So let me understand this. If NTRP succeeds, there's a 50% chance the company fails. But if the data is negative, there's also a 50% chance of failure. That old adage about "damn statitics" comes to mind. Time will tell us, and soon, whether NTRP's MOA works. But why are posters posting about AVXL.
"Bryostatin fails to correct the cause of the Alzheimers, mitochondrial dysfunction. The first thing to show up in pre Alzheimers patients is mitochondrial dysfunction, not low levels of PKE epsilon."
Let's do this. Show us the source of your statement that "mitochondrial dysfunction" is "the cause" of Alzheimer's.
Let's be real. No one knows what causes Alzheimer's. There are just lots of unproven hypotheses about it's root cause.
"There are currently five dominant hypotheses on the etiology of AD and these are: the amyloid hypothesis (AH), the tau hypothesis (tH), the in ammation hypothesis (IH), oxidative stress hypothesis (OSH) and the vascular hypothesis (VH). These theories are not mutually exclusive. For example, the OSH can accommodate both the in ammation hypothesis, the VH, elements of the Ab-AH and tH. There are other theories such as mitochondrial de cits, parasitic infections, bacterial infections, viral infections and post-trau- matic brain injury. These will not be discussed in detail here. Many of these are also subsets of the OSH (Figure 1) [16]. Finally, there is the theory of neuronal hibernation that has been proposed by Swaab and colleagues [17]."
Would you like to see one current hypothesis that supports Neurotrope's approach?
Alzheimer’s may be caused by haywire immune system eating brain connections
"Stevens has spent much of her career studying a normal immune mechanism that prunes weak or unnecessary synapses as the brain matures from the womb through adolescence, allowing more important connections to become stronger. In this process, a protein called C1q sets off a series of chemical reactions that ultimately mark a synapse for destruction. After a synapse has been “tagged,” immune cells called microglia—the brain’s trash disposal service—know to “eat” it, Stevens says. When this system goes awry during the brain’s development, whether in the womb or later during childhood and into the teen years, it may lead to psychiatric disorders such as schizophrenia, she says.
Stevens hypothesized that the same mechanism goes awry in early Alzheimer’s disease, leading to the destruction of good synapses and ultimately to cognitive impairment. Using two Alzheimer’s mouse models—each of which produces excess amounts of the ß amyloid protein, and develops memory and learning impairments as they age—she and her team found that both strains had elevated levels of C1q in brain tissue. When they used an antibody to block C1q from setting off the microglial feast, however, synapse loss did not occur, the team reports today in Science.
To Stevens, that suggests that the normal mechanism for pruning synapses during development somehow gets turned back on again in the adult brain in Alzheimer’s, with dangerous consequences. “Instead of nicely whittling away [at synapses], microglia are eating when they’re not supposed to,” she says."
So as soon as I see a comment like "(fill in the blank) is the cause of Alzheimer's", I think to myself: that's funny because not even the most brilliant people in the world seem to agree on the cause of Alzheimer's, but somehow the author of that statement knows? Unlikely imho.
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