Not all forms of memory loss are equal. AD changes the brain in different ways as does age related memory loss as examples; while both affect the hippocampus each target completely different areas within the region, with AD beginning in the entorhinal cortex and age related memory loss beginning in the dentate gyrus.
RbAp48 protein deficiency is a significant contributor to age related memory loss but not in Alzheimer’s disease, research has shown levels decline with age in both mice and humans. When levels were increased in aging mice dentate gyrus the decline was counteracted and mice memory was observed to improve in 2013. Infusions of osteocalcin were also found to have had positive effects on memory in 2017.
This study connects RbAp48 and osteocalcin suggestion key drivers of memory improvements lay in interplay between these molecules. A series of experiments found that RbAp48 controls expression levels of GPR158 and BDNF proteins regulated from osteocalcin in events that appear to be critical: inhibiting RbAp48 leads to infusions of osteocalcin having no effect on memory, osteocalcin needs RbAp48 to kick start the process.
The complex sequence of molecular signals is completely different to those associated with AD, and provides even more evidence that AD and age related memory loss are distinct disease according to the researchers.
Findings also provide evidence in favor of what may be a good method to stave off age related memory loss in humans via exercise which triggers release of osteocalcin within the body which overtime makes its way to the brain and encounters RbAp48 which may have long term positive effects on memory and the brain. Researchers are eager to further explore this line of inquiry, as their latest findings are almost certainly not the entire story, rather just the beginning.
