Alzheimer's Disease and Tau and several other neurodegenerative diseases, page-9

Just looking further into this and what part Tau proteins play, it seems to me that there may be much more to this than first meets the eye? and if so? then I very much doubt that they would be Licensing out any of the IP?
After I first posted about a connection to with Tau proteins, I decided to look into it further and found this -:

Tau protein is a highly soluble microtubule-associated protein (MAP). In humans, these proteins are found mostly in neurons compared to non-neuronal cells. One of tau's main functions is to modulate the stability of axonal microtubules. Other nervous system MAPs may perform similar functions, as suggested by tau knockout mice that did not show abnormalities in brain development - possibly because of compensation in tau deficiency by other MAPs.

Now that word microtuble rang a bell somewhere in my head, please forgive me if I am reading this wrong? as I am not someone from a medical background, but I like researching!

I went back looking for what Novogen had written about microtubles in the SBR literature?but it wasn't there! so I googled microtubles and Novogen and guess what? it comes in under the ATM program Anisina!
see here-: http://www.novogen.com/pdf/Anisina.pdf
it says this-:
The microfilaments are cable like structures which are made up of a backbone actin protein chain (light green) sur-rounded by a double chain of tropomyosin protein (red). Tropomyosin functions by pro-tecting the actin component of the microfila-ment from falling apart. It does this by form-ing a “head” to “tail” chain essentially wrap-ping around the actin.
For cell division and survival cancer cells rely on actin filaments that contain a particular isoform of tropomyosin, Tpm3.1. The anti-tropomyosin compound, Anisina, selectively binds to and impairs Tpm3.1 function resulting in the collapse of the actin cytoskeleton. Disabling this component of the cell’s cytoskeleton makes the cancer cell significantly more sensitive to microtubule targeting agents.

Am I wrong in thinking there may also be a connection with Anisina?

So Pbnewby and also Novogenbuyer you may both be right?
I say that because to me it looks as if Anisina may also play a part revolving around this Tau protein and it's relationship with microtubles, is it possible like Novogenbuyer said, about using the delivery system they intend to use with Anisina to get it through the BBB also with Jacob's Hope, we were always told that Jacob's Hope revolved around Genistein and the SBP program, but I have a sneaky suspicion that it may revolve around both perhaps?
See here-:

http://www.ncbi.nlm.nih.gov/pubmed/11948687

J Cell Biochem. 2002;85(2):315-24.
Tubulin, actin, and tau protein interactions and the study of their macromolecular assemblies.

Farias GA1, Muñoz JP, Garrido J, Maccioni RB.
Author information


Abstract

The intracellular polymerization of cytoskeletal proteins into their supramolecular assemblies raises many questions regarding the regulatory patterns that control this process. Binding experiments using the ELISA solid phase system, together with protein assembly assays and electron microscopical studies provided clues on the protein-protein associations in the polymerization of tubulin and actin networks. In vitro reconstitution experiments of these cytoskeletal filaments using purified tau, tubulin, and actin proteins were carried out. Tau protein association with tubulin immobilized in a solid phase support system was inhibited by actin monomer, and a higher inhibition was attained in the presence of preassembled actin filaments. Conversely, tubulin and assembled microtubules strongly inhibited tau interaction with actin in the solid phase system. Actin filaments decreased the extent of in vitro tau-induced tubulin assembly. Studies on the morphological aspects of microtubules and actin filaments coexisting in vitro, revealed the association between both cytoskeletal filaments, and in some cases, the presence of fine filamentous structures bridging these polymers. Immunogold studies showed the association of tau along polymerized microtubules and actin filaments, even though a preferential localization of labeled tau with microtubules was revealed. The studies provide further evidence for the involvement of tau protein in modulating the interactions of microtubules and actin polymers in the organization of the cytsokeletal network.

Combine that with this which I posted earlier


Friday, September 18, 2015 | 8:30 AM - 4:30 PM
Alzheimer's Disease and Tau: Pathogenic Mechanisms and Therapeutic Approaches

Speakers: George S. Bloom (University of Virginia), Peter Davies (Feinstein Institute for Medical Research), Marc I. Diamond (University of Texas, Southwestern Medical Center), Michael Hutton (Eli Lilly and Company), Khalid Iqbal (New York State Institute for Basic Research in Developmental Disabilities), Hartmuth C. Kolb (Johnson & Johnson, Janssen R&D), Nicole Leclerc (Université de Montréal), Richard Ransohoff (Biogen)

Speakers at this symposium will address novel tau-centered mechanisms of neurodegeneration and new therapeutic approaches for many devastating neurological disorders.


It seems to me like the SBP's and the ATM technology cross over in some areas in relation to degenerative diseases?

If this is the case I can't see Novogen letting the ATM technology end up in another companies hands! I don't believe they will license it, I reckopn they will partner and Novogen will be in control I believe.