Ok so the article says this successfully destroys the amyloid plaques, but does it help cognition or slow the disease?
Specifically for “slowing” it seems entirely plausible that breaking up the plaques will allow misfolded proteins to migrate (due to reduced size).
Ignoring entirely the there have been multiple drugs that successfully reduced amyloid build up, with no actual benefit. Eg they did exactly what they were designed for to no avail.
There's a theory on beta amyloid that it's merely the by-product of other causative agents, and that as a surrogate end-point for Alzheimer's outcomes, it's not nearly as useful as symptom reduction, as you state. My professor who studied AD and dementia likened beta-amyloid to the garbage leftover in a stadium or outdoor concert: you know something went down, this leftover trash isn't great, but hard to determine what actually did occur just based on beta-amyloid.
Of course, the AD research field is still divided and there are many competing theories. Solving AD and dementia is one of the greatest challenges in modern science.
It’s moving to a phase I trial, that means it’s just being tested for tolerability and adverse effects. A firm conclusion about outcome won’t be available until a phase III trial is completed, that’s years down the line. So we don’t know, but looks promising.
The information around Alzheimers seems to be heading the direction that the beta-amyloid plaques are an immune response to the HSV1 herpes virus that help prevent the spread of the virus.[1]
I suppose it can't be ruled out yet that this immune response could still cause damage, but it does make me wonder if the plaques are actually responsible at all for the symptoms seen, since like you said, other drugs reduce the plaques with no improvement in symptoms.
It's interesting that this treatment seems to work when others do not- when they seem to be accomplishing the same thing (reduction of beta-amyloid plaques)
"the team has worked to further test and refine the technique, successfully proving the treatment both clears toxic proteins and restores memory function safely in several different rodent models, including an older mouse model designed to resemble human brains of 80 to 90 years old."
Alzheimer is weird in that plenty of treatment works in mice but fails in humans. I suspect it's primarily because we do not fully understand the cause of Alzheimer.
My understanding is that "mice studies" cost less than clinical trials, therefore more "mice studies" with (correct/incorrect) conclusions are created.
Most likely there is no singular cause, but a slew of contributing factors that prevent amyloid clearance and promote plaque formation. That's why overlapping,
holistic solutions like the Bredesen protocol, ketagenic diets and now possibly ultrasound are the best treatment than waiting for a panacea that is unlikely to ever exist.
Probably more harm than good- you probably don’t want ultrasonic waves shaking your neurons around without a good reason. This sounds like a “kick a TV and it works again” sort of technology.
[+] [-] olliej|7 years ago|reply
Specifically for “slowing” it seems entirely plausible that breaking up the plaques will allow misfolded proteins to migrate (due to reduced size).
Ignoring entirely the there have been multiple drugs that successfully reduced amyloid build up, with no actual benefit. Eg they did exactly what they were designed for to no avail.
[+] [-] WhompingWindows|7 years ago|reply
Of course, the AD research field is still divided and there are many competing theories. Solving AD and dementia is one of the greatest challenges in modern science.
[+] [-] jf-|7 years ago|reply
[+] [-] kup0|7 years ago|reply
I suppose it can't be ruled out yet that this immune response could still cause damage, but it does make me wonder if the plaques are actually responsible at all for the symptoms seen, since like you said, other drugs reduce the plaques with no improvement in symptoms.
It's interesting that this treatment seems to work when others do not- when they seem to be accomplishing the same thing (reduction of beta-amyloid plaques)
[1] http://www.virology.ws/2018/11/08/herpes-simplex-virus-and-a...
[+] [-] DennisP|7 years ago|reply
"the team has worked to further test and refine the technique, successfully proving the treatment both clears toxic proteins and restores memory function safely in several different rodent models, including an older mouse model designed to resemble human brains of 80 to 90 years old."
[+] [-] ganeshkrishnan|7 years ago|reply
[+] [-] JamesBarney|7 years ago|reply
I think there is a better chance for this therapy because of the way it works, by transition the microglia over to an anti-inflammatory mode.
If this procedure passed safety trials I wouldn't be surprised if a similar therapy worked for schizophrenia, anxiety, and depression.
[+] [-] newsbinator|7 years ago|reply
[+] [-] nonbel|7 years ago|reply
My understanding is that "mice studies" cost less than clinical trials, therefore more "mice studies" with (correct/incorrect) conclusions are created.
[+] [-] heyjudy|7 years ago|reply
[+] [-] jobigoud|7 years ago|reply
[+] [-] maxander|7 years ago|reply
[+] [-] jbb999|7 years ago|reply
[+] [-] 49para|7 years ago|reply
[+] [-] jhayward|7 years ago|reply
[+] [-] usmanshaikh06|7 years ago|reply
[+] [-] heyjudy|7 years ago|reply