Tao Synergies Inc (TAOX)

[SF Wolf]

Maple tree, this study (which I posted earlier) along with the Aphios data confirm the role of PKC epsilon in AD progression:

Independent Confirmation of Dr. Alkon's research

The scholarly article below was referenced twice by Dr. Alkon in recent presentations at both the Oppenheimer and Sachs Forums. I believe for Dr. Alkon this study independently confirms an element of his theoretical framework for the role of PKC epsilon in modulating Alzheimer’s disease. The study addresses one aspect of the multi-modal effect of treatment with Byrostatin. The reduction of amyloid plaque pathology.

Briefly, the study took mice that genetically express AD at an early stage in their life cycle. Then this mouse model was further genetically manipulated with a gene to produce higher than normal levels of PKC epsilon (the brain agent that Byrostatin stimulates to treat AD). The premise was, will higher levels of PKC epsilon prevent AD symptoms in animals that always develop the disease. This study showed that these double transgenic mice had lower amyloid plaque deposits and Alzheimer’s disease expression confirming an important theoretical aspect of Dr. Alkons work.
PKCe increases endothelin converting enzyme activity and reduces amyloid plaque pathology in transgenic mice
Choi et. al.
March 31, 2006

Abstract
Deposition of plaques containing amyloid ß (Aß) peptides is a neuropathological hallmark of Alzheimer's disease (AD). Here we demonstrate that neuronal overexpression of the e isozyme of PKC decreases Aß levels, plaque burden, and plaque-associated neuritic dystrophy and reactive astrocytosis in transgenic mice expressing familial AD-mutant forms of the human amyloid precursor protein (APP). Compared with APP singly transgenic mice, APP/PKCe doubly transgenic mice had decreased Aß levels but showed no evidence for altered cleavage of APP. Instead, PKCe overexpression selectively increased the activity of endothelin-converting enzyme, which degrades Aß. The activities of other Aß-degrading enzymes, insulin degrading enzyme and neprilysin, were unchanged. These results indicate that increased neuronal PKCe activity can promote Aß clearance and reduce AD neuropathology through increased endothelin-converting enzyme activity. http://www.pnas.org/content/103/21/8215.full