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 Gene Therapy Reverses Memory Loss In Mice Models

​Researchers have developed a novel gene therapy that reverses the loss of memory in mice models with initial stages of Alzheimer’s disease, according to a study published Wednesday in The Journal of Neuroscience.

The therapy, developed by researchers from the Institute of Neuroscience at the Universitat Autònoma de Barcelona, consisted of injecting a gene that causes the production of a protein blocked in patients with Alzheimer’s (Crtc1, the CREB-regulated transcription coactivator-1) into the hippocampus of mice.

“This study opens up new perspectives on therapeutic prevention and treatment of Alzheimer’s disease, given that we have demonstrated that a gene therapy which activates the Crtc1 protein is effective in preventing the loss of memory in lab mice,” said Carlos Saura, head of research at the Institute of Neuroscience.

According to a statement from the university, the protein gives way to the signals needed to activate the genes involved in long-term memory consolidation.

In order to identify this protein, researchers compared gene expression in the hippocampus of healthy control mice with that of transgenic mice that had developed the disease. The genes were identified through DNA microchips, and the proteins expressed themselves in each of the mice in different phases of the disease.

The researchers observed that the set of genes involved in memory consolidation coincided with the genes regulating Crtc1, a protein that also controls genes related to the metabolism of glucose and to cancer. The alteration of this group of genes could cause memory loss in the initial stages of Alzheimer’s disease.

“When the Crtc1 protein is altered, the genes responsible for the synapsis or connections between neurons in the hippocampus cannot be activated and the individual cannot perform memory tasks correctly,” Saura said.

One of the main challenges in finding a treatment for the disease in the future is the research and development of pharmacological therapies capable of activating the Crtc1 protein, with the aim of preventing, slowing down, or reversing cognitive alterations in patients, the university said in its statement.
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