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Exposure to lead can hinder the brain’s ability to recover from injury, a recent study in laboratory animals shows. The results have implications for the effects of environmental lead exposure on brain injuries such as stroke, say researchers at Jefferson Medical College, who led the work.

Lead exposure early in life is known to increase the risk for cancer, renal disease, hypertension and cardiovascular disease later in life, and as a result, also increases the risk for stroke and brain damage. Jay Schneider, Ph.D., professor of Pathology, Anatomy and Cell Biology and Neurology at Jefferson Medical College of Thomas Jefferson University in Philadelphia and research associate, Emmanuel Decamp, wanted to know if it was possible that lead might alter the potential for plasticity, the ability of the brain to compensate for an injury. They studied young rats that were fed a diet supplemented with lead and compared them to others on a diet without lead. In earlier work in the lab, they found that even brief exposures to lead affected neurotrophic factors in the brain important for growth and maintenance of neurons and their connections.

They ran each group through some simple behavioral tests before causing a small stroke in a specific part of the brain that affected a hind limb. Reporting in the journal NeuroToxicology, Dr. Schneider, who is director of the Parkinson’s Disease Research Unit at Thomas Jefferson University, and his group saw significant recovery after a brief period of time in the control group, “as compensatory processes take over,” though the limb function was not completely back to normal.

“In contrast, those animals that were exposed to lead earlier in life had worse outcomes in the same period after the stroke,” he says. “There was significant difference in the brain’s ability to compensate for that injury.”

Because the study was brief, he says, they don’t know if in a longer period of time the lead-exposed animals would catch up in their recovery to the controls. There was some recovery in the lead group, but then it leveled off. The control group continued to get better.

“That’s one of the questions we would like to pursue in further studies – whether lead exposure slows or attenuates the recovery process after a brain injury,” Dr. Schneider notes. “Have they recovered as much as they will recover or given more time, would they recover to the same extent? Is lead exposure affecting the rate of recovery or the recovery potential?”

According to Dr. Schneider, it is well known that lead exposure had detrimental effects on learning and memory, other forms of brain plasticity. “Brain plasticity generally refers to the brain’s ability to be molded by experience as well as its ability to reorganize anatomically and functionally and recover from injury,” Dr. Schneider says. “It’s why people who have relatively small strokes can recover function. The brain has an innate ability to reorganize and repair itself. Our data suggest that lead exposure may compromise or alter this capacity for remodeling that may impair recovery of function following brain injury.”

Next, the group would also like to see if such a trend translates to recovery from other types of injury, such as traumatic brain injury. They would also like to explore the notion that childhood lead exposure increases the risk of a child having a poorer outcome from an acquired brain injury.

Dr. Schneider explains that one important aspect of lead poisoning is impairment of plasticity. “The data we have begin to support that,” he says. “We want to look at the effects of different levels of lead exposure on the outcome from acquired brain injury and see how different types and extents of exposures correspond with the expression of injury and recovery of function. Then, we want to try to nail down the biological processes responsible.”