27 April 2009

A 'burnt-out' brain can cause Alzheimer's






It has recently been established that variants in the APOE gene (this gene codes for protein thought and for maintaining and repairing neuronal connections) in particular the epsilon 4 variant increases the risk of getting Alzheimer’s. For individuals who have one copy of the gene variant they have an increased risk of up to four times. However, people who have two copies of the variant have an increased risk of up to twelve times more likely of getting Alzheimer’s.

A recent study was undertaken where thirty-six (18 adults who had the epsilon 4 variant and 18 controls who didn’t have the variant) participants took part in an investigation. The participants took part in memory tests and also did nothing to test the activity in the hippocampus (the hippocampus stores new information in an individual’s memory so that they can remember it later on). The results showed that the participants that carried epsilon 4 had greater activity in their hippocampus than the participants that didn’t. However, there were no significant differences in the way they performed in the tests, signifying that for an individual with the epsilon 4 variant to be able to achieve the same result as an individual without the variant requires more energy in their hippocampi. When the participants were doing nothing, the researchers concentrated on the default mode network (DMN) which are sites located in the brain that is still active when an individual is resting. It was found that the participants that had the epsilon 4 variant of the gene had greater activity in there DMN (which is located in the hippocampus) than participants without the gene variant. Therefore, this suggests that participants with the epsilon 4 variant have brain regions that get overworked which can result in their brains ‘burning out.’



Therefore, the gene variant epsilon 4 can cause overworking of the hippocampus. However, it is not sufficient to say that it causes Alzheimer’s; although, it is a strong possibility. This is because the differences must be detected in the functioning of the brain with those who carry the gene variant and suffer from Alzheimer’s and those who carry the gene variant and are free of Alzheimer’s. In discovering these differences, certain interventions could be made in individuals before the disease has the chance to develop.