Brain Inflammation a Hallmark of Autism, Study Shows
- Created on December 11, 2014
WEDNESDAY, Dec. 10, 2014 (HealthDay News) -- Brain inflammation, triggered by an overactive immune system, is common among people with autism, a new study finds.
However, this inflammation does not cause the developmental disorder. Rather, it's a response to the different factors that can trigger autism, the researchers stressed.
Their findings are based on autopsies performed on 72 brains of people with and without autism. In the brains of those who had autism when they were alive, a certain type of cell had its genes for inflammation permanently turned on.
"There are many different ways of getting autism, but we found that they all have the same downstream effect," study author Dan Arking, an associate professor at the Institute for Genetic Medicine at Johns Hopkins University School of Medicine in Baltimore, said in a university news release.
"What we don't know is whether this immune response is making things better in the short term and worse in the long term," he added.
The next step is to find out whether treating this inflammation would reduce symptoms of autism, Arking said.
The study was published online Dec. 10 in the journal Nature Communications.
"This type of inflammation is not well understood, but it highlights the lack of current understanding about how innate immunity controls neural circuits," study co-author Andrew West, an associate professor of neurology at the University of Alabama at Birmingham, said in the news release.
The U.S. National Institute of Neurological Disorders and Stroke has more about autism.
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Study suggests potential therapy for second most common form of dementia
- Created on December 04, 2014
Written by Bob Shepard
Drugs that boost the function of a specific type of neurotransmitter receptor may provide benefit to patients with the second most common type of dementia, according to research by scientists at the University of Alabama at Birmingham published today in the Journal of Neuroscience.
Frontotemporal dementia, known as FTD, is a devastating disease in which patients have rapid and dramatic changes in behavior, personality and social skills. The age of onset for FTD is relatively young, usually striking patients in their mid- to late 50s. The prognosis is grim; patients quickly deteriorate and usually die within 10 years after onset. Currently, there is no effective treatment for FTD.
The UAB research team’s effort focused on mutations in certain genes, primarily in the Microtubule Associated Protein Tau gene. An accumulation of tau protein is associated with Alzheimer’s disease, the most common form of dementia; but little is known how tau mutations affect specific brain regions and cause FTD.
The UAB researchers used a new mouse model expressing human tau with an FTD-associated mutation. These mice demonstrate physical behaviors similar to those seen in humans with FTD — compulsive, excessively repetitive actions such as grooming, for example. The mice also had impaired synaptic and network function in certain brain network regions.
“We found that mutant tau impairs synapses — the connections between neurons — by reducing the size of the anchoring sites of an essential glutamate receptor called NMDA,” said Erik Roberson, M.D., Ph.D., associate professor in the Department of Neurology and primary investigator for the study. “Reduction of the anchoring sites left fewer NMDA receptors available at the synapse to receive excitatory signals, thus limiting synaptic firing and network activity.”
The team then employed cycloserine, a drug already approved for use by the FDA, which is known to assist NMDA receptor function. This boost of NMDA receptor function was able to restore synaptic firing and thereby restore network activity in the animal model. The restoration of normal network activity reversed the behavioral abnormalities seen in the mice.
“This study provides mechanistic insight into how a tau mutation affects specific brain regions to impair a network,” said Roberson. “It also provides a potential therapeutic target, the NMDA receptor, which appears to correct the network and behavioral abnormalities.”
Roberson’s team hypothesizes that increasing NMDA receptor function may benefit human FTD patients. With further preclinical validation, this hypothesis could be tested in clinical trials using the already available drug cycloserine.
Dr. Marissa Natelson Love Awarded ACA Grant
- Created on November 18, 2014
Dr. Marissa Natelson Love, a UAB Memory Disorders Fellow, was awarded a grant November 14, 2014, from Alzheimer’s of Central Alabama (ACA) at their Annual Meeting to assist in funding research at UAB on Clinical Correlates of Family Quality of Life in Dementia. Dr. Natelson is pictured here accepting the award from Alacare President John Beard, ACA Executive Director Miller Piggott, and ACA Vice President for Research Dr. Lindy Harrell.
Investing in Breakthroughs
- Created on September 30, 2014
The Jurenko name is indelibly linked with the UAB Department of Neurology, so consistent has been the Huntsville couple’s support of the department’s goals. Since 2007, John Jurenko, the retired vice president of sales and marketing at ADTRAN, a company he co-founded in 1985, and his wife, Ruth, have made gifts to advance numerous initiatives within the department. Among these are the John A. and Ruth R. Jurenko Neurological Research Laboratory, the John A. and Ruth R. Jurenko Research Scholar Fund, and the UAB-HudsonAlpha Collaborative Project in the Genetics and Genomics of Parkinson’s Disease.
Their latest gift, to establish the John A. and Ruth R. Jurenko Endowed Professorship in Neurology, enabled department chair David G. Standaert, M.D., Ph.D., to recruit one of the country’s leading Parkinson’s disease researchers. In 2007, Andrew B. West, Ph.D., was recruited from Johns Hopkins University to UAB, where he was named the John A. and Ruth R. Jurenko Research Scholar and became director of the John A. and Ruth R. Jurenko Neurological Research Laboratory in the UAB Center for Neurodegeneration and Experimental Therapeutics (CNET). In February 2013, he became the inaugural holder of the John A. and Ruth R. Jurenko Endowed Professorship in Neurology.
John Jurenko first encountered the Department of Neurology as a Parkinson’s patient, but was quickly impressed by the innovative research taking place. “My original contact with the department was because of the disease, but then I got to know the people there. They are exceptional people, both professionally and personally,” he says. “In discussion with them, I learned that they wanted to grow the department, and I figured I could help. They mentioned Andy West and his talent and that they’d like to have him. So I said, ‘Well, let’s go get him.’”
According to Standaert, philanthropic support like the Jurenkos’ has been key to making the UAB Department of Neurology and its associated divisions and centers the hives of innovation they are today. “Almost all of the major faculty recruitments we have done have been based on philanthropic gifts,” he says. “Their willingness to support our vision has enabled the tremendous growth we have experienced in less than a decade. When I first came to UAB in 2006 to lead CNET, it was just me. Now the center comprises more than 50 scientists, students, postdocs, and staff.” This philanthropic investment in research has contributed to an explosion in Parkinson’s discoveries, Standaert says. “The amount we’ve learned in the past five years exceeds everything we knew from the previous 200 years. We are deeply grateful to John and Ruth Jurenko for helping us achieve so much in such a relatively short period of time.”
According to West, “Meaningful advances in neurodegeneration research are very hard won. The John A. and Ruth R. Jurenko Professorship in Neurology allows us to accelerate the process and provides key resources to address critical questions that can’t wait for traditional funding mechanisms. With the support of the Jurenkos, we can focus on addressing critical bottlenecks and hasten the identification of novel neuroprotective therapeutics.”