I finally got around to reading the two latest papers. Here's some notes for the first paper if anyone's interested:
- "In the brain, ePKC interacts with several neuronal receptors and neuromediators including N-methyl-d-aspartate(NMDA), gamma-aminobutyric acid (GABA) synapses, BDNF (Brain-derived neurotrophic factor), SIRT1 (Sirtuin1), and SIRT5 [34,35]."
The effect on NMDA receptors isn't anything new, but independent confirmation is always nice. What really caught my attention though was that it also has an effect on SIRT1, which if I recall correctly is a gene being studied at Harvard for life extension purposes. Not really relevant for Neurotrope, but still interesting to know.
- "These results suggested that the activation of ePKC reduced ischemic/reperfusion damage by a significant decrease in blood flow during reperfusion after ischemia [32]. Similar protective evidences for ePKC were reported by using an Oxygen Glucose Deprivation (OGD) model, (in vitro ischemia) highlighting the role of NMDA receptors in cerebral ischemic tolerance [36]."
"PKCs phosphorylate and regulate the dopamine transporter, -amino-3-hydroxy-5-methyl-5-isoxazolepropionic acid(AMPA)-type glutamate receptors (AMPARs), NMDA-type glutamate receptors (NMDARs), -aminobutyric acid (GABA) receptors, -opioid receptor, and metabotropic glutamate receptor 5 (mGluR5) receptors [51–53]."
Memantine is an NMDAR blocker. If Bryostatin works by activating endogenous repair mechanisms and those mechanisms need NMDAR to work properly, it makes perfect sense why patients on Memantine showed no improvement in the last trial.
- "In the brain of patients with AD, the levels of PKCs are significantly reduced and PKCs signaling is impaired in terms of activity and translocation to the cellular membrane [48,49]. Therefore, a direct effect of PKCs in AD, as an etiopathogenic cause or as consequence of neurological damage, is highly suggestive [44]."
"However, ePKC levels were 21% and 30% lower in the particulate fraction of aged hippocampi (78.92 2.85, p < 0.05) compared to the young (100 8.68, p < 0.05) and middle-aged (108.85 9.54, p < 0.05) groups respectively (Figure 2c)."
"Loss in PKCs expression and function have been indicated as one among the first markers of neuronal death [21]. Therefore, impairment in PKCs is surely implicated in neurological age-related disorders, such as cerebral ischemia, brain injury, and cognitive impairment [4,18]."
If PKCs are involved in protecting the brain, and their levels drop as we age, it could explain why AD mostly affects older people.
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