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Wednesday, March 23, 2016

Viruses Could Be Causing Alzheimer’s

Dear Readers,
An international team of 31 researchers wrote an editorial in the Journal of Alzheimer’s Disease suggesting that viral and bacterial infections caused by viruses such as herpes, generate plaque build-up in the brain, the hallmark of Alzheimer’s. They suggested that treating these infections with antimicrobial drugs might stop dementia. The herpes virus, Chlamydia bacteria and spirochaete bacteria were named as major triggers.

The authors pointed out that viruses and bacteria are common in the brains of older people, and while they are usually dormant, they can come to life from stress or if the immune system is compromised. It is well known that the herpes virus can damage the central nervous system. In addition they brought up that a gene mutation - APOEe4 - also raises vulnerability to infectious disease. Viral infections in the brain are known to cause symptoms similar to Alzheimer’s; the experts say the link has been ignored for too long.

“Alzheimer’s disease causes great emotional and physical harm to sufferers and their carers as well as having enormously damaging economic consequences,” they wrote. “We write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest Alzheimer’s disease progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain.”

The authors propose further research on the role of infectious agents in Alzheimer’s disease development, saying that the inclusion of antimicrobial therapy in clinical trials is now justified.”

They added that new findings could also have significance for future treatment of Parkinson’s Disease, and other progressive neurological conditions.

To read the full editorial, please visit:

Thanks for reading,

Jeffree Itrich, M.S.W., M.J.
Mgr, ADCS Communications
Author: Jeffree Itrich at 10:41 AM 0 Comments

Wednesday, March 16, 2016

Ohio State University Researchers Establish Link Between Chronic Stress and Short Term Memory Loss

Dear Readers,

According to a new mouse study out of Ohio State University, continuous stress wears down memory. Lead researcher Jonathan Godbout, associate professor of neuroscience at Ohio State says the type of stress they looked at is not everyday stress that everyone encounters, but chronic stress. The study appeared in the March 2nd issue of Journal of Neuroscience and built upon earlier work corroborating associations between chronic stress and lasting anxiety.

In the new study, researchers trained mice on the location of an escape hole in a maze. All the mice mastered the escape route. Later, researchers introduced an aggressive intruder mouse into the maze. The mice that were repeatedly exposed to the intruder had difficulty recalling the location of the escape hole, whereas the mice that were not exposed to the intruder and were not stressed, easily found it.

In addition, the researchers discovered quantifiable changes in the mice brains, such as signs of inflammation instigated by the immune system’s response to outside pressure. They associated this finding to the presence of macrophages (immune cells) in the brains of the stressed out mice. The research team was able to isolate the short-term memory loss to the inflammation as well as the immune system, which the team called important new discoveries. In the future the team hopes to interrupt the inflammation, possibly by identifying targets that could be treated pharmacologically or by employing behavior changes.

This new study focused on the hippocampus, the brain’s center of memory and emotional response. The researchers found that the stressed mice had trouble with spatial memory that resolved within 28 days. They also found that the mice exhibited social avoidance, which measures depressive-like behavior that continued after four weeks of monitoring. Moreover, they were also able to calculate deficits in the development of new neurons 10 days and 28 days after the prolonged stress ended. When they gave the mice a compound that hindered inflammation, neither the depressive symptoms nor brain-cell problems resolved. However, the memory loss and inflammatory macrophages did disappear. This led the researchers to deduce that the post-stress memory issue was directly linked to inflammation – and the immune system – rather than to other damage to the brain. They hope that this type of finding can pave the way for immune-based treatments.

Thanks for reading,

Jeffree Itrich, M.S.W., M.J.
Mgr, ADCS Communications

Author: Jeffree Itrich at 11:25 AM 0 Comments

Wednesday, March 02, 2016

Connectivity Disruptions May Cause Cognitive Deficits in Traumatic Brain Injury

Each year approximately 1.7 million Americans suffer a traumatic brain injury (TBI). Cognitive impairment following a TBI is not uncommon. Researchers at the Center for BrainHealth at The University of Texas at Dallas wondered if connectivity disruptions could be the reason behind the development of cognitive deficits in these patients.

To test their theory, the researchers analyzed 40 MRI scans of TBI patients against MRI scans of 17 healthy individuals matched for gender, age and years of education. Participants were aged 19 to 45 years. Although everyone in the TBI group was at least six months post-injury at the time of the study, the average length of time since injury was eight years with no history of any noteworthy, clinically-diagnosed neurological or psychiatric disorders prior to suffering their TBI.

The researchers discovered that people who are at least six months post-TBI display between-network, long-range and inter-hemispheric connectivity interruptions in the default mode and dorsal attention networks, as well as the frontoparietal control networks. This is key because interactions among the networks are essential for achieving daily life goals such as controlling internal trains of thought and accomplishing daily tasks such as planning, learning and problem solving. The research indicates that cognitive deficits could be the end result of brain network communications inefficiency.

Kihwan Han, Ph.D., served as the study’s lead author and is a post doctoral research associate at the Center for BrainHealth. Daniel Krawczyk, Ph.D. served as principal investigator he is associate professor of cognitive neuroscience and cognitive psychology at the Center for BrainHealth and Debbie and Jim Francis Chair at The University of Texas at Dallas. Their study was recently published in the Journal of International Neuropsychological Society.

Previously most research has focused on separating out individual brain networks. The researchers say this is the first study of its kind to show the relationships among different networks and disruptions in individuals with TBI. In the future the group hopes to study how networks can be improved, even after a TBI.

Funding was provided by US Department of Defense and The Meadows Foundation.
Author: Jeffree Itrich at 10:08 AM 0 Comments

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The Alzheimer's Disease Cooperative Study (ADCS) was formed in 1991 as a cooperative agreement between the National Institute on Aging (NIA) and the University of California, San Diego. The ADCS is a major initiative for Alzheimer's disease (AD) clinical studies in the Federal government, addressing treatments for both cognitive and behavioral symptoms. This is part of the NIA Division of Neuroscience's effort to facilitate the discovery, development and testing of new drugs for the treatment of AD and also is part of the Alzheimer's Disease Prevention Initiative.

The ADCS was developed in response to a perceived need to advance research in the development of drugs that might be useful for treating patients with Alzheimer's disease (AD), particularly drugs that might not be developed by industry.