biOasis Technologies Ord Shs V.BTI.H

RE:Prothena and Management's Reporting

[prophetoffactz]

"Bioasis needs to clarify some stuff. If not then shareholders ought to get a leadership team in there that is capable or willing to do it."

You can't wait and tell us after they've clarified because you may be competing with everyone else for shares. It's free. At least we know that Prothena has an xB3 liscense and the options were extended a number of times before expiring. What was it working on? This new success in the field may spark renewed interest. With Prothena's new market cap buying BTI at US$100 million would only be 3.33% of its market cap. The new potential success in Alzheimer's is injecting significant excitement into the sector and capital. 

BTI's acquisition had Alzheimer's in its pipeline:

Alzheimer Disease

Alzheimer’s is a neurodegenerative disease in which protein deposits form amyloid plaques and tau tangles in the brain: neurons stop functioning, lose connections and die; the brain shrinks dramatically.
The disease begins with memory impairment; evolution progressively leads to communication problems, addiction and eventually death.
There is no disease-modifying treatment. Only symptomatic treatments somehow delay progression.

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Inflammation and remyelination may both be important in Alzheimer's with amyloid-β and tau:

 

J Alzheimers Dis

 

•  
•  
•  

. 2017;58(3):597-612.

 doi: 10.3233/JAD-170036.

Remyelination: A Potential Therapeutic Strategy for Alzheimer's Disease?

Junjun Sun, Hong Zhou, Feng Bai, Zhijun Zhang, Qingguo Ren

 

• PMID: 28453483
•  
• DOI: 10.3233/JAD-170036

Abstract

Myelin is a lipid-rich multilamellar membrane that wraps around long segments of neuronal axons and it increases the conduction of action potentials, transports the necessary trophic support to the neuronal axons, and reduces the energy consumed by the neuronal axons. Together with axons, myelin is a prerequisite for the higher functions of the central nervous system and complex forms of network integration. Myelin impairments have been suggested to lead to neuronal dysfunction and cognitive decline. Accumulating evidence, including brain imaging and postmortem and genetic association studies, has implicated myelin impairments in Alzheimer's disease (AD). Increasing data link myelin impairments with amyloid-β (Aβ) plaques and tau hyperphosphorylation, which are both present in patients with AD. Moreover, aging and apolipoprotein E (ApoE) may be involved in the myelin impairments observed in patients with AD. Decreased neuronal activity, increased Aβ levels, and inflammation further damage myelin in patients with AD. Furthermore, treatments that promote myelination contribute to the recovery of neuronal function and improve cognition. Therefore, strategies targeting myelin impairment may provide therapeutic opportunities for patients with AD.

J Alzheimers Dis

 

•  
•  
•  

. 2017;58(3):597-612.

 doi: 10.3233/JAD-170036.

Remyelination: A Potential Therapeutic Strategy for Alzheimer's Disease?

Junjun Sun, Hong Zhou, Feng Bai, Zhijun Zhang, Qingguo Ren

 

• PMID: 28453483
•  
• DOI: 10.3233/JAD-170036

Abstract

Myelin is a lipid-rich multilamellar membrane that wraps around long segments of neuronal axons and it increases the conduction of action potentials, transports the necessary trophic support to the neuronal axons, and reduces the energy consumed by the neuronal axons. Together with axons, myelin is a prerequisite for the higher functions of the central nervous system and complex forms of network integration. Myelin impairments have been suggested to lead to neuronal dysfunction and cognitive decline. Accumulating evidence, including brain imaging and postmortem and genetic association studies, has implicated myelin impairments in Alzheimer's disease (AD). Increasing data link myelin impairments with amyloid-β (Aβ) plaques and tau hyperphosphorylation, which are both present in patients with AD. Moreover, aging and apolipoprotein E (ApoE) may be involved in the myelin impairments observed in patients with AD. Decreased neuronal activity, increased Aβ levels, and inflammation further damage myelin in patients with AD. Furthermore, treatments that promote myelination contribute to the recovery of neuronal function and improve cognition. Therefore, strategies targeting myelin impairment may provide therapeutic opportunities for patients with AD.