on MRI scans and their results on cognitive tests.

“We wanted to describe these individuals to raise awareness about the early clinical and brain features of PPA to develop metrics which would advocate for their inclusion in clinical trials targeting Alzheimer’s disease,” Rogalski said.

“These individuals are often excluded because they don’t have memory deficits, but they share the same disease [Alzheimer’s] that’s causing their symptoms.”

The study was published online in the journal Neurology Aug. 26.

Dr. Marsel Mesulam, director of the Cognitive Neurology and Alzheimer's Disease Center and the Ruth Dunbar Davee Professor of Neuroscience at Northwestern University Feinberg School of Medicine, is senior author of the paper.

The study was funded by grants DC008552 from the National Institute on Deafness and Other Communication Disorders, AG13854 from the National Institute on Aging, NS075075 from the National Institute of Neurological Disorders and Stroke, all of the National Institutes of Health.

Memory Loss Caused by West Nile Virus Explained

Study identifies targets for prevention, treatment

Newswise, June 23, 2016— Every year as mosquito season arrives, so does West Nile virus, causing fever in thousands of people nationwide and life-threatening brain infections in an unlucky few. About half the people who survive that infection – West Nile encephalitis – are left with permanent neurological deficits such as memory loss.

New research shows that these long-term neurological problems may be due to the patient’s own immune system destroying parts of their neurons, which suggests that intervening in the immune response may help prevent brain damage or help patients recover.

The study is published June 22 in Nature.

Since 1999, when West Nile arrived in the Western Hemisphere via an infected flamingo in the Bronx Zoo, the virus has spread throughout the Americas, infecting millions of people.

Ten thousand West Nile survivors are living with long-term neurological problems such as fatigue, weakness, difficulty walking and memory loss, and the number goes up by about a thousand every year following mosquito season. There is no vaccine or specific treatment for West Nile infection.

“When I talk with other doctors about West Nile patients with these persistent neurological deficits, many say, ‘The virus in their brains must have killed neurons, and there’s nothing we can do about it,’” said Robyn Klein, MD, PhD, a professor of medicine and the study’s senior author.

“My thinking has been, if we can determine what triggers this brain damage, maybe we can prevent this from happening or stop it afterwards.’”

Klein, postdoctoral researcher Michael Vasek, PhD, and colleagues developed a mouse model of West Nile encephalitis by injecting a weakened strain of the virus directly on top of the mouse hippocampus, a region of the brain important for memory.

A month after the mice had recovered from the infection, the researchers tested the animals’ ability to navigate a maze.

Much like West Nile survivors who cannot navigate their neighborhood, the infected mice could not remember how to navigate the maze. But contrary to conventional wisdom, their hippocampal neurons hadn’t been killed by the virus.

Instead, the researchers found that microglial cells, a kind of immune cell that lives in the brain, were clustered around the neurons at the site of infection and were highly activated – “on fire,” as Klein put it.

Moreover, levels of an immune protein called complement were high in the brains of mice with memory loss. Neurons make connections to each other at junctions called synapses, allowing information to be passed from cell to cell. During normal brain development, many more synapses are formed than needed and only those that are strengthened should persist. Complement tags the weak synapses to be removed, and activated microglia destroy them.

In the mice with memory loss, viral infection seems to have sent this system into overdrive, leading to the destruction of needed synapses. Synapses must be formed or strengthened for learning and memory to occur.

While the neurons near the activated microglia were still alive, they were lacking synapses. The more synapses that were destroyed, the worse the mouse’s memory problems.

“There’s never been any model of cognitive dysfunction due to brain infection that shows that eliminating synapses without loss of neurons could cause these symptoms,” said Klein, who is also a professor of pathology and immunology, and of neurosciences.

“It’s really a paradigm-shifting idea that a viral infection can do this. It also makes us wonder whether these mechanisms are involved in other diseases associated with memory loss.”

Healthy people create new synapses throughout life as they learn new things. West Nile survivors, however, may be unable to grow new synapses to replace the ones lost during their bouts of encephalitis.

“The microglia remain activated long after the virus is cleared, and this may be preventing the synapses from recovering,” Klein said. “But that gives us hope that we can develop interventions directed at the immune response. We think we can treat this. And that’s what we’re trying to do.”