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XenaLives

04/07/18 11:05 AM

#146700 RE: Amatuer17 #146699

In is a biomarker, but it does not fit the clinical practice of what is defined as "Alzheimer's", it is also not clear if it is a cause or an effect of the disease.

Approaching amyloid beta as causative or treatable is what has failed.

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Investor2014

04/07/18 11:48 AM

#146708 RE: Amatuer17 #146699

The issue is that that Amyloid has been seen as causative, when in reality the beta-amyloid deposits appear to be a pathological and possible an immune response in many, but not all, patients that are diagnosed with AD.

The plaque removal drug attempts fail because they do not address the issue or issues upstream of the beta-amyloid deposits. Despite the recently aborted BP attempts at amyloid removal some, possibly in error, cling on to the idea that treating early with plaque preventing drugs may delay or avoid the onset of a clinical AD diagnosis.

So beta-amyloid may be a biomarker of AD at some point in disease progression, but not necessarily a good early signal.

As a biomarker Amyloid might be useful e.g. for Anavex A2-73 or A3-71 to be taken early or perhaps still as a prophylactic. This because it would appear that a growing number of researchers, independent of Anavex, conclude that the Sigma-1 receptor is a potent drug target upstream of neurodevelopmental and neurodegenerative disease.

Check out my recent two posts with YouTube presentations.
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Steady_T

04/08/18 3:15 AM

#146755 RE: Amatuer17 #146699

If you read the paper it is CSF and PET scans detecting levels of Aß42 and the transition from CSF high levels and PET scan normal levels to CSF high levels and PET scan high levels that the authors found as indicative of early stage AD.

This was not a study discussing treatment, only early diagnosis based on biological factors.