As more and more people are diagnosed with Alzheimer’s disease, it’s becoming increasingly important to find some way to cure or at least slow down its progress. Now, new findings from a study carried out at the Biodesign Neurodegenerative Disease Research Center suggests that the protein, p62, may play a critical role in the development of the disease.
The p62 protein already has associations with one of the two tell-tale neurological symptoms of the disease, neurofibrillary tangles. Now, it’s been shown that it’s also got an association with the other trademark symptom, the accumulation of plaques of amyloid beta. However, for the first time, this study has shown that p62 may help to reverse the effects of these plaques. This means that it may offer clues that could lead to the development of successful treatments.
Known to perform several vital functions within our cells, p62 was interesting to the scientists as it is involved in both the aggregation and degradation of the two proteins involved in Alzheimer’s disease. The researchers already knew that p62 played some part in the regulation of tau protein in the brain, noting that the protein makes bonds with the tau tangles. They thought that this was probably a mechanism to identify them for degradation.
By using mice which had been bred without the p62 protein, the team were able to show that the cognition levels of the mice improved when they were able to restore the level of p62. The mice also demonstrated reduced levels of the amyloid beta protein and associated plaques, following restoration of p62.
In order to assess the memory and cognition of the mice, they were given a simple test which required them to remember the locations of platforms submerged within a circular water maze. The mice were tested four times per day for five days in a row. While all the mice improved their ability to remember the location of the platforms over the test period, those who had been given the p62 were seen to perform much better.
As a result of their research, the team hope that it may be possible to restore the function of the neurons by introducing p62 in order to remove the tau and amyloid beta proteins. However, further research will be needed to more fully understand this process.
The research was funded by the National Institutes of Health and the results were published online in the journal Molecular Psychiatry.