When mice are missing a key brain protein, they have difficulty learning, a problem that can be corrected using a potential Alzheimer's drug, Canadian researchers have found.
In Tuesday's issue of the journal PLoS Biology, geneticist Roderick McInnes of Toronto's Hospital for Sick Children and his colleagues describe their experiments showing the protein leads to learning impairments when it is missing or malfunctions.
The protein, called Neto1, helps brain cells communicate with each other.
Networks of brain cells or neurons are able to adapt to learn through a process called synaptic plasticity.
Scientists knew that the NMDA receptor complex is an important part of synaptic plasticity, but how it works remains a major question in neurobiology.
Drug to the rescue
In the study, researchers discovered that Neto 1 is a key player in the NMDA receptor complex, which is crucial for forming memories and learning. The receptors are like gates that open and close to allow signals to pass.
Mice missing the Neto1 gene had fewer NDMA receptors in their brain cells, the researchers said.
But a drug that is being tested to help people with Alzheimer's disease indirectly seemed to keep the receptors open longer in the mutant mice, which were then able to perform as well on cognitive tests as normal mice, the team found.
"This is the first report of a pharmacological rescue of an NMDAR impairment, and consequently, our results extend the principle that in vertebrates, an inherited defect in synaptic plasticity and spatial learning can be corrected in the adult," the study's authors concluded.
It's not known whether the drug could safely help humans with learning disabilities.
