- The focus of ALS research has expanded from motor neurons alone to central nervous system support cells (glia), which include astrocytes, microglia and oligodendrocytes.
- MDA's Neuron Symposium, held May 22, 2012, in Tucson, Ariz., provided the chance for more than a dozen of the world's top scientists to focus on the role of glia in ALS.
- The Neuron Symposium is the second of four in MDA’s 2012 Symposium Series, which is designed to help accelerate therapy development for ALS and the other diseases in its program.
The contribution of nervous system support cells called glia to the degeneration of motor neurons in amyotrophic lateral sclerosis (ALS)was the topic of serious discussion among researchers at MDA's Neuron Symposium on May 22, 2012.
The meeting, held at MDA's national headquarters in Tucson, Ariz., brought together ALS researchers studying the toxic role played in that disease by glia, and scientists who specialize in these key support cells.
The symposium opened with a keynote address by Don Cleveland, professor and chair of Cellular and Molecular Medicine at the University of California, San Diego.
Stanley H. Appel and Jeffrey Rothstein co-chaired the event. Appel, a longtime and current MDA research grantee, is chairman of the Department of Neurology at the Methodist Neurological Institute (MNI) in Houston, where he directs the MDA/ALS center. Appel is also a longtime MDA adviser, serving on MDA’s Board of Directors and chairing its Medical Advisory Committee. Rothstein, a longtime and current MDA research grantee, directs both the Robert Packard Center for ALS Research and the MDA/ALS Center at Johns Hopkins University in Baltimore.
The symposium marked the second in a series of four MDA symposia scheduled for 2012, each of which is focused on a particular aspect of disease processes or therapy development for the neuromuscular diseases in MDA’s program.
Glial cells more important than previously thought
Years ago, nearly all ALS research focused solely on the nerve cells called motor neurons. It was thought that somehow repairing or replacing these muscle-activating cells would cure the disease.
Over time, however, it's become clear that motor neuron degeneration in ALS occurs in large part because surrounding cells (such as astrocytes, microglia and oligodendrocytes) don't perform their normal support functions. Instead, these normally protective cells develop other functions that are toxic to motor neurons.
"While it is clear that glial cells play a critical role in the degeneration of neurons in ALS, a lot remains to be deciphered about how this actually happens," said Sanjay Bidichandani, MDA vice president for research. "MDA’s Neuron Symposium was designed to bring together the top minds in the field to discuss the plans and tools that will be necessary to unravel the role of glial cells in ALS."
Top scientists share expertise
Speakers at the May 22 symposium included experts in ALS and scientists whose specialties include glial cells. Among those making presentations were:
- Jean-Pierre Julien, an MDA grantee and professor at Laval University in Quebec. Julien, who has conducted extensive research on microglia (the innate immune cells of the central nervous system), noted that increased activity (upregulation) of the ALS-associated gene TDP43 increases the sensitivity of motor neurons to a toxic environment.
- Serge Przedborski, co-director of the Center for Motor Neuron Biology and Disease at Columbia University in New York. Przedborski studies the ways in which microglia and astrocytes contribute to neurodegeneration. He discussed results from previously published studies that have shown that, at least under some circumstances, astrocytes appear to be toxic in both familial and sporadic ALS. Astrocytes have been implicated in the ALS disease process.
- Brian Popko, director of the University of Chicago Center for Peripheral Neuropathy. Popko, who holds a particular interest in interactions between motor neurons and glial cells, discussed the relationship between oligodendrocyte function, inflammation and a particular type of stress — ER stress — that damages the cell membrane known as the endoplasmic reticulum. ER stress is one of a number of processes that are thought to play a part in ALS progression.
Two more MDA symposia in 2012
MDA will sponsor two additional research symposia in 2012:
- MDA Translational Research Symposium, focusing on enhancing collaboration and technology transfer between academia and industry, June 17, in New Orleans; and
- MDA Muscle Symposium, focusing on developing newborn screening for DMD, Sept. 11-12, in Washington, D.C.
"MDA’s new symposium series is designed to address cutting-edge issues in neuromuscular disease research," said Bidichandani. "Science is advancing at a rapid pace, and these small and focused meetings will allow us to be nimble in tackling multiple issues every year."
The Association's 2012 symposium series was launched May 17, 2012, in Philadelphia, with the MDA-AFM Gene Therapy Symposium. Held in conjunction with the 2012 meeting of the American Society of Gene & Cell Therapy, this examination of challenges in developing gene therapy for neuromuscular disease was jointly sponsored by MDA and the Association Française Contre les Myopathies (French Association Against Myopathies).
For background information on the role of glial cells in ALS, see: