The mitochondria in brain cells are especially important. Mitochrondria, also referred to as the powerhouse portion of cells, are diminutive structures that transform energy from food into nutrition for cells. The brain cells’ mitochondria are rife with calcium ions that control the energy required for optimal brain functionality. It is clear the brain requires just the right level of calcium to function as designed.
The research was led by Pooja Jadiya, a postdoctoral fellow at Temple University. Jadiya’s team of researchers studied brain samples derived from Alzheimer’s patients along with a mouse model genetically modified to simulate symptoms suffered by those plagued with Alzheimer’s disease.
The study also included a mutant cell with Alzheimer’s as well. The research group analyzed mitochondrial alterations in the context of calcium processing, membrane potential, the generation of reactive oxygen species, the metabolism of active amyloid proteins and cell death.
A healthy human brain has calcium ions that flee neuron mitochondria to prevent excessive accumulation. The protein transporter, referred to as the mitochondrial sodium calcium exchanger, facilitates this process. Jadiya determined the amounts of sodium-calcium exchanger were quite low in tissue impacted by Alzheimer’s disease. The protein level was so small that it was difficult to pinpoint.
The research team believes such a phenomenon could trigger numerous reactive oxygen species (ROS) that cause neurodegeneration to speed up. ROS are molecules that can damage protein, lipids and DNA when present at high levels. This process causes oxidative stress.
The Progression of Alzheimer’s
In order for Alzheimer’s to progress, there has to be considerable activity in the calcium exchanger. The research team determined a higher rate of neuronal death is correlated to an inactive sodium-calcium exchanger. Data from the mouse model indicates the gene necessary for encoding the exchanger is relatively inactive when Alzheimer’s sets in.
Minimal activity in the gene’s expression is further proof protein exchangers serve an important role in the advancement of the disease. The researchers analyzed this mechanism in a cell culture model impacted by Alzheimer’s disease by forcing higher exchanger levels. As expected, affected cells bounced back to the point that they were nearly indistinguishable from regular cells.
Furthermore, the level of adenosine triphosphate (ATP) increased, ROS levels decreased and few neurons perished. Biologists consider ATP to be the energy currency necessary for human life. The human body requires ATP for all of the activities it performs, from brain functionality to walking, talking and beyond.
The Importance of the Research
Prior studies proved excess calcium causes neurons to die. There is a strong link between calcium imbalance and the neurodegeneration that takes place during the onset of Alzheimer’s. The study noted above is the first sign of an exact mechanism connecting the imbalance of mitochondrial calcium to the onset of Alzheimer’s.
Jadiya’s research group was the first to make use of the different model systems as noted above. In layman’s terms, the research outlined above is making it that much easier for medical professionals to diagnose and predict Alzheimer’s. The medical community is now pushing forward to determine if it is possible to significantly alter calcium imbalances.
Jadiya’s research has paved the way for new Alzheimer’s treatment options. Medical researchers are now working to reverse Alzheimer’s neurodegeneration with the use of mouse models. The researchers are stimulating the gene expression necessary to encode the sodium-calcium exchanger. This stimulation might be possible with the use of new drugs or gene therapy. There is hope altering the exchanger’s expression level or activity will help serve as a form of therapy that wards off Alzheimer’s.
Though it is not yet known if such actions can completely prevent Alzheimer’s for the entirety of a patient’s life, it might be possible to prevent this debilitating disease from setting in before one can truly enjoy the golden years. Perhaps those who are cured of Alzheimer’s in the future will credit Jadiya’s work for their newfound mental health.
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