Tuesday, January 02, 2018 by Zoey Sky
According to research published early in 2017, calcium in the mitochondria (the powerhouse of the cell), could be “one of the keys to understanding and treating Alzheimer’s disease and dementia.”
A group of scientists at the Center for Translational Medicine at Temple University has revealed that they determined how “an imbalance of calcium ions in the mitochondria may contribute to cell death and, specifically, neurodegeneration in brain cells during Alzheimer’s and dementia.”
In a neuron’s mitochondria, calcium ions are initially believed to regulate the energy production required so the brain can function. However, an imbalance in calcium, such as what happens in individuals with Alzheimer’s, can lead to cell death.
Based on earlier research, the imbalance of calcium in neurons could be significant when it comes to the onset of Alzheimer’s. Yet this imbalance and its connection to mitochondrial dysfunction and neurodegeneration remain unknown. (Related: Boost mitochondrial function naturally.)
Pooja Jadiya, a postdoctoral fellow working in John Elrod’s lab at Temple University who also led the research team, discovered that the removal of calcium from mitochondria is a “possible mechanism of Alzheimer’s disease.” Because of the mitochondrial sodium/calcium exchanger, a transporter protein, calcium ions can exit a neuron’s mitochondria.
The scientists looked at human brain samples from Alzheimer’s patients, and they determined that the levels of the exchanger were barely detectable in the diseased tissues. The low calcium levels caused a calcium build up in the diseased mitochondria.
Jadiya and his team posited that this could prompt the “excessive production of reactive oxygen species,” or molecules that can wreak havoc in the cell and add to neurodegeneration. The scientists also found that the reduced activity of this exchanger is linked to impaired energy production and increased cell death, which can both contribute to the neurodegeneration that leads to Alzheimer’s disease.
While observing mice that were genetically altered to develop Alzheimer’s, the researchers also discovered that prior to the onset of the disease, “the gene that encodes the exchanger protein was much less active.” This could mean that a drop in the gene’s expression might have something to do with disease progression.
The scientists observed this gene in an Alzheimer’s cell culture model to study this mechanism further. Like their observations concerning the mice, the cells were “genetically altered to exhibit the cellular symptoms of Alzheimer’s.”
The diseased cells recovered and were nearly identical to the control healthy cells after the researchers genetically boosted the levels of the mitochondrial sodium-calcium exchanger. ATP production was increased while reactive oxygen species decreased and cell death was minimized.
The scientists are collaborating with representatives from the lab of Domenico Praticò, also at Temple University, to see if it is possible to reverse the development of Alzheimer’s in mutant mouse models by increasing the gene that encodes the sodium-calcium exchanger. If this is possible, this mechanism could soon pave the way for new treatments that can boost the function of the mitochondrial sodium-calcium exchanger through new drugs or gene therapy.
While the root cause of Alzheimer’s still hasn’t been determined, there’s no harm in trying these natural ways to prevent it:
You can read more articles about disease prevention at Prevention.news.