Scientists found that by altering a single gene, they could create "genius" mice that were resistant to anxiety and less likely to recall fear.

The findings could provide a basis for new research on treatments for age-related cognitive decline, psychiatric disorders like schizophrenia, and problems associated with traumatic experiences the University of Leeds reported.

""In the future, medicines targeting PDE4B may potentially improve the lives of individuals with neurocognitive disorders and life-impairing anxiety, and they may have a time-limited role after traumatic events," said Alexander McGirr, a psychiatrist in training at the University of British Columbia, who co-led the study.

To create these incredible mice, a team of researchers altered a gene to inhibit the activity of an enzyme called phosphodiesterase-4B (PDE4B), which is present in the brain. The technique proved to enhance the cognitive abilities of the treated mice, allowing them to learn more quickly, solve complex puzzles, and hold onto memories longer than normal mice. The PDE4B-inhibited mice howed less recall of frightening events after several days and less general anxiety when compared to average mice. The treated mice also displayed a reduced fear towards cats and cat urine than what would be seen in non-treated mice.The diminished memory of fear seen in the PDE4B-inhibited mice could be a clue as to how to treat fear-related disorders such as Post-Traumatic Stress Disorder (PTSD).

The researchers are now working on the development of drugs that will specifically inhibit PDE4B, and will test these drugs on animals to determine if they are suitable for clinical trials in humans.

"This study highlights a potentially important role for the PDE4B gene in learning and memory in mice, but further studies will be needed to know whether the findings could have implications for Alzheimer's disease or other dementias. We'd need to see how this gene could influence memory and thinking in people to get a better idea of whether it could hold potential as a target to treat Alzheimer's," said Laura Phipps of Alzheimer's Research UK, who were not involved in the study.

The findings were published in a recent edition of the journal Neuropsychopharmacology