Doctors finding links of Tau with Alzheimer’s
Doctors and researchers in Georgetown University’s Laboratory for Dementia and Parkinsonism have recently unveiled some interesting findings on their constant studies of Alzheimer’s disease. They are quickly regarding a malfunction of a protein called tau as the main suspect in what causes the disease and other different forms of dementia. Recently the investigation team was performing tests and research with lab mice, and they have found that when Tau malfunctions and it fails to clear the cells of unwanted toxic proteins. After this malfunction neurons appear to die. What this could mean is that there could be a possibility that if drugs were to replace the functions of tau in these cells the progression of Alzheimer’s could slow down, or at least that is what they are hoping to demonstrate in the new stages of their research.
This is not the first time Tau has been brought up as a probable suspect in the search of the elusive cause of Alzheimer’s disease. Alzheimer’s patients have their brains congested with twisted protein threads made of tau in areas important to memory functions. So far scientists have been unable to explain why Tau might cause Alzheimer’s, considering that there are other factors that could very well fit the profile. However this research has been able to get some results that can further shed some light in this complicated matter.
These mentioned studies have shown in their results that whenever tau begins to malfunction, the neurons begin to split a protein called amyloid beta, that protein fills the spaces between the brain’s nerve cells. Now the discovery this investigation with mice has shown is that Tau has been successfully able to keep neurons naturally free of amyloid beta and other toxic proteins. When malfunction of tau is present, the neurons start to exude amyloid beta out into the space between the brain cells, where protein sticks together and forms plaques. What this study is saying that could be a possibility is that these plaques can deteriorate the brains functions to eventually form and cause Alzheimer’s and other forms of dementia.
Representatives of the Investigation Staff have expressed to be optimistic but cautious at the same times. The next step in their research is to gather enough evidence that can cement and clear the air when it comes to the causes of Alzheimer’s disease. If they do so, the world might be able to start a new discussion of the real and valid possibilities of curing and/or preventing the disease.