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.

Friday, January 5, 2024

Opening Blood-Brain Barrier to Deliver Alzheimer's Drug Shows Promise

 Because of your risk of dementia post stroke you'll want your doctor to know about this. So be prepared to train them.

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:

Opening Blood-Brain Barrier to Deliver Alzheimer's Drug Shows Promise


Focused ultrasound helped aducanumab reduce amyloid-beta levels

Last Updated January 4, 2024
A computer rendering of a patient who is receiving focused ultrasound

Aducanumab (Aduhelm) infusions combined with focused ultrasound led to lower cerebral amyloid-beta levels in Alzheimer's disease, a proof-of-concept trial showed.

The investigational treatment involved creating an opening in the blood-brain barrier with MRI-guided focused ultrasound to boost drug delivery.

In each of three participants who received aducanumab infusions, amyloid reduction was greater in brain regions targeted with focused ultrasound than in regions not exposed to focused ultrasound, said Ali Rezai, MD, of West Virginia University Rockefeller Neuroscience Institute in Morgantown, and co-authors in a New England Journal of Medicineopens in a new tab or window brief report.

From baseline to the 26-week assessment, PET scans showed that focused ultrasound combined with aducanumab led to a drop in amyloid levels from 224.2 to 115.2 centiloids in participant 1, from 185.6 to 104.6 centiloids in participant 2, and from 251.5 to 84.9 centiloids in participant 3. Contralateral brain regions that did not have focused ultrasound showed little change in amyloid levels from baseline to 26 weeks.

"We observed an average 32% reduction in SUVR [standardized uptake value ratio] for the three participants combined after 26 weeks in the regions that had received treatment to open the blood-brain barrier and six combination treatments," Rezai and colleagues wrote.

Headaches were the most common adverse events and were mild except for one moderate headache. One participant had two severe adverse events during the focused ultrasound treatment due to discomfort with head and neck positioning; this resolved immediately after the procedure. No amyloid-related imaging abnormalities were seen.

Low-intensity focused ultrasound has reversibly opened the blood-brain barrier in people with Alzheimer's disease or other neurologic disorders, including Parkinson's disease, brain tumors, and amyotrophic lateral sclerosis.

Previous work by Rezai's group showed that focused ultrasound alone -- without a therapeutic agent like aducanumab -- slightly reducedopens in a new tab or window amyloid-beta levels, noted Kullervo Hynynen, PhD, of the University of Toronto in Canada. "The reduction observed in the current trial was numerically greater than in the previous studies," he wrote in an accompanying editorialopens in a new tab or window.

"The blood-brain barrier safeguards the brain from harmful substances while allowing essential nutrients to pass through," Hynynen said. "However, it also impedes the delivery of drugs to the brain."

The three participants were a 77-year-old man (participant 1), a 59-year-old man (participant 2), and a 64-year-old woman (participant 3). All received a diagnosis of Alzheimer's disease within the year before enrollment. None had previously received aducanumab therapy and none carried an APOE4 allele.

For 6 months, participants received monthly intravenous aducanumab, escalated up to 6 mg/kg rather than the on-label doseopens in a new tab or window of 10 mg/kg, as a risk mitigation strategy.

Opening the blood-brain barrier with focused ultrasound started 2 hours after each infusion. The blood-brain barrier closed within 24 to 48 hours after the procedure.

Focused ultrasound was applied to areas with high beta-amyloid in the frontal or temporal lobe or the hippocampus. In the contralateral hemisphere, homologous brain regions that were not exposed to focused ultrasound served as controls.

Participants 1 and 2 had no neurologic, cognitive, or behavioral changes at their last follow-up visit. At day 30 of follow-up, participant 3's cognitive test scores declined, but she showed no neurologic change or change in activity of daily living scores.

These findings are consistent with those of mouse studiesopens in a new tab or window that demonstrated increased penetration of aducanumab when combined with focused ultrasound to open the blood-brain barrier, Rezai and colleagues noted.

"However, our trial did not quantify monoclonal antibody penetration, and therefore enhanced delivery of the monoclonal antibody was not directly shown," they acknowledged.

The study involved small tissue volumes in one side of the brain of only three patients, Hynynen pointed out. Larger trials are needed and expanding treatment to both sides of the brain is crucial to determine efficacy, he observed.

"That all being said, the results spark optimism that this approach to treatment, together with agents that remove [amyloid-beta], could eventually slow the progression of Alzheimer's disease," he wrote.

  • Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

This study was funded by the Harry T. Mangurian, Jr. Foundation and the West Virginia University Rockefeller Neuroscience Institute.

Rezai had no disclosures.

Co-authors reported relationships with Insightec, AbbVie, Genentech, Neurocrine Biosciences, Teva Pharmaceuticals USA, and Taylor & Francis Group.

Hynynen is a founder of FUS Instruments and holds patents related to focus ultrasound methods.

Primary Source

New England Journal of Medicine

Source Reference: opens in a new tab or windowRezai AR, et al "Ultrasound blood–brain barrier opening and aducanumab in Alzheimer's disease" N Engl J Med 2024; DOI: 10.1056/NEJMoa2308719.

Secondary Source

New England Journal of Medicine

Source Reference: opens in a new tab or windowHynynen K "Sounding out the blood–brain barrier" N Engl J Med 2024; DOI: 10.1056/NEJMe2311358.

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