Alzheimer\'s disease could be a Result of Two Defective Proteins Present in the Brain Cells
Two defective proteins can collude together to hamper the working of the mitochondria present in the brain cells in patients of Alzheimer’s disease, resulting in the death of these cells. The research, published in the Neurobiology of Aging, states that the coming together of two pathological proteins, namely amyloid beta and tau, can spell doom for the brain cells.
The brain cells, as like any other cells are dependant upon the mitochondria for their energy supply. Mitochondria are the cellular components which are responsible for the release of glucose. Besides that, they maintain the calcium levels present in the cells at an optimal level. Any damage to the mitochondria, results in insufficient glucose supply to the cell, an imbalance in the calcium levels and the release of certain oxidative molecules which can damage the cell. These events may result in improper functioning of the brain cells and ultimately their death.
The researchers of the study exposed the mitochondria present in the nerve cells of a rat to amyloid beta, to the regular tau protein, to the truncated version of tau, and to combinations of amyloid beta and the two versions of tau. They then tracked the movement of the mitochondria inside the cell by taking its image every 10 seconds for a period of five minutes. The researchers found that those mitochondria, which had been exposed to a combination of amyloid beta and truncated tau, were severely damaged. They clumped together abnormally in certain parts of the cell and were not able to supply energy to all the parts. They could not maintain their electrical potential which is crucial for energy production. These damaged mitochondria also released 60% more free radicals and became fragmented.
According to the scientists, these cellular changes begin taking place inside the brain, much before the symptoms of Alzheimer’s disease, such as memory loss become apparent. And once the cells are dead, it’s too late to do anything about it. That is why, researchers are trying to identify the changes that take place at the cellular level much before the advent of the disease symptoms. Once the causative agents of these changes are identified, treatment can be started at that stage, so that the progression of Alzheimer’s and other brain diseases is halted.
The information gained from the study, about the role of amyloid beta and truncated form of tau proteins on the degeneration of neuronal mitochondria, can open new channels for a therapeutic intervention at an early stage of Alzheimer’s disease.