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Tuesday, May 12, 2020 5:44:02 PM
New report from neurologists at Massachusetts General Hospital: “Mass General Researchers Link High Calcium Levels in Mitochondria to Neuronal Death in Alzheimer’s Disease.”
For us, we know that one of the functions of the activated sigma-1 receptors in neurons is to properly modulate calcium concentrations and exchanges in mitochondria. Blarcamesine (Anavex 2-73) activates sigma-1 receptor proteins, allowing them to function normally.
This new study demonstrates that elevated calcium ions in mitochondria (in transgenic mice with Alzheimer’s) are pathogenic: “Their studies demonstrate that increased mitochondrial Ca2+ levels are associated with plaque deposition and neuronal death in this model, indicating that abnormal Ca2+ levels in mitochondria could play a role in neuronal cell death in Alzheimer’s disease.”
Ok, then, let’s get some blarcamesine into these mice with Alzheimer’s, and using the new calcium detection methods see if our drug prevents or reverses calcium accumulation in mitochondria. Would such mice then be free of Alzheimer’s symptoms?
Chances for this are very high.
https://www.massgeneral.org/news/press-release/researchers-link-high-calcium-levels-in-mitochondria-to-neuronal-death-in-alzheimers
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