Mice with symptoms that mimic Bardet-Biedl syndrome (BBS) have difficulty learning and generating new neurons in the hippocampus. However, according to a new study by Thomas Pak, Calvin Carter and Val Sheffield of the University of Iowa, published on April 22 in the journal PLOS Genetics, these mental defects can be successfully treated with lithium.
BBS is a rare genetic disorder that results in intellectual disability, vision loss and obesity, and sometimes kidney problems and additional fingers and toes. It is one of many ciliopathies, which are diseases that arise from defective cilia – tiny finger-like projections on the surface of cells that play an important role in moving fluids, sensing the environment, and signaling between cells. Pak, Carter, Sheffield and their colleagues wanted to learn more about how ciliopathies cause intellectual disability, so they studied a type of mouse with the same symptoms as people with BBS.
In the new study, the researchers showed that normal mice could be quickly trained to associate a specific environment with a frightening event, but BBS mice had a harder time remembering fear. Further investigation has shown that these learning problems stem from an inability to make new neurons in the hippocampus. However, treating mice with lithium increased cell production and improved learning and memory.
Intellectual disability is the most common type of neurodevelopmental disorder, but few drugs are available to treat it. New study suggests lithium may be an effective treatment for learning and memory defects caused by BBS, and researchers suggest more studies should be done to test the use of this FDA-approved drug . The new findings also demonstrate a new role for cilia in learning and memory in the brain, potentially improving our understanding of the mechanisms that cause intellectual disability.
Pak adds: “A mouse model of an eyelash disease, Bardet-Biedl syndrome, impaired fear memory and hippocampal neurogenesis. In this mouse model, lithium treatment improves memory of fear and hippocampal neurogenesis. “
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