Search the Bridge

Mailing List

Contact Us


Research Briefs

Search Research Briefs
| Browse Research Briefs

Impaired communication. As many as 1.5 million Americans, mostly boys, are afflicted by autism, an inherited neurological disorder that interferes with the normal development of the brain and causes difficulty in social interaction and communication. Gene Blatt, a MED associate professor of anatomy and neurobiology, is director of the Laboratory of Autism Neuroscience Research, which is part of the National Institutes of Health–funded Autism Center of Excellence at BU. He and his colleagues investigate the alterations in the sensory and motor systems and the changes in the brain that underlie the social and emotional behavior characteristics of those with autism.

“By determining what neurochemicals are affected in the autistic brain,” Blatt says, “we can begin to understand the underlying mechanisms that give rise to the behaviors we see with autism.”

In recent studies, Blatt focused on three different neurotransmitter systems, including the inhibitory GABA and serotonin systems, and the excitatory cholinergic system in autism. Neurotransmitters attach, or bind, to specific receptors, or sites, on neurons in the brain. Binding signals the neuron either to begin or to stop sending signals to other neurons. A complex pattern of signaling throughout the brain ultimately results in behavior. Blatt hypothesizes that the delicate balance between starting, or exciting, and stopping, or inhibiting, signaling is upset in autism.

The researchers examined tissue samples from the brains of both autistic and nonautistic individuals, finding in the brains of the autistic subjects fewer type-2 muscarinic receptors — one type of receptor for the the major neurotransmitter acetylcholine. They found this deficit in a specific area of the brain called the medial accessory olive, a subregion of the inferior olive, a structure in the brain that communicates directly with the cerebellum.

Blatt and his colleagues hope that new data about how neurotransmitter systems operate differently in autistic brains, together with knowledge about where these differences are located, may one day lead to the development of new pharmaceuticals that target the underlying causes of autism, rather than just its behavioral symptoms.

Healing news. Most people heal quickly from minor cuts, scrapes, and bruises, but for people with diabetes such wounds can quickly become serious, leading to severe infection or even amputation of an affected limb. This is also true for bacteria-induced injuries such as periodontal disease, which can cause tissue damage in the gums and jaw.

It has been commonly believed that diabetes somehow impairs the body’s ability to fight bacteria at the site of such an injury. But new evidence implicates an additional mechanism. Recent research led by Dana Graves, an SDM professor of periodontology and oral biology, indicates that diabetes also interferes with the work of fibroblasts, the cells that spring into action to repair damaged tissue.

In nondiabetic individuals, fibroblasts move in large numbers to the site of an injury and begin to build new tissue to fill in the area damaged by bacteria. During the later stages of healing, enzymes signal the fibroblasts to self-destruct, a process known as apoptosis, to avoid creating excessive scar tissue.

The experiments, which were done by Rongkun Liu and others in Grave's laboratory found a high rate of fibroblast apoptosis during the peak phase of healing in diabetic mice. The researchers speculate that hyperglycemia, the high blood sugar levels characteristic of unregulated diabetes, may stimulate a cascade of events that leads to activation of an enzyme known as caspase-3, which initiates apoptosis.

More than 17 million Americans have diabetes, and many times that number worldwide, so the impact of diabetes-related infection is profound. The researchers hope that by improved understanding of how healing is short-circuited by diabetes, they will be better able to design ways to put the healing process back on track.

This research was published in the June 2004 issue of the journal Endocrinology.

"Research Briefs" is written by Joan Schwartz in the Office of the Provost. To read more about BU research, visit


15 May 2003
Boston University
Office of University Relations