People Want an Alzheimer’s Drug. This Isn’t the One. NY Times

Given our lack of effective treatments, some may argue that aducanumab is better than nothing. We strongly disagree.
Click to expand...

Consequence1 : Side effects that are hard to differentiate from the disease
In the aducanumab trials, three out of 10 patients exposed to a high dose had brain swelling as a complication, and although this was usually asymptomatic, in some patients it led to confusion, disorientation and falls. The swelling was detected with the use of rigorous safety screening, including routine M.R.I. scans. Such regular screening is unlikely to occur outside of the clinical trials, and because similar symptoms can be seen in progressive Alzheimer’s, distinguishing these adverse effects from disease progression would be especially difficult.
Click to expand...


Consequence 2: Slowed progress to find a good drug
Approval of aducanumab will also, inevitably, slow progress in finding a new drug that is clearly safe and effective. A lot of continuing and forthcoming drug trials require regular infusions of the drugs being tested and safety M.R.I. scans. Conducting these trials will be more challenging in a setting where many patients are already on monthly infusions of an F.D.A.-approved drug that frequently causes brain swelling. Some patients and caregivers may be reluctant to enroll in a study if they are taking a newly approved drug they presume works. Others, while taking aducanumab, might be ineligible for new trials, since it would be hard to know whether adverse effects such as confusion or brain swelling were from aducanumab or any new investigational drug.
Click to expand...
I'd add that having a treatment in the arsenal, even one that doesn't really work, reduces the political pressure on funders to keep looking for a good treatment.
 
Last edited:
If I remember rightly, Professor Steven Rose was on about amyloid beta in connection with Alzheimer's many years ago, despite the fact that he found results similar to these. I challenged him vigorously at the Open University about it. Isn't it time that they sought the actual cause of this disease?
 
MeSci said:
If I remember rightly, Professor Steven Rose was on about amyloid beta in connection with Alzheimer's many years ago, despite the fact that he found results similar to these. I challenged him vigorously at the Open University about it. Isn't it time that they sought the actual cause of this disease?
Click to expand...

Sure you're aware that @Simon M has pointed out that GWAS has suggested clues re Alzheimer's.
 
Hutan said:
Consequence1 : Side effects that are hard to differentiate from the disease

Consequence 2: Slowed progress to find a good drug
Click to expand...

Consequence 3: Doctors in the USA getting pressure from families to prescribe it off-label for loved ones with more advanced Alzheimer’s (for which it’s not indicated, only early MCI stage) because this is such a devastating disorder, burdening patient families and insurance companies with huge costs (cuz you know this is USA we move with the $ it’s gonna be $$$$) for a drug that likely will not work for more advanced Alzheimer’s.
 
Last edited:
MeSci said:
If I remember rightly, Professor Steven Rose was on about amyloid beta in connection with Alzheimer's many years ago, despite the fact that he found results similar to these. I challenged him vigorously at the Open University about it. Isn't it time that they sought the actual cause of this disease?
Click to expand...

I think since then not only discovery of the role of tau protein plus I believe very importantly the role of blood brain barrier damage/breakdown and insulin resistance and diabetes in the pathogenesis and progression of Alzheimer’s. BBB damage and leakage from diet, high blood pressure, diabetes, as well as brain cellular metabolic dysfunction due to insulin resistance I think are very plausible causes or major factors in the development of idiopathic (non APOE4 mutation) Alzheimer’s.
 
You must log in or register to reply here.
Back
Top Bottom