I agree. I forget to include these possible therapeutic signals, they give 2-73 commercial potential as well. The Phase 2/3 will no doubt include these as end points and will hopefully prove out.
Excellent post. Improving sleep would definitely be something that Alzheimer’s patients and caregivers could both benefit from.
I particularly like your last paragraph. I probably need to add a statement like that to all of my posts as well.
Just because I post things which might seem to be negative does not mean that anyone should use them as a basis to sell Anavex stock that they own and for goodness sakes never short any stock if you don’t use something to protect against a huge price surge. Imagine being short and some sort of partnership is announced. You can lose MORE than the amount you have invested! Don’t do it.
I think you might enjoy reading the rest of the following link if you have not already read it. (Very in-depth and loaded with jargon)
I thought the following quote was very intriguing especially since this is an ‘Australian” trial.
“We have to mention one more time about the recent genetic study, which has discovered a tight association between Sig-1R gene mutations and FTLD-MND [29]. This finding provides enormous implication of Sig-1Rs in the pathophysiology of human neurodegenerative disorders. The study found that, among a particular Australian pedigree (Aus-14), carriers of mutations at the UTR of the Sig-1R gene all suffer from FTLD, indicating the mutations may serve as a specific marker for a prediction of FTLD. Importantly, mutations that either increase or decrease the transcription of Sig-1Rs can both cause neuronal damages by inducing inclusion bodies composed of heterogeneous nuclear ribonucleoproteins in vitro. The specific brains regions and some motor neuron subcomponents appear to need to set the Sig-1R level within a precise range to cope with misfolded proteins. Since some other causal mutations of FTLD have been discovered (e.g., proglanulin, VPC)[29], the mutations of the Sig-1R gene may not be, however, always necessary for the onset of FTLD. These causal mutations and others related to neurodegenerative disorders phenotypically similar to FTLD (i.e., ALS) are all known to lead to dysregulation of protein sorting and degradation that often cause the ER dysfunction. The unexpected convergence in the concept of the Sig-1R derived from this clinical study (i.e., the gene study of FTLD) and from basic studies (e.g., the identification of the Sig-1R as an ER chaperone) now begins to elucidate a clear picture of the pathophysiological implication of Sig-1Rs in human diseases.”