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.
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.”
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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.
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