This week, researchers report evidence that a statin drug already shown to be safe for use in humans has proven effective at correcting cell-cell communication and curing learning disfunction in a mouse model of Neurofibromatosis type I, a human genetic disorder that causes learning disabilities in millions of people worldwide.
Learning disabilities affect 5% of the world’s population, have a profound impact on countless lives, and cost billions of dollars, but there is little or nothing that we are currently able do to prevent or treat this enormous problem. At the heart of this challenge is our lack of understanding of the mechanisms underlying this complex class of brain problems. In an effort to understand these disorders and develop treatments, Dr. Alcino Silva and colleagues at UCLA have focused research on the study of the most common genetic cause for learning disabilities: Neurofibromatosis type I (NF1). The idea behind the NF1 research is that if we understand this particular learning disability, which is caused by a single defective gene, and manage to develop effective and sustainable treatments, we may be able to use the information learned to tackle this general class of learning and memory problems.
Because of the difficulties and limitations of studying mechanisms of memory in human patients, the researchers decided to study NF1 in mice. The scientists had previously shown that mice with the mutations that cause NF1 in human patients possess many of the features of this complex disorder, including deficits in spatial learning, attention, and motor coordination. Studies of these mutant mice showed that the learning deficits are caused by the overactivity of a molecule called Ras, causing an imbalance between signals that activate brain cells and those that inhibit them, and leading to deficits in cell-cell communication needed for learning.
Heidi Hardman | EurekAlert!
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