While present thinking in the research community is leaning towards tau rather than amyloid-β as the primary cause of cell death and dysfunction in later stage Alzheimer’s disease, it is still the case that too much amyloid-β is toxic to cells. Researchers here propose a treatment based on suppressing one of the mitochondrial mechanisms of programmed cell death that is triggered by the presence of amyloid-β. This is in many ways a classic example of what I consider to be a problematic focus in medical research: ignoring the root cause damage, the amyloid-β, in favor of tinkering with cellular mechanisms in the hope of improving the dysfunctional, damaged state of cells and tissues.
There are no doubt a hundred places in which one could reasonably try to intervene downstream of the presence of amyloid-β – and a good twenty of those are probably fairly independent of one another, requiring separate research and development project to address. But why build twenty projects when you could build one to achieve the same effect? Target the root causes. Don’t mess with the downstream state. I wish that more of that philosophy of development was in evidence
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