Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, October 25, 2023

Donanemab slows disease progression, reduces amyloid in early symptomatic Alzheimer’s

Do you have any proof your doctors follow and implement research? Because you will likely need this, better start shopping for doctors now before you need this. If we had any brains at all in stroke, trials would be done on stroke survivors to see if using this prevents getting dementia,

Your chances of getting dementia.

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018 

The latest here:

Donanemab slows disease progression, reduces amyloid in early symptomatic Alzheimer’s

Key takeaways:

  • The randomized, double-blind study included 1,219 individuals with early symptomatic Alzheimer’s disease.
  • Donanemab performed superior to placebo for both carriers and noncarriers of the APOE ε4 allele.

Compared with placebo, donanemab slowed disease progression and reduced amyloid presence at 76 weeks for carriers and noncarriers of the APOE ε4 allele in early symptomatic Alzheimer’s disease, according to data presented at CTAD.

“The APOE 4 allele increases the risk of developing Alzheimer’s disease, and is associated with amyloid accumulation, cerebral amyloid angiopathy risk and an earlier age of disease onset,” Cynthia D. Evans, PhD, a neuroscientist at Eli Lilly & Co., said in her presentation.

Source: Adobe Stock.
Results of a randomized, double-blind, placebo-controlled clinical trial found donanemab effective in slowing disease progression, reducing amyloid presence in early symptomatic Alzheimer’s. Image: Adobe Stock

Evans and colleagues sought to examine safety and efficacy of donanemab (Eli Lilly & Co.) by APOE ε4 carrier status for those with early symptomatic AD in the TRAILBLAZER-ALZ 2 clinical trial.

Their randomized, double-blind, placebo-controlled study included 1,729 individuals, 1,219 of whom were APOE ε4 carriers (mean age 72.6 years; 57.2% female) and 510 who were not (mean age 73.9 years; 58.0% female), with separate subsets of low-medium tau and high tau populations. Participants engaged in a screening period of up to 7 weeks, which included an MRI as well as amyloid and tau positron emission tomography scans. This was followed by a double-blind treatment period of 76 weeks during which IV donanemab was administered initially at three doses of 700 mg every 4 weeks for the first 12 weeks, then at 1400 mg every 4 weeks through week 76, or placebo administered every 4 weeks through week 76. Participants could enter a long-term extension of the study preceding a follow-up interval of up to 44 weeks.

Results showed that treatment with donanemab slowed clinical decline in both allele carriers and noncarriers at similar rates (36% vs. 35%) over 76 weeks, while clinical decline was faster for carriers and noncarriers given placebo.

In addition, efficacy rates for both allele carriers and noncarriers were similar in low-medium tau populations, but higher across all scales compared with the overall study population.

Data further showed that amyloid reduction for both carriers and noncarriers was significant at week 76 in the donanemab-treated population compared with placebo.

“Mean amyloid clearance was robust among all donanemab-treated participant groups,” Evans said. “Noncarriers decline faster than carriers on clinical scales in amyloid selected early symptomatic [Alzheimer’s disease] populations.”

Sources/Disclosures

Collapse

Source:

Evans CD, et al. Efficacy of donanemab by APOE ε4 carrier status in TRAILBLAZER ALZ 2, a phase 3 randomized clinical trial in early symptomatic Alzheimer’s disease. Presented at: CTAD; Oct. 24-27, 2023; Boston.

Disclosures: Evans is employed by Eli Lilly & Co., which sponsored the study and has a pending patent application on the blood test used in the research.

No comments:

Post a Comment