thoughts on hd and pbt2, page-11

Hi Skint,

Glad to have you back by the way!

I am sure you have been monitoring things while away from your normal desk : )

I started on this trail because of all of the negativity around the HD trial outcome. I feel and have always felt that the primary endpoints for it and AD are more or less a slam dunk. It is just that concentration by skeptics is pointing ever at the secondary endpoints. I know I am just talking to the air in most cases because many new share holders and potential new share holders are in it for a fast buck and do not care which way the SP moves in order for them to turn the dollar.

I didn't mean to say that PBT2 does not have a positive affect on (on Mitochondria's inner cell and wall and particularly on the ROS) CLK1 to Prana's benefit as well as for all the AD, HD and PD not to mention other sufferers of NeuroDegen Diseases, but as I understand true control of CLK1 is by the sensor protein.
What I like is the aspect of the sensor protein being able to instruct the repair of the affected DNA (to what extent I do not know).
"Recent models depict the DSB response as developing through a series of steps . According to these models, DSBs might first be detected by sensor proteins
that recognize the DNA lesion itself or possibly chromatin alterations that follow DNA breakage. The broken ends are then processed — their chemical nature is random,
so they cannot serve directly as substrates for repair mechanisms. Then, the transducers are brought into action; these convey the damage signal to downstream effectors. It is this relay system from transducers to effectors that enables a single transducer to quickly affect the
operation of many pathways. The transducers might also be involved in the assembly of DNA-repair complexes at the site of the damage, so DSB repair and signaling are probably concomitant and functionally linked. In the case of DSBs, the initial and primary transducer is ATM
although related protein kinases are also involved which transmits the message via a standard signaling mode:protein phosphorylation."

I agree that PBT2 is hitting the right targets!

Speaking only of the HDD protein misfolded formation, I wonder if we can stop/correct its creation in the first place?

This perhaps may be where Prana heads once they have plenty of research dollars flowing in!

Again, glad to have you back!!