Lead Exposure May Be Linked to Schizophrenia

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Exposure to lead may contribute to the development of schizophrenia, based on a study in rats.

Scientists at the Mailman School of Public Health at Columbia University found that, in rats, lead had a deleterious impact on three brain areas: the medial prefrontal cortex, the hippocampus, and the striatum. Those areas are also implicated in schizophrenia.

The rats were exposed to lead both before birth and in their early life.

Lead exposure was linked to a decline of about one-third in the density of Parvalbumin-Positive GABAergic interneurons, or PVGI, a type of brain cells. This level of decline is on par with that seen in schizophrenia patients in these cells. The rats also had higher levels of a dopamine receptor known as D2R. Again, the magnitude of the increase was similar to what has bene seen in schizophrenia patients, the researchers reported in the journal Translational Psychiatry.

“The similarities in the brain structure and neuronal systems between what we see in lead-exposed rats and human schizophrenia patients is striking, and adds to a growing body of literature suggesting that early lead exposure primes the brain for schizophrenia later in life,” senior author Tomás Guilarte, PhD, said in a statement.

In a related finding, the researchers found that the lead exposed rats had a much stronger reaction to cocaine than healthy controls.

Lead Exposure May Be Linked to Schizophrenia
Lead Exposure May Be Linked to Schizophrenia

A study of the brains of rats exposed to lead has uncovered striking similarities with what is known about the brains of human schizophrenia patients, adding compelling evidence that lead is a factor in the onset of schizophrenia.

Results of the study by scientists at Columbia University's Mailman School of Public Health appear in the journal Translational Psychiatry.

The researchers found that lead had a detrimental effect on cells in three brain areas implicated in schizophrenia: the medial prefrontal cortex, the hippocampus, and the striatum of rats exposed to lead before birth and in the early part of their lives. Density of brain cells known as Parvalbumin-Positive GABAergic interneurons, or PVGI, declined by approximately a third — at roughly the same percentage decline seen in schizophrenia patients. And, using imaging technology, they identified higher levels of a dopamine receptor called D2R. Again, the magnitude of the increase matched what has been documented in human schizophrenia patients, and in a previous study of genetically engineered mice.

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