In fact this is not a new indication (see below) but an example of post anesthesia delirium or cognitive dysfunction after anesthesia which could be perhaps be prevented by PBT2 as earlier animal studies done by Prana scientist would support. IMO it would be much easer and quicker study (Ph 2b and Ph 3) to do than the one Prana has been planning now almost 2 years. The big AD study needs to be done, but with smaller indication Prana perhaps could go to the market earlier so that there would be no need for additional money from investors or even from big pharma.
In any case, most likely PBT2 is also indicated before big operations. It is big need! At least 200 million operations are done every year. I hope we are now closer to an intervention study by PBT2 to get also this indication for PBT2.
I hope Kempler and Cherny (one of the authors of this paper)will have a serious discussion.


Ann Thorac Surg. 2009 Nov;88(5):1426-32.

Plasma amyloid beta42 and amyloid beta40 levels are associated with early cognitive dysfunction after cardiac surgery.
Evered LA, Silbert BS, Scott DA, Maruff P, Laughton KM, Volitakis I, Cowie T, Cherny RA, Masters CL, Li QX.

Centre for Anaesthesia and Cognitive Function, Department of Anaesthesia, St. Vincent's Hospital, University of Melbourne, Melbourne, Victoria, Australia.

Comment in:

Ann Thorac Surg. 2009 Nov;88(5):1432.

BACKGROUND: Decreased cognitive function associated with coronary artery bypass graft surgery is common. These deficits may be similar to the cognitive dysfunction seen in the spectrum of mild cognitive impairment to Alzheimer's disease, which are believed to result from the accumulation of amyloid beta (Abeta) peptide in the brain. We measured cognition both before and after coronary artery bypass graft surgery and assayed Abeta levels to investigate whether the cognitive dysfunction of cardiac surgery was associated with Abeta levels. METHODS: The plasma of 332 patients, who had undergone neuropsychological testing before and 3 and 12 months after coronary artery bypass graft surgery, was analyzed for Abeta(42) and Abeta(40). Patients were classified as having preexisting cognitive impairment if cognitive function was decreased in two or more tests compared with a healthy control group, and postoperative cognitive dysfunction was defined as a decline in two or more tests compared with the group mean baseline score. RESULTS: Preexisting cognitive impairment was present in 117 patients (35.2%), and postoperative cognitive dysfunction was present in 40 (12%) at 3 months and 41 (13%) at 12 months after surgery. Both plasma Abeta(42) and Abeta(40) levels assessed before the surgery were significantly lower in patients who later had postoperative cognitive dysfunction at 3 months. CONCLUSIONS: Decreased preoperative plasma levels of Abeta(42) and Abeta(40) in patients who exhibit postoperative cognitive dysfunction at 3 months suggest that postoperative cognitive dysfunction at this time may share a common mechanism with mild cognitive impairment and Alzheimer's disease. This process may be exacerbated by anesthesia.