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Thursday, 08/30/2018 12:15:04 AM

Thursday, August 30, 2018 12:15:04 AM

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Here's another recent study from Finland confirming our PKC activation theory: https://www.ncbi.nlm.nih.gov/pubmed/30138694

"Abnormal protein kinase C (PKC) function contributes to many pathophysiological processes relevant for Alzheimer's disease (AD), such as amyloid precursor protein (APP) processing. Phorbol esters and other PKC activators have been demonstrated to enhance the secretion of soluble APPa (sAPPa), reduce the levels of ß-amyloid (Aß), induce synaptogenesis, and promote neuroprotection."

"Finally, bryostatin-1, but not HMI-1a3, increased the number of mushroom spines in proportion to total spine density in mature mouse hippocampal neuron cultures. These results suggest that the PKC activator HMI-1a3 exerts neuroprotective functions in the in vitro models relevant for AD by reducing the production of TNFa and increasing the secretion of neuroprotective sAPPa."
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