To fight inherited autism
Divya Gandhi
Scientists reverse genetic autism in mice; clinical trials on
Bangalore: A treatment for inherited autism and developmental disorders may be
closer than thought, with new understanding of the Fragile X syndrome, the
most common inherited cause of mental impairment, emerging.
In a research paper published in the international journal Neuron on December
20, scientists have demonstrated that the symptoms of Fragile X can be reversed
in mice that were genetically engineered to manifest the symptoms found in
humans. Fragile X syndrome is associated with developmental disorders such as
learning disorders, attention deficit disorder and vulnerability to seizures. A
third of individuals with the syndrome are autistic.
The paper is co-authored by seven scientists, including two Bangalore-based
scientists: Sumantra Chattarji, Professor, National Centre for Biological
Sciences
(NCBS); and B.S. Shankaranarayana Rao, Associate Professor, National Institute
of Mental Health and Neurosceince . The others are from the Massachusetts
Institute of Technology, and Brown Medical School in the U.S.
The paper discusses the "major therapeutic implications" of this finding, and
possibilities of developing drugs to treat the disorder.
"We have known for a long time now that individuals with the Fragile X syndrome
have very low concentrations of an important protein, FMRP (Fragile X Mental
Retardation Protein), which is instrumental in the development of the brain and
in the forming of synaptic connections," explains Professor Chattarji.
The new understanding pertains to its interaction with another protein, called
mGluR5 (metabotropic glutamate receptor), the level of which increases
dramatically
in people with reduced FMRP. This contributes to the disorder, also preventing
neural connections from maturing, he says.
Says Dr. Rao: "What our research shows is that by reducing mGluR5 by 50 per
cent in mice, immature connections in the brain grew into mature synapses, the
ability of the brain to process information improved, the incidence of seizures
reduced and social interaction increased."
"Now that we have established this link between these two brain proteins,
designing drug therapy will become easier," says Dr. Rao. Clinical trials are
under way for a drug that blocks mGluR5.
Earlier this year Professor Chattarji and Dr. Rao, among others, identified the
role of a brain enzyme PAK (p21-activated kinase) in mental retardation.
"But our new findings about mGluR5 will take us much faster towards drug
therapy. We could have a drug much sooner than we expected, perhaps even within
five years," says Professor Chattarji.
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