The specially bred rodents were genetically engineered without the enzyme Cdk5 which causes the death of brain cells in Alzheimer's patients.

The mice were found to be much smarter and learned quicker than other mice and the researchers say their work could lead to new treatments for Alzheimer's disease.

The team at the University of Texas (UT) Southwestern Medical Center, say they have demonstrated that a gene in an adult animal can be switched off and that has never been done before.

Lead researcher Dr. James Bibb says when the genetically modified mice were closely examined it was seen that areas of their brains which were responsible for memory and learning appeared to be much more active.

The engineered mice were found to be more adept at learning to navigate a water maze and remembering that being in a certain box involves a mild shock; when the situation changed, such as the water maze being rearranged, the engineered mice were much faster to realize that things were different and work out the new route.

Dr. Bibb says being able to make mice "smarter" is very rare and this has many cognitive implications.

Dr. Bibb says any time the brain loses neurons, Cdk5 may be contributing to that process as Cdk5 made them have a much stronger associative memory.

The scientists are now looking at the long-term effects of deleting the enzyme, and are also searching for drugs which can be used to suppress the enzyme that when broken down, appears to boost levels of the learning compound.

Dr. Bibb says the findings could have applications in the treatment of post-traumatic stress disorder, and addiction to drugs of abuse, as well as Alzheimer's disease.

He says understanding how the enzyme affects the brain and behavior might aid in the development of new treatments for these and other conditions.

The research appears in the online edition of the journal Nature Neuroscience.

"While preliminary, these results may allow investigators to identify biomarkers of disease progression," said Dr King, who is the Chief of Medicine at San Francisco General Hospital and an internationally renowned expert in research and management of pulmonary fibrosis.

The senior author on this paper, Dr Naftali Kaminski, who is the Director of the Simmons Center for Interstitial Lung Disease at the University of Pittsburgh, added that this research highlighted the need to collect as much information on patients with IPF as possible. "We are only now starting to really understand the disease and characterize it," he said, "therefore, it is critical for patients with the disease to be seen in centers that are actively involved in IPF research."

Better identification and understanding of these differences may provide insights into the pathogenesis of IPF and assist in the development of therapeutic interventions for this devastating lung disease.

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