Mitochondria are tiny organelles inside the cell that produce the energy for the cell and regulate its metabolism. Changes to the mitochondria have been linked with a range of disorders, including Alzheimer's disease. Finding out more about these changes could help us to understand how Alzheimer's disease develops, and perhaps even lead to new therapeutics, according to researchers publishing in PLoS One.
The team from the Mayo Clinic studied the neurons from three groups of mice that each had a gene tweak causing familial, or early-onset, Alzheimer's disease. Each showed changes in the mitochondria--the mitochondria in the mouse neurons moved less and the cell's metabolome (the profile of all the molecules involved in metabolism) showed changes linked with mitochondria. These changes occurred even before the mice showed any symptoms of memory loss or dementia, or any development of plaques in the brain. Later, the mitochondria started to break down and lose function, along with the onset and progression of Alzheimer's disease. The researchers also found dysfunctional mitochondria in the neurons linked with memory.
"One of the most significant findings of this study is our discovery of the impact of mitochondrial dysfunction in Alzheimer's disease," says Eugenia Trushina, Ph.D., Mayo Clinic pharmacologist and senior investigator on the study. "We are asking: Can we connect the degree of mitochondrial dysfunction with the progression of symptoms in Alzheimer's disease?"
These are mouse model studies, so the next step is to validate the metabolomic changes in humans with Alzheimer's disease. Using metabolomic biomarkers linked with mitochondrial changes could help identify the early mechanisms underlying Alzheimer's disease, perhaps leading to new therapies and ways to diagnose Alzheimer's disease, predict its progression and monitor its progress.