Why hasn't our competent? doctors and hospitals looked at this and said: 'Hey, maybe this could help in stroke!' But that won't occur, there aren't two functioning neurons to rub together to get a spark of intelligence in all of stroke!
With your chances of getting dementia post stroke you need solutions. YOUR DOCTOR IS RESPONSIBLE FOR PREVENTING THIS!
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
Send me hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name and my response in my blog. Or are you afraid to engage with my stroke-addled mind? I need an explanation of whom you go to in stroke to ensure valid stroke research get done.
Small molecule oligomer antagonist for Alzheimer’s disease boosts brain connectivity
Results of an ongoing clinical trial showed that an oral, small molecule oligomer antagonist used to treat mild to moderate Alzheimer’s disease boosted connectivity between regions of the brain as a promising sign of cognitive improvement.
Cognition Therapeutics Inc. reported in a press release that data from the SEQUEL study demonstrated treatment with its novel lead therapeutic, CT1812, led to consistent improvement across all prespecified electroencephalography (EEG) parameters, including significant positive change in relative theta power in the central region of the brain and AEC-c, which assesses connectivity between brain regions.
SEQUEL is a phase 2 randomized, double-blind, single-site study that measured brain wave patterns in 16 adults with mild to moderate AD after 29 days of treatment with either CT1812 or placebo.
According to additional data cited in the release, treatment with once-daily CT1812 — which penetrates the blood-brain barrier and binds selectively to the sigma-2 receptor complex — produced a consistent reduction in global relative theta power and in relative theta power across all regions of the brain. The treatment also resulted in an increased prominence of slower EEG frequencies associated with AD-related cognitive decline.
CT1812 was also well-tolerated, with mild or moderate treatment-emergent adverse events observed in 11 patients in the CT1812-treatment group compared with six in the placebo group, and no adverse events leading to treatment discontinuation, the company said in the release.
Full data were published in The Journal of Prevention of Alzheimer's Disease.
”The gradual slowing of brain wave patterns and impaired connectivity that is a hallmark of Alzheimer’s disease is due to the loss of synapses, which are the connection points between neurons,” Anthony O. Caggiano, MD, PhD, chief medical officer and head of research and development at Cognition Therapeutics, said in the release. “The changes we observed across EEG parameters in SEQUEL may indicate that CT1812 is normalizing brain wave patterns and facilitating communication between different brain regions.”
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