Researchers at Harvard University have found that fibroblast of Alzheimer patient have defective mitochondria metabolic potential
Alzheimer disease is a neurodegenerative disease caused due to damage to neurons which causes loss of memory and cognitive decline. Approximately, 200,000 Americans under the age of 65 have early onset Alzheimer’s disease. Alzheimer can be in two forms i.e. early onset which is an inherited disease develops at the age of 50s. This is rare as compared to the second form which is called late onset. It is also called as sporadic Alzheimer which strikes after the age of 65 and could be an aberration of normal aging.
Researchers do not fully understand why the changes that lead to Alzheimer’s disease occur. Previous research explains the cause of Alzheimer disease by amyloid cascade hypothesis. According to this hypothesis, this disease is caused by plaque formation by a protein called amyloid beta which triggers another protein named as Tau which causes inflammation in brain cell leading to degeneration of neuron.
Plaques are formed from the build-up protein and are found between the dying cell and other protein called tau which gets disintegrated and forms tangles. But this hypothesis is yet not completely believed because when an Alzheimer’s drug was made to target beta-amyloid, it failed to revert the disease. Additionally, plague is also found in old people after their death which does not have this disease. Even growth of amyloid beta protein occurs in all of us as well as phosphorylation of tau. High level of this protein is also found in postmortem brains.
In the Harvard University, the researchers are working on the relation of Alzheimer’s disease with the energy production of the cell. They found out that during this disease, the energy production became low due to the defect in the mitochondria. Cells get most of their cellular energy from mitochondria only.
Our brain demands 20 times more energy than any part of our body. So brain when the brain does not get as much energy as required, it will kill or damage the nerve cell. Such disrupted energy production also explain the cognitive decline associated with the disease. The research led by Cohen previously discovered that there is a big role of cellular energy in psychiatric diseases. Energy produced by cells is reduced with aging and Alzheimer’s, particularly the late-onset form, tied to aging.
A study was done in McLean by Cohen, Sonntag, and colleagues published recently in a scientific journal in which they took fibroblast from Alzheimer patient and normal person of same age. They found out that fibroblast of Alzheimer patient has defective mitochondria metabolic potential. Actually, the cell produces 98% of energy through respiration in mitochondria and only small amount through glycolysis. So because of the defective mitochondria, production of energy is compensated through glycolysis. Neuron use only mitochondrial respiration for energy source and don’t have the process of glycolysis as a backup due to which neurons cell get damaged and killed.
This study helped us to know that Alzheimer disease and formation of plaque and tangles are not completely correlated and cellular energy dysfunction could be the reason. The next step of the researcher will be to do a similar study on a neuron-like they did on fibroblast to know whether similar dysfunction of energy will take place there or not.