Alzheimer disease (AD) is characterized by the accumulation of beta-amyloid (Aβ) plaques and neurofibrillary tangles composed of hyperphosphorylated tau, which together lead to neurodegeneration and cognitive decline. Current therapeutic approaches have primarily aimed to reduce pathological aggregates of either Aβ or tau, yet phase 3 clinical trials of these approaches have thus far failed to delay disease progression in humans. Strong preclinical evidence indicates that these two abnormally aggregated proteins interact synergistically to drive downstream neurodegeneration. Therefore, combinatorial therapies that concurrently target both Aβ and tau might be needed for effective disease modification.
Just recently I read an article in a magazine about a clinical trial for an Alzheimer’s drug. People on the trial were noticing a clear improvement, the first time a drug has apparently reversed the symptoms of Alzheimer’s. But the trial was declared a failure and ended. After a lot of people, patients and medical people, said how can you call this a failure when so many people noticed a drastic improvement (and then deterioration after the trial ended) the trial was studied. Somehow the parameters were changed and the results were misreported. Anyhow the trial is now being reinstated and there will be no placebos. This will be a trial of how the drug performs. I’m pretty sure the article said this is the first time a same trial has been reinstated. It sounds hopeful. Also it made me think of people here saying they were part of clinical trials and the drug seemed to be successful but the trial was ended and the drug came to nothing. Could it be that other drugs have wrongly been declared a failure in spite of the obvious actual success 🤔
Very informative HH. As usual, you are clued in to advanced research and its foibles. What do you think the report means by"downstream neurodegeneration"?
There are a lot of phrases in that report that I don’t understand! I am really not all that clued in. My general understanding of it is the dual targeting of the plaques and tau could help to stop neurodegeneration.
I can only guess that in the current modern scientific idiom HH the metaphor applies to developing neurodegeneration which the subject is about to experience or is lying in wait for the brain. Or should researchers think more carefully about their use of figures of speech?
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