In June 2021, the US Food and Drug Administration (FDA) granted accelerated approval for aducanumab to treat patients with mild cognitive impairment (MCI) or mild dementia due to Alzheimer disease (AD), despite limited evidence of clinical benefit. The 2 phase 3 clinical trials of aducanumab, EMERGE and ENGAGE, were stopped prematurely based on prespecified futility thresholds.1 Both trials also showed an increased risk of adverse events with aducanumab, including microhemorrhages and vasogenic brain edema, headache, and possibly falls.1 Though both trials excluded patients based on age, certain chronic diseases, and use of antiplatelet agents and anticoagulants, FDA approval was granted without contraindications or precautions for these unstudied patient populations. We evaluated whether patients enrolled in the trials of aducanumab were representative of patients with dementia enrolled in Medicare by estimating the proportions of Medicare beneficiaries with AD or MCI who would have been excluded from the trials.
Showing posts with label Aducanumab. Show all posts
Showing posts with label Aducanumab. Show all posts
Friday, January 12, 2024
Alzheimer's Mysterious Origins May Lie in Exhausted Cells Unable to Cope
4. Dementia Risk Doubled in Patients Following Stroke September 2018
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
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.
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.
Saturday, August 27, 2022
Combined therapy of focused ultrasound and aducanumab induces neurogenesis and decreases of beta-amyloid plaques in a mouse model of Alzheimer’s disease
20 pages for your doctor to apply for preventing your likely Alzheimers and better stroke recovery.
Combined therapy of focused ultrasound and aducanumab induces neurogenesis and decreases of beta-amyloid plaques in a mouse model of Alzheimers disease
Directed by Professor Jin Woo Chang Doctoral Dissertation submitted to the Department of Medicine, the Graduate School of Yonsei University in partial fulfillment of the requirements for the degree of Doctor of Philosophy Chanho Kong
Tuesday, September 14, 2021
Representativeness of Participants Eligible to Be Enrolled in Clinical Trials of Aducanumab for Alzheimer Disease Compared With Medicare Beneficiaries With Alzheimer Disease and Mild Cognitive Impairment
From an analysis:
About 90% of people with Alzheimer's disease or mild cognitive impairment had at least one condition -- like cardiovascular disease, prior stroke, blood thinner use, chronic kidney disease, or age over 85 -- that would have excluded them from aducanumab (Aduhelm) clinical trials, an analysis of Medicare data found.
With the possible side effects I will never take something like this. Hopefully I'm still cognizant enough to object.
Representativeness of Participants Eligible to Be Enrolled in Clinical Trials of Aducanumab for Alzheimer Disease Compared With Medicare Beneficiaries With Alzheimer Disease and Mild Cognitive Impairment
Saturday, May 8, 2021
Boosting brain’s waste removal system could improve Alzheimer’s outcomes
But is side sleeping better? I'd love to see you research that in mice.
The Brain’s Waste-Removal System Side sleeping in here.
The latest here:
Boosting brain’s waste removal system could improve Alzheimer’s outcomes
At a Glance
- A study in mice suggests that antibody therapies targeting amyloid-beta protein may be more effective after enhancing the brain’s waste drainage system.
- The findings point to a potential strategy to help slow the progression of Alzheimer’s.
The lymphatic system is sometimes called the body’s waste removal system. It’s a vital part of the immune system that helps organs remove waste and protect from infection. Lymphatic vessels run alongside blood vessels to transport immune cells and cellular waste products. The lymph fluid is then filtered through glands called lymph nodes and returned to the bloodstream.
Just a few years ago, researchers discovered that the human brain has a lymphatic system of its own to remove waste. Recent studies suggest that problems with the brain’s lymphatic clearance may play a role in Alzheimer’s disease. One of the hallmarks of Alzheimer’s is an abnormal buildup of amyloid-beta protein. A 2018 study found that impairing lymphatic vessels in a mouse model of Alzheimer’s led to higher levels of amyloid-beta deposits in the brain as the mice aged.
A study led by Drs. Jonathan Kipnis, Oscar Harari, and Carlos Cruchaga of Washington University in St. Louis set out to investigate whether altering lymphatic drainage could make experimental antibody treatments that target amyloid-beta more effective. The study was funded in part by NIH’s National Institute on Aging (NIA). Findings appeared in Nature on April 28, 2021.
Using a mouse model of early-onset Alzheimer’s, the researchers removed some of the lymphatic vessels in the brains of one group of mice. They treated the mice, as well as a control group, with injections of antibody therapies, or “immunotherapies,” including a mouse version of the drug aducanumab.
The mice with impaired lymphatic systems had greater buildup of amyloid-beta plaques and immune cells that cause inflammation. Brain inflammation is thought to play a role in Alzheimer’s progression. These mice also performed more poorly on a test of learning and memory.
The researchers then tested whether boosting the brain’s lymphatic system could have the opposite effect. They injected mice with a growth factor to enhance growth of cells that line the brain’s lymph vessels. They then followed this with the amyloid-beta antibody therapies. The treated mice showed lower accumulations of amyloid-beta in the brain’s meninges—the membranes surrounding the brain and spinal cord.
A genetic analysis showed that microglia—the brain’s “trash collector cells”—were greatly affected by manipulations of the brain’s lymphatic system. When the team compared microglia in the brains of Alzheimer’s patients with those of the mice whose lymphatic systems had been impaired, they found significant similarities.
Taken together, these findings support the role of impaired lymphatic drainage in the brain inflammation seen in Alzheimer’s disease. The study also suggests that improving lymphatic clearance in people with Alzheimer’s while administering immunotherapies could lead to better outcomes. Starting treatment early in the disease when the lymphatic system is more intact may be an important factor.
“A broad range of research on immunotherapies in development to treat Alzheimer’s by targeting amyloid-beta has not to date demonstrated consistent results,” says NIA Director Dr. Richard J. Hodes. “While this study’s findings require further confirmation, the link it has identified between a well-functioning lymphatic system in the brain and the ability to reduce amyloid-beta accumulation may be a significant step forward in pursuing this class of therapeutics.”
Monday, August 10, 2020
'Game-changing' drug that could halt Alzheimer’s may be available in the US by March
Interesting that they don't tell you this is intravenous, once a month. From this earlier piece on it here:
Clinicians view new Alzheimer’s drug with guarded optimism
But is this the correct path to go down or should tau proteins be
addressed? Is this just cleaning up existing plaque but not addressing
new plaque being generated by tau? Cause and effect once again. Ask your doctor to clarify.
The real cause of Alzheimer’s is a dysfunctional ‘tau’ protein, a new study of over 3,600 brains finds.
The latest here:
'Game-changing' drug that could halt Alzheimer’s may be available in the US by March
An Alzheimer’s drug that could halt the progression of the disease has been hailed a “game changer”.
The memory-robbing disorder has no cure, with existing treatments working to ease its symptoms.
In severe cases, patients may become aggressive, struggle to move or even hallucinate.
Hopes have been raised after the US Food and Drug Administration (FDA) granted the medication aducanumab fast-track approval.
Read more: Gum disease linked to double the risk of dementia
Trials have demonstrated aducanumab helps to untangle Alzheimer’s tell-tale protein clumps in the brain, potentially reversing the disease.
The FDA has not considered a new treatment for the condition in 17 years, with aducanumab’s fate being decided by 7 March 2021.
If licensed, it would be the first therapy approved to delay Alzheimer’s progression.
‘A new era for Alzheimer’s treatments’
“The FDA’s acceptance of the aducanumab with priority review is an important step in the path to potentially having a treatment that meaningfully changes the course of Alzheimer’s disease,” said Michel Vounatsos, CEO of the manufacturer Biogen, as reported by Global News Wire.
“We believe aducanumab marks the beginning of a new era of potential treatments for Alzheimer’s disease that will inspire even more discovery and innovation to bring hope to those affected by this devastating disease.”
Read more: 'Game changing' Alzheimer's blood test edges closer
More than 5 million people in the US have Alzheimer’s, which is expected to increase to over 13 million by 2050.
In the UK, around 850,000 people have dementia – the umbrella term for conditions that cause a gradual decline in brain function.
Alzheimer’s is the most common type of dementia, affecting between 50% and 75% of patients in the UK.
The disease is thought to be caused by the abnormal build-up of proteins in and around brain cells.
Two of these are amyloid – which forms plaques, and tau – which develops into tangles.
Over time, the chemical messengers that send signals between brain cells decline.
Different areas of the vital organ then shrink, usually starting with those responsible for memories.
Trials have shown aducanumab works to untangle these clumps, slowing memory loss.
The drug was also linked to improvement in a patient’s ability to carry out day-to-day tasks, like household chores and leaving the home alone.
Read more: Elderly who distinctly smell roses 'have half the risk of dementia'
“I am heartened by what this progress may mean for people living with Alzheimer’s disease and their families,” said Dr Christopher van Dyck, from the Yale Alzheimer’s Disease Research Center.
“If aducanumab is determined to be effective in reducing the decline in cognition and activities of daily living resulting from progression of this disease by addressing the underlying disease pathology, it will deliver meaningful benefits to those who most need them.”
Keeps patients ‘in a better place for a longer time’
Aducanumab has had a bumpy road. Studies were scrapped in March 2019 after two late-stage trials suggested it was of no benefit.
Several months later, Biogen looked at a larger amount of data that became available after the trials stopped.
It found the drugs were effective providing they were given early enough and at a sufficient dose.
Experts hope aducanumab will benefit those with early signs of dementia, helping to halt or slow the disease before patients became incapacitated.
The FDA has been set an “action date” of 7 March 2021, but “plans to act early on this application under an expedited review”.
Michael Yee, an analyst at the investment bank Jefferies, expects a verdict in the first quarter of 2021, adding the data demonstrating the drug’s effectiveness is “mixed and still inconclusive”, Fierce Biotech reported.
Nevertheless, the fast-track approval suggests the FDA is “comfortable with the totality of the data, recognises high unmet need and really wants to get an Alzheimer’s drug approved”, he added.
Analyst Brian Abrahams, from RBC Capital Markets, has given aducanumab a 30% chance of approval.
Dr Dennis Selkoe from Harvard told wbur: “I think there’s a reasonable chance that aducanumab, if approved and we don’t know that yet, will be the first disease-modifying agent for Alzheimer’s, and that will be a huge milestone, and patients of mine and others can access the drug.
“Having cared for hundreds of patients with this disease, this would be a game changer.
“At least for some of my patients, if aducanumab is approved, [it would be] something that will slow down their deterioration, that will keep them in a better place for a longer time.”
The FDA only accepts drugs for priority review if they offer major advances in treatments or provide a therapy where none existed.
If approved in the US, experts are confident other health watchdogs around the world will consider doing the same.
In the meantime, Biogen is planning further studies, which will offer high doses to all eligible participants from the earlier trials.
Monday, February 24, 2020
Clinicians view new Alzheimer’s drug with guarded optimism
What reason do you have to think your stroke hospital knows about this AND knows you need it? A call to the president and board of directors will be required.
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
5. Parkinson’s Disease May Have Link to Stroke March 2017
Clinicians view new Alzheimer’s drug with guarded optimism
This year, Biogen is
expected to submit a Biologics License Application to the FDA for its
anti-amyloid antibody, aducanumab. If approved, it will be the first new
drug available to patients with Alzheimer’s disease in 16 years.
Administered intravenously once a month, aducanumab clears some of the plaque materials that may cause cell death and tissue loss in the brain caused by Alzheimer's disease, according to Barry Reisberg, MD, one of the clinical investigators who developed the Alzheimer’s drug memantine, which was approved back in 2003.
Although it is not curative, aducanumab could be a valuable addition to the clinician’s armamentarium, according to Sharon A. Brangman, MD,
chair of the geriatrics department and director of the Center for
Excellence for Alzheimer’s Disease at Upstate Medical University in New
York.
“Aducanumab is exciting in terms of adding more information to our knowledge of Alzheimer’s disease and maybe offering potential treatment, but it is not a cure,” she said.
The Alzheimer’s Association estimates that 5.8 million Americans live
with Alzheimer’s, and the disease cost the country about $290 billion
in 2019. Healio Primary Care discussed aducanumab with several experts
to see where the drug fits in the treatment landscape and what its
approval could mean for patients.
What is aducanumab?
The mechanism behind aducanumab, an anti-amyloid antibody, is different than donepezil, rivastigmine, memantine and galantamine — which are cholinesterase inhibitors or glutamate modulators and the three currently approved medications to treat patients with Alzheimer’s dementia.
Researchers have previously reported that aducanumab is a human monoclonal antibody that selectively binds to amyloid fibrils and soluble oligomers. Donepezil is a centrally acting, reversible, rapid inhibitor of acetyl cholinesteras that binds reversibly to acetylcholinesterase and impedes the hydrolysis of acetylcholine. Memantine is an antagonist of the N-Methyl-D-Aspartate subtype of glutamate receptors in the central nervous system, while donepezil. rivastigmine and galantamine are cholinesterase inhibitors and reversibly inhibit acetylcholine esterase and improve the intrinsic action of acetylcholine on cholinergic receptors.
According to Biogen, aducanumab was evaluated in two, phase 3 randomized controlled trials — EMERGE (n = 1,638) and ENGAGE (n = 1,647). Although the EMERGE trial met its primary endpoint showing a significant reduction in clinical decline, the trials were discontinued in March 2019 following the results of a futility analysis, which the company said “relied on an earlier and smaller data set.”
Biogen then conducted an additional analysis with a larger data set that yielded positive results.
“They found that there was a subgroup of patients who had mild cognitive impairment but did not meet the criteria for Alzheimer’s disease or any dementia who got higher doses, [and those patients] did have improvement in their cognition,” Brangman said. “Then, when Biogen did a PET scan, these patients did not have amyloid buildup. So, the thinking is that if you remove this amyloid, you may be treating their Alzheimer’s disease.”
The price of aducanumab could be a factor in whether or not patients request or adhere to the medication.
The authors of a recent Neurology study found that a $50 increase in out-of-pocket costs was associated with a 12-percent decrease in the time that a person had access to medication. For example, in 2015, when the cost of the drug donepezil was about $3 for a 30-day supply, patients filled those prescriptions about 70% of the time. Patients prescribed rivastigmine, which cost about $100 for a 30-day supply in 2015, filled their prescriptions about 45 percent of the time.
Biogen declined to answer questions about the price of the drug for this story.
Administered intravenously once a month, aducanumab clears some of the plaque materials that may cause cell death and tissue loss in the brain caused by Alzheimer's disease, according to Barry Reisberg, MD, one of the clinical investigators who developed the Alzheimer’s drug memantine, which was approved back in 2003.
“Aducanumab is exciting in terms of adding more information to our knowledge of Alzheimer’s disease and maybe offering potential treatment, but it is not a cure,” she said.
What is aducanumab?
The mechanism behind aducanumab, an anti-amyloid antibody, is different than donepezil, rivastigmine, memantine and galantamine — which are cholinesterase inhibitors or glutamate modulators and the three currently approved medications to treat patients with Alzheimer’s dementia.
Researchers have previously reported that aducanumab is a human monoclonal antibody that selectively binds to amyloid fibrils and soluble oligomers. Donepezil is a centrally acting, reversible, rapid inhibitor of acetyl cholinesteras that binds reversibly to acetylcholinesterase and impedes the hydrolysis of acetylcholine. Memantine is an antagonist of the N-Methyl-D-Aspartate subtype of glutamate receptors in the central nervous system, while donepezil. rivastigmine and galantamine are cholinesterase inhibitors and reversibly inhibit acetylcholine esterase and improve the intrinsic action of acetylcholine on cholinergic receptors.
According to Biogen, aducanumab was evaluated in two, phase 3 randomized controlled trials — EMERGE (n = 1,638) and ENGAGE (n = 1,647). Although the EMERGE trial met its primary endpoint showing a significant reduction in clinical decline, the trials were discontinued in March 2019 following the results of a futility analysis, which the company said “relied on an earlier and smaller data set.”
Biogen then conducted an additional analysis with a larger data set that yielded positive results.
“They found that there was a subgroup of patients who had mild cognitive impairment but did not meet the criteria for Alzheimer’s disease or any dementia who got higher doses, [and those patients] did have improvement in their cognition,” Brangman said. “Then, when Biogen did a PET scan, these patients did not have amyloid buildup. So, the thinking is that if you remove this amyloid, you may be treating their Alzheimer’s disease.”
The price of aducanumab could be a factor in whether or not patients request or adhere to the medication.
The authors of a recent Neurology study found that a $50 increase in out-of-pocket costs was associated with a 12-percent decrease in the time that a person had access to medication. For example, in 2015, when the cost of the drug donepezil was about $3 for a 30-day supply, patients filled those prescriptions about 70% of the time. Patients prescribed rivastigmine, which cost about $100 for a 30-day supply in 2015, filled their prescriptions about 45 percent of the time.
Biogen declined to answer questions about the price of the drug for this story.
Thursday, September 1, 2016
Antibody Reduces Harmful Brain Amyloid Plaques in Alzheimer's Patients
But is this the correct path to go down or should tau proteins be addressed? Is this just cleaning up existing plaque but not addressing new plaque being generated by tau? Cause and effect once again.
The real cause of Alzheimer’s is a dysfunctional ‘tau’ protein, a new study of over 3,600 brains finds.
Antibody Reduces Harmful Brain Amyloid Plaques in Alzheimer's Patients
Aducanumab, an antibody developed by the University of Zurich, has been shown to trigger a meaningful reduction of harmful beta-amyloid plaques in patients with early-stage Alzheimer's disease. These protein deposits in the brain are a classic sign of Alzheimer's disease and contribute to the progressive degeneration of brain cells. The researchers furthermore demonstrated in an early stage clinical study that, after one year of treatment with Aducanumab, cognitive decline could be significantly slowed in antibody-treated patients as opposed to the placebo group.Although the causes of Alzheimer's disease are still unknown, it is clear that the disease commences with progressive amyloid deposition in the brains of affected persons between ten and fifteen years before the emergence of initial clinical symptoms such as memory loss. Researchers have now been able to show that Aducanumab, a human monoclonal antibody, selectively binds brain amyloid plaques, thus enabling microglial cells to remove the plaques. A one-year treatment with the antibody, as part of a phase Ib study, resulted in almost complete clearance of the brain amyloid plaques in the study group patients. The results, which were realized by researchers at UZH together with the biotech company “Biogen” and the UZH spin-off “Neurimmune,” have been published in the renowned science journal “Nature.”
Reduction of brain amyloid plaque is dependent on treatment duration and dosage
“The results of this clinical study make us optimistic that we can potentially make a great step forward in treating Alzheimer's disease,” says Roger M. Nitsch, professor at the Institute for Regenerative Medicine at UZH. “The effect of the antibody is very impressive. And the outcome is dependent on the dosage and length of treatment.” After one year of treatment, practically no beta-amyloid plaques could be detected in the patients who received the highest dose of the antibody.
The antibody was developed with the help of a technology platform from “Neurimmune.” Using blood collected from elderly persons aged up to one hundred and demonstrating no cognitive impairment, the researchers isolated precisely those immune cells whose antibodies are able to identify toxic beta-amyloid plaques but not the amyloid precursor protein that is present throughout the human body and that presumably plays an important role in the growth of nerve cells. The good safety profile of Aducanumab in patients may well be attributed to the antibody’s specific capacity to bond with the abnormally folded beta-amyloid protein fragment as well as the fact that the antibody is of human origin.
Investigational treatment also curbs cognitive decline
165 patients with early-stage Alzheimer's disease were treated in the phase 1b clinical trial. Although not initially planned as a primary study objective, the good results encouraged researchers to additionally investigate how the treatment affected the symptoms of disease. This was evaluated via standardized questionnaires to assess the cognitive abilities and everyday activities of the patients. “Aducanumab also showed positive effects on clinical symptoms," is how Nitsch sums up the findings. “While patients in the placebo group exhibited significant cognitive decline, cognitive ability remained distinctly more stable in patients receiving the antibody.”
Some of the trial participants temporarily suffered from amyloid-related imaging abnormality (ARIA), an adverse effect that can be detected via magnetic resonance imaging. In a minority of cases, this was accompanied by temporary mild to moderate headaches. The UZH researchers believe that ARIA is a measurable biological effect of amyloid clearance.
The promising effects of Aducanumab are currently being investigated in two large phase three clinical studies to further evaluate safety and efficacy. Involving over 300 centers in 20 countries throughout North America, Europe, and Asia, these studies are evaluating the effectiveness and safety of the antibody on a total of 2,700 patients with early-stage Alzheimer's disease.
http://www.media.uzh.ch/en/Press-Releases/2016/alzheimer-aducanumab.html
Subscribe to:
Posts (Atom)