Scientists From Japan Show How The Intranasally Delivered Oxytocin Derivative Could Be Used To Treat Alzheimer’s Disease
- Date:
- Tokyo University of Science
- Summary:
- Alzheimer’s disease , characterized by an accumulation of beta-amyloid protein in brain tissue, is a leading cause of dementia. Researchers now show that an oxytocin derivative with modifications to enhance brain perfusion can reverse cognitive impairment in mice.
Alzheimer’s disease , characterized by an accumulation of -amyloid protein in brain tissue, is a leading cause of dementia. Researchers at Tokyo University of Science have previously reported on the oxytocin-induced reversal of impaired synaptic plasticity triggered by amyloid peptide . They now show that an oxytocin derivative with modifications to enhance brain perfusion can reverse A25-35-induced cognitive impairment in mice.
The cognitive decline and memory loss observed in Alzheimer’s disease is attributed to the accumulation of -amyloid protein , which impairs neural function in the brain. Experimentation has shown that oxytocin, a peptide hormone primarily responsible for parturition, bonding, and lactation, also regulates cognitive behavior in the rodent central nervous system . This finding, along with the identification of oxytocin receptors in CNS neurons, has spurred interest in the potential role of oxytocin in reversing memory loss tied to cognitive disorders like AD.
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Alzheimers Disease Causes Major Metabolic Changes In The Brain
Concept of memory loss and dementia disease and losing brain function memories as an alzheimers health symbol. Credit: Shutterstock
A collaboration between Weill Cornell Medicine scientists and other leaders in Alzheimers disease research has revealed widespread metabolic changes in the brains of individuals with Alzheimers disease. The findings could lead to the development of new treatments aimed at ameliorating the metabolic effects of the disease.
For the study, published July 13 in Alzheimers and Dementia, the investigators compared the levels of about 670 metabolites in postmortem human brain tissue samples obtained from people with Alzheimers disease and from those who did not have the condition. These metabolites are small molecules produced during key metabolic processes in the brain, such as producing energy for brain cells or processing fats essential for efficient transmission of information in the brain. Levels of more than half of the metabolites were altered in individuals diagnosed with Alzheimers. The team linked the metabolic changes with memory loss and the characteristic build-up of protein tangles in the brains of individuals with Alzheimers disease. In addition, the investigation revealed a new connection between cellular osmotic regulation and the disease.
This is a potential new mechanism in Alzheimers disease, he said.
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Online Program Helps People Move Toward Better Health Camraderie
When Dave Elliott was diagnosed with mild cognitive impairment in 2018, many services werent available to him and his wife, Susan. Mild cognitive impairment is an early stage of losing memory or other cognitive abilities, such as language or visual/spatial perception. The COVID-19 pandemic made it even more difficult for
Amyloid Hypothesis Fails To Find Treatments
Scientists had been hopeful that amyloid which has been the primary focus of Alzheimers treatment research for the past three decades would be the key to solving Alzheimers. The plaque builds up around neurons the cells responsible for sending and receiving signals from the brain eventually leading to impaired memory and thinking in patients.
However, the recent controversy around Biogens aducanumab, allegations of falsified research and a series of failed clinical trials over the years targeting amyloid have left some in the field demoralized.
Most recently, pharmaceutical company Roche announced in June that its amyloid targeting drug, crenezumab, failed to slow or prevent cognitive decline in people with a rare genetic mutation that causes early-onset Alzheimers disease. The phase 3 trial, which the National Institute on Aging supported, enrolled around 250 people.
The amyloid hypothesis has been taking a lot of hits lately, said Donna Wilcock, the assistant dean of biomedicine at the University of Kentucky. The drug trials keep coming through and for the most part, failing.
Experts expect diagnosis and treatment of the disease may have to consider multiple mechanisms.
“Its an all-hands-on-deck kind of situation with research to try to identify better diagnosis and treatment options,” Ramanan said.
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Optimal Subcutaneous Lecanemab Dose Found In Modeling Study
The optimal dose of under-the-skin lecanemab, Eisais experimental therapy for early Alzheimers disease, has been determined in a modeling study. The dose is currently being evaluated in the Phase 3 Clarity AD open-label extension study . Eisais broad clinical program for lecanemab continues to deliver data
Dementia Alzheimer’s Not An Inevitable Part Of Aging: Study
The study showed centenarians without cognitive decline despite risk factors.
Dementia and Alzheimer’s disease may not be an inevitable part of aging, according to a recent Dutch study, which identified 100-year-olds with high cognitive performance despite risk factors for decline.
This six-year study of centenarians — people who are over 100 years old — found that despite high levels of a brain marker associated with cognitive decline, called amyloid beta, these centenarians were still sharp and performed well on cognitive tests. The researchers concluded these elderly subjects may have resilience mechanisms protecting them from memory loss.
In fact, they said the risk of dementia may not necessarily increase once you pass your 100th birthday.
“A person between 70 and 95 years old is exposed to the same dementia risk as a person who lives between age 100 and 102,” said Henne Holstege, Ph.D., of Amsterdam University Medical College in the Netherlands, who was involved in the study.
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But Does The Drug Work
In a prior blog post I reviewed the publicly available data and the daylong FDA hearing on aducanumab. In a nutshell, there were two large clinical trials to assess effectiveness, side effects, safety, and how the drug might be used in clinical practice. One of the studies was positive, meaning that the drug worked to slow down the decline of thinking, memory, and function that is usually impossible to stop in Alzheimers. The other large study was negative. In my view and that of the FDA advisory panel these results mean that we dont know if the drug works or not.
Another factor to consider is that the potential benefit if the drug works as well as it did in the positive study was fairly small. Looking at the two objective measures, in the positive trial, the high dose made a 0.6-point change on the 30-point Mini-Mental State Examination. On the 85-point Alzheimers Disease Assessment ScaleCognitive Subscale-13, the high dose made a 1.4-point change.
New Study Expands Range Of Potential Alzheimer’s Drugs
Alzheimer’s disease is associated with a reduction of insulin receptors in brain microvessels, which may contribute to brain insulin resistance and the formation of amyloid plaques, one of the disease’s hallmarks. That’s according to a study published today in the journal Brain by a team from Université Laval and Rush University Medical Center in Chicago.
The work leading to the discovery was headed by Frédéric Calon, a professor at the Faculty of Pharmacy and a researcher at the Institute of Nutrition and Functional Foods and the CHU de QuébecUniversité Laval Research Center.
The findings could affect the search for new Alzheimer’s drugs. “Several clinical trials are underway to assess the efficacy of diabetes drugs for Alzheimer’s disease,” said Professor Calon.”Our study shows that drugs do not need to cross the bloodbrain barrier of microvessels to affect brain insulin resistance. Instead, they can target insulin receptors located in cerebral microvessels. That expands the range of drugs that could be tested for Alzheimer’s.”
The research was made possible by a longitudinal study that began in 1993 and involves about 1,100 members of some 30 religious congregations in the United States. The participants have agreed to undergo annual medical and psychological tests and donate their brains after death. The Brain article is based on data from 60 deceased individuals who participated in this extensive study.
Examination of their brains revealed that:
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Clarity In The Future
Part of the FDAs approval of aducanumab requires Biogen to conduct an additional study to try to determine if it really works. So, we may have more clarity in the future. However, this additional study will likely take three to four years, and thus its results will be too late for those trying to decide today whether to take the medication.
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Not Giving Up On Amyloid
While research outside amyloid is accelerating, former Food and Drug Administration scientist, Dr. Yaning Wang, now the CEO of a clinical-stage biotech firm, is urging scientists to not wholly abandon the development of amyloid-fighting drugs.
Likewise, Dennis Selkoe, a neurologist at Harvard Medical School and Brigham and Womens Hospital, is also pushing for the continued development of drugs that target amyloid.
He co-authored a paper published in the journal PLOS Biology last month that noted that amyloid is still likely one of several factors that play a role in the development of the disease and that clinical trials targeting the plaque have been fraught with missteps.
Both Wang and Selkoe said scientists are eagerly awaiting data from another amyloid-targeting drug, from Biogen and Eisai, expected in the fall.
At the same time, Selkoe is calling for more research into treatments that target tangled tau proteins, also commonly found in Alzheimers patients, and the activation of microglia, the immune cells of the central nervous system that play a role in brain inflammation.
Tau and microglia appear to be important additional factors, but they appear to be precipitated by amyloid accumulation, he said.
He said its only a matter of time before we see more research discoveries that show potential for slowing Alzheimers disease, possibly within the next year or two.
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As pioneers in neuroscience, we believe defeating this disease will require multiple approaches and treatment options, and we look forward to continuing the discussion about the significance of these findings with the patient, scientific, and medical communities, he said.
News of the milestone study, known as Clarity AD, also rippled in the finance world Biogens stock soared around $73 to $270 upon the major announcement, Yahoo! Finance reported.
We think that lecanemab holds mega blockbuster potential, likely in the $6 to $8 billion range, Guggenheim Partners analyst Yatin Suneja wrote in a client memo on Wednesday.
Lecanemab represents a major rebound for Biogen after Aduhelm the companys previous try at an Alzheimers treatment failed when brought to market in 2021, the New York Times reported.
The new drugs intended, neurological purpose is to clear away plaques formed on the brain by an Alzheimers-connected protein called amyloid, thus reducing the diseases major effects.
Eisai representatives will present the Clarity AD study findings to the Clinical Trials on Alzheimers Congress in late November and will publish the research to a peer-reviewed medical journal.
Eisai believes these findings will create new horizons in the diagnosis and treatment of Alzheimers disease as well as further activate innovation for new treatment options, company CEO Haruo Naito said.
Discuss With Your Doctor
Should you or a loved one take aducanumab? You should discuss this decision with your doctor. Because we dont know if aducanumab works or not, deciding to take it is similar to deciding to participate in a clinical trial. As mentioned above, the known side effects are that 30% of people experienced reversible brain swelling and more than 10% had tiny brain bleeds. Although it does clear amyloid plaques from the brain, we dont know if it will slow down the dementia or not.
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How Do You Take The Drug And Is It Safe
To take the drug, you need an intravenous infusion every four weeks forever. Thirty percent of those who took the drug had a reversible swelling of the brain, and more than 10% had tiny brain bleeds. These side effects need to be watched closely by an expert neurology/radiology team who understand how to monitor for these events and know when to pause or stop the drug.
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For decades, a leading theory stated that the amyloid beta protein formed sticky plaques in the brain that were the main cause of Alzheimers.
The 2006 study in Nature identified a subtype of the protein A*56, or “amyloid beta star 56” as the cause of memory loss in rats.
The paper caused “a big splash at the time,” said Donna Wilcock, the assistant dean of biomedicine at the University of Kentucky.
But Science magazine said it found evidence that the paper’s images and images in other studies on A*56 by Lesné had been doctored to inflate the protein’s role in the progression to Alzheimers, according to experts like Wilcock who reviewed the images for Science.
Other researchers expressed concern that Lesné’s results couldnt be replicated, a key part of the scientific process to confirm the validity of certain findings.
“In my own work, was not a species … that we had ever observed,” said Dr. Thomas Wisniewski, a professor of neurology at the New York University Alzheimers Disease Center.
Wisniewski, who wasnt involved in the investigation, said he looked at the images Monday and saw “evidence of what looks like copy and paste” to make a composite picture.
Wilcock said she also noticed small areas of the images that appeared to have been “selectively enhanced.”
Kat Dodge, a spokesperson for the University of Minnesota Medical School, said the institution is aware of questions surrounding studies published by Lesné and Ashe.
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Can Exercise Prevent Alzheimer’s
Since new pharmaceutical treatments may be years from being available for patients, some Alzheimers researchers are looking more to early detection and prevention such as exercise to slow the onset or progression of the disease.
Data from the longest-ever phase 3 trial of exercise on cognition released at the conference on Tuesday found that exercise may stall cognitive decline in Alzheimers patients.
Three hundred patients in the trial by Alzheimers Disease Cooperative Study in partnership with Wake Forest and the YMCA were randomized to moderate intensity aerobic training, or to stretching, balance and range of motion for 18 months. Neither group showed 12-month declines in cognitive tests.
The data suggest exercise “may be a mechanism of potentially reducing risk for not only developing dementia” but “an overall healthy, balanced lifestyle approach to risk reduction,” said Edelmayer, of the Alzheimers Association.
A key benefit of an exercise program is that doctors could prescribe it to patients right away to reduce their risk of the disease, without waiting years for clinical drug trials.
One In 10 Older Americans Has Dementia
In the first nationally representative study of cognitive impairment prevalence in more than 20 years, Columbia University researchers have found almost 10% of U.S. adults ages 65 and older have dementia, while another 22% have mild cognitive impairment. People with dementia and mild cognitive impairment are more likely to be older, have lower levels of education, and to be racialized as Black or Hispanic. Men and women have similar rates of dementia and mild cognitive impairment.
Although dementia and mild cognitive impairment are known to be common in the United States, accurate, up-to-date measures of their national prevalence were scarce.
Such data are critical for understanding the causes, costs, and consequences of dementia and mild cognitive impairment in the United States and for informing policies aimed at reducing their impact on patients, families, and public programs, says Jennifer J. Manly, PhD, the studys lead author and professor of neuropsychology in neurology at the Gertrude H. Sergievsky Center and the Taub Institute for Research on Alzheimers Disease and the Aging Brain at Columbia University.
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Study Shows Lecanemab Drug Slows Down Cognition Decline By 27% Compared To Placebo
Biogen Inc. headquarters are shown March 11, 2020, in Cambridge, Mass. Shares of Biogen and other drugmakers researching Alzheimers disease soared early Wednesday, Sept. 28, 2022, after Japans Eisai Co. said its potential treatment appeared to slow the fatal diseases progress in a late-stage study. Eisai announced results late Tuesday from a global study of nearly 1,800 people with early-stage Alzheimers.
Steven Senne, Associated Press
After an 18-month trial, pharmaceutical companies Biogen and Eisai report that results from a new study indicate a new clinical drug called lacanemab could be the next step in helping the Alzheimer’s community.
Dr. Susan Kohlhaas of Alzheimers Research UK told The Guardian that this is the first clinical trial in phase 3 to show a significant change in cognitive decline in a generation, and called it a historic moment for dementia research.
Whats the risk? Out of about 1,800 patients who participated in the trial, about 1 in 5 experienced side effects including brain swelling or bleeding, that have occurred with other medications similar to lecanemab.
The new medicine specifically targets amyloid plaques which are associated with Alzheimers disease, along with neurofibrillary tangles , per the National Institute of Aging.
Long-term effects are still being monitored.
Were not ready to deliver this at scale and we need to address that now, he said.
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