Chronic stress associated with Alzheimer's disease protein accumulation

University of California San Diego School of CAMK1D Medicine researchers published in a mention in the March 26 online early edition of NationalAcademy of Sciences study, repeated stress to trigger rat brain cells, insoluble microtubule-associated protein aggregates production and accumulation. Its total amount of CAMK1G neurofibrillary tangles, or NFTs similar modification of the protein structure is one of the physiological characteristics of Alzheimer's disease. Lead author and assistant professor of neuroscience, RobertA Dr. Rissman said the findings may at least partially explain why clinical studies have found the CAMK2A body produce stress and Alzheimer disease (AD) between the occurrence of strong contact, such cases accounted for 95% of all AD cases accounted for.

In a mouse model, we found that repeated episodes of emotional stress, has proven to be a problem often encountered in ordinary life, can lead to neuron microtubule-related protein phosphorylation and solubility change. Rissman said, "These events are essential for the development of CAMK2B Alzheimer's disease pathology NFT. The most obvious effect in the hippocampus, Rissman said, the region of the brain associated with memory formation, organization and storage. In AD patients, the hippocampus is usually the first region of the pathological effects of brain, and accompanied by the serious impact of a large number of cell death and contraction. Not all forms of pressure have the same threat. In earlier research, Rissman and his colleagues reported that CAMK2D acute stress (a single sexual attacks) will not lead to the accumulation of phosphorylated proteins and lasting. He said that the cells in the acute stress-induced modification is transient, on the whole, it might be useful.

Acute stress may promote the role of brain plasticity and learning have some help. Chronic stress and continuous stress pathway activation may lead to pathological changes in the stress circuit, which was originally the views of a good thing. "With the increasing age of the human perhaps their neural circuits become stronger, he said, it might not be able to fully restore the effects of stress. "Age is the primary risk factors for Alzheimer's disease is known, it may be because the neuron is no longer as it was before the plasticity of the increase with age."

The researchers observed that tension affect the two key corticotropin-releasing factor receptor, which means that there is a potential therapeutic target goal. The Rissman pointed out already undergoing human trials of drugs (other conditions) to regulate the activities of these receptors. "You can not eliminate the tension. We all need some ability to cope with a certain excitement level, this idea is the use of antagonists to reduce stress on neurons. Pressure system still can be fed, but this feedback in the brain and the hippocampus area will be diluted, so that it does not cause harmful permanent damage. "

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