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ByJocelyn Kaiser A common genetic variant called APOE4 raises a person’s risk of Alzheimer’s disease. It also poses a puzzle: If APOE4 is so bad for us, why hasn’t it been weeded out from the population? A new study finds that, surprisingly, the APOE4 variant has positive cognitive impacts: It may not only boost short-term memory, but also protect against subtle memory loss early in the course of Alzheimer’s disease. “There is something about the possession of an APOE4 allele which is providing some positive impacts on your cognitive function,” even in people whose brains are primed for Alzheimer’s, says neurologist Jonathan Schott of University College London (UCL), co-leader of the study. That could not only help explain why the variant persists, but also guide Alzheimer’s treatments, he says. The APOE gene codes for a protein called apolipoprotein E, which helps metabolize fats. About one in four people carry one copy of the version called APOE4 that roughly triples the risk for late-onset Alzheimer’s disease. (A few people have two copies of APOE4, which raises the risk 12-fold or more.) When a harmful gene remains in a population across hundreds of thousands of years, one possible explanation for its staying power is that one copy is beneficial. For example, people with one copy of the sickle cell gene are protected from malaria. Scientists have known for years that people with APOE4 are more likely to develop sticky amyloid protein plaques in their brains; many researchers think these may contribute to Alzheimer’s by triggering other changes that lead to neuronal death. Yet several small studies have hinted that APOE4 could have benefits, such as boosting fertility and cognition. Last year, a larger study found that APOE4 carriers across a range of ages perform slightly better than noncarriers on a test requiring them to quickly recall an object and its location. © 2021 American Association for the Advancement of Science.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28028 - Posted: 10.09.2021

By Judith Graham The approval of a controversial new drug for Alzheimer’s disease, Aduhelm, is shining a spotlight on mild cognitive impairment (MCI) — problems with memory, attention, language or other cognitive tasks that exceed changes expected with normal aging. After initially indicating that Aduhelm could be prescribed to anyone with dementia, the Food and Drug Administration now specifies that the prescription drug be given to individuals with MCI or early-stage Alzheimer’s, the groups in which the medication was studied. Yet this narrower recommendation raises questions. What does a diagnosis of MCI mean? Is Aduhelm appropriate for all people with MCI, or only some? And who should decide which patients qualify for treatment: dementia specialists or primary care physicians? Debate surrounds Aduhelm because its effectiveness has not been proved, its cost is high (an estimated $56,000 a year, not including expenses for imaging and monthly infusions), and its potential side effects are significant (41 percent of patients in the drug’s clinical trials experienced brain swelling and bleeding). Furthermore, an FDA advisory committee strongly recommended against Aduhelm’s approval, and Congress is investigating the process leading to the FDA’s decision. Medicare is studying whether it should cover the medication, and Veterans Affairs has declined to do so under most circumstances. Clinical trials for Aduhelm, developed by Biogen, based in Cambridge, Mass., excluded adults over 85, people taking blood thinners, people who had experienced a stroke, and those with cardiovascular disease or impaired kidney or liver function, among other conditions. If those criteria were broadly applied, 85 percent of people with MCI would not qualify for the drug, according to a research letter in the Journal of the American Medical Association.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28007 - Posted: 09.29.2021

Emma Yasinski Some genetic risk factors for alcohol use disorder overlap with those for neurodegenerative diseases like Alzheimer’s, scientists reported in Nature Communications on August 20. The study, which relied on a combination of genetic, transcriptomic, and epigenetic data, also offers insight into the molecular commonalities among these disorders, and their connections to immune disfunction. “By meshing findings from genome wide association studies . . . with gene expression in brain and other tissues, this new study has prioritized genes likely to harbor regulatory variants influencing risk of Alcohol Use Disorder,” writes David Goldman, a neurogenetics researcher at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), in an email to The Scientist. “Several of these genes are also associated with neurodegenerative disorders—an intriguing connection because of alcohol’s ability to prematurely age the brain.” Over the past several years, researchers have published a handful of massive genome-wide association studies (GWAS) studies identifying loci—regions of the genome that can contain 10 or more individual genes—that likely influence a person’s risk of developing an alcohol use disorder (AUD). In a study published two years ago, Manav Kapoor, a neuroscientist and geneticist at the Icahn School of Medicine at Mount Sinai and first author on the new paper, and his team found evidence that the immune system might be overactive in people with AUD, but the finding left him with more questions. The first was whether excessive drinking directly causes immune dysfunction, or if instead some people’s genetic makeup puts them at risk for both simultaneously. The second was which of the dozen or so genes at each previous GWAS-identified locus actually influences drinking behaviors. Lastly, he wanted to know if there is a genetic difference between people who consume higher numbers of alcoholic beverages per week but are not diagnosed with AUD and those who have received the diagnosis. © 1986–2021 The Scientist.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 13: Memory and Learning
Link ID: 27995 - Posted: 09.18.2021

Andrew Gregory Health editor Millions of people with eye conditions including age-related macular degeneration, cataracts and diabetes-related eye disease have an increased risk of developing dementia, new research shows. Vision impairment can be one of the first signs of the disease, which is predicted to affect more than 130 million people worldwide by 2050. Previous research has suggested there could be a link between eye conditions that cause vision impairment, and cognitive impairment. However, the incidence of these conditions increases with age, as do systemic conditions such as diabetes, high blood pressure, heart disease, depression and stroke, which are all accepted risk factors for dementia. That meant it was unclear whether eye conditions were linked with a higher incidence of dementia independently of systemic conditions. Now researchers have found that age-related macular degeneration, cataracts and diabetes-related eye disease are independently associated with increased risk of dementia, according to a new study published in the British Journal of Ophthalmology. The research examined data from 12,364 British adults aged 55 to 73, who were taking part in the UK Biobank study. They were assessed in 2006 and again in 2010 with their health information tracked until early 2021. More than 2,300 cases of dementia were documented, according to the international team of experts led by academics from the Guangdong Eye Institute in China. After assessing health data, researchers found those with age-related macular degeneration had a 26% increased risk of developing dementia. Those with cataracts had an 11% increased risk and people with diabetes-related eye disease had a 61% heightened risk. Glaucoma was not linked to a significant increase in risk. © 2021 Guardian News & Media Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 7: Vision: From Eye to Brain
Link ID: 27990 - Posted: 09.15.2021

By Daniel R. George, Peter J. Whitehouse Aducanumab, marketed as “Aduhelm,” is an antiamyloid monoclonal antibody and the latest in a procession of such drugs to be tested against Alzheimer’s disease. Over the last several decades, billions have been spent targeting the amyloid that clumps together to form the neuritic plaques first documented by German psychiatrist Alois Alzheimer in 1906. This class of drugs has reduced amyloid aggregation; however, since 2000, there has been a virtual 100 percent fail rate in clinical trials, with some therapies actually worsening patient outcomes. In 2019, Aducanumab failed in a futility analysis of two pooled phase III randomized controlled trials, but was later claimed to have yielded a small benefit for a subset of patients in a high-dosage group. The biologic was granted accelerated approval by the FDA based not on its clinical benefit but rather on its ability to lower amyloid on PET scans. Biogen immediately priced the treatment at $56,000 annually, making it potentially one of the most expensive drugs in the country’s history. This predicament is all the more surreal because—in the absence of more decisive evidence—there is no adequate proof that the drug actually clinically benefits people who take it. Aducanumab, which is delivered intravenously, was observed to cause brain swelling or bleeding in 40 percent of high-dose participants as well as higher rates of headache, falls and diarrhea. The FDA’s decision flew in the face of a near-consensus recommendation from its advisory committee not to approve. Three members of that committee have since resigned; several federal investigations have been launched to examine the close relationship between Biogen and the FDA; and the Department of Veterans Affairs and numerous private insurers and high-profile hospital systems have already signaled they want nothing to do with the drug. Meanwhile, Biogen has launched a Web site and comprehensive marketing campaign called “It’s Time,” quizzing potential consumers on their memory loss and ultimately guiding them to experts, imaging and/or infusion sites. © 2021 Scientific American,

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27967 - Posted: 08.28.2021

Emma Yasinski Some genetic risk factors for alcohol use disorder overlap with those for neurodegenerative diseases like Alzheimer’s, scientists reported in Nature Communications on August 20. The study, which relied on a combination of genetic, transcriptomic, and epigenetic data, also offers insight into the molecular commonalities among these disorders, and their connections to immune disfunction. “By meshing findings from genome wide association studies . . . with gene expression in brain and other tissues, this new study has prioritized genes likely to harbor regulatory variants influencing risk of Alcohol Use Disorder,” writes David Goldman, a neurogenetics researcher at the National Institute on Alcohol Abuse and Alcoholism (NIAAA), in an email to The Scientist. “Several of these genes are also associated with neurodegenerative disorders—an intriguing connection because of alcohol’s ability to prematurely age the brain.” Over the past several years, researchers have published a handful of massive genome-wide association studies (GWAS) studies identifying loci—regions of the genome that can contain 10 or more individual genes—that likely influence a person’s risk of developing an alcohol use disorder (AUD). In a study published two years ago, Manav Kapoor, a neuroscientist and geneticist at the Icahn School of Medicine at Mount Sinai and first author on the new paper, and his team found evidence that the immune system might be overactive in people with AUD, but the finding left him with more questions. The first was whether excessive drinking directly causes immune dysfunction, or if instead some people’s genetic makeup puts them at risk for both simultaneously. © 1986–2021 The Scientist.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 4: Development of the Brain
Link ID: 27966 - Posted: 08.28.2021

By Paula Span Learning your odds of eventually developing dementia — a pressing concern for many, especially those with a family history of it — requires medical testing and counseling. But what if everyday behavior, like overlooking a couple of credit card payments or habitually braking while driving, could foretell your risk? A spate of experiments is underway to explore that possibility, reflecting the growing awareness that the pathologies underlying dementia can begin years or even decades before symptoms emerge. “Early detection is key for intervention, at the stage when that would be most effective,” said Sayeh Bayat, the lead author of a driving study funded by the National Institutes of Health and conducted at Washington University in St. Louis. Such efforts could help identify potential volunteers for clinical trials, researchers say, and help protect older people against financial abuse and other dangers. In recent years, many once-promising dementia drugs, particularly for Alzheimer’s disease, have failed in trials. One possible reason, researchers say, is that the drugs are administered too late to be helpful. Identifying risks earlier, when the brain has sustained less damage, could create a pool of potential participants with “preclinical” Alzheimer’s disease, who could then test preventive measures or treatments. It could also bring improvements in daily life. “We could support people’s ability to drive longer, and have safer streets for everyone,” Ms. Bayat offered as an example. © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 27959 - Posted: 08.25.2021

Nicola Davis Science correspondent It’s been used to detect eye diseases, make medical diagnoses, and spot early signs of oesophageal cancer. Now it has been claimed artificial intelligence may be able to diagnose dementia from just one brain scan, with researchers starting a trial to test the approach. The team behind the AI tool say the hope is that it will lead to earlier diagnoses, which could improve outcomes for patients, while it may also help to shed light on their prognoses. Dr Timothy Rittman, a senior clinical research associate and consultant neurologist at the University of Cambridge, who is leading the study, told the BBC the AI system is a “fantastic development”. “These set of diseases are really devastating for people,” he said. “So when I am delivering this information to a patient, anything I can do to be more confident about the diagnosis, to give them more information about the likely progression of the disease to help them plan their lives is a great thing to be able to do.” It is expected that in the first year of the trial the AI system, which uses algorithms to detect patterns in brain scans, will be tested in a “real-world” clinical setting on about 500 patients at Addenbrooke’s hospital in Cambridge and other memory clinics across the country. “If we intervene early, the treatments can kick in early and slow down the progression of the disease and at the same time avoid more damage,” Prof Zoe Kourtzi, of Cambridge University and a fellow of national centre for AI and data science the Alan Turing Institute, told the BBC. “And it’s likely that symptoms occur much later in life or may never occur.” © 2021 Guardian News & Media Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 27941 - Posted: 08.11.2021

Jon Hamilton Scientists are working to develop new treatments for Alzheimer's disease by looking beyond amyloid plaques, which have been the focus of most Alzheimer's drug development in the past 20 years. Science Photo Library — ZEPHYR./Getty Images Immune cells, toxic protein tangles and brain waves are among the targets of future Alzheimer's treatments, scientists say. These approaches are noteworthy because they do not directly attack the sticky amyloid plaques in the brain that are a hallmark of Alzheimer's. The plaques have been the focus of most Alzheimer's drug development in the past 20 years. And the drug Aduhelm was given conditional approval by the Food and Drug Administration in June based primarily on the medication's ability to remove amyloid from the brain. But many researchers believe amyloid drugs alone can't stop Alzheimer's. "The field has been moving beyond amyloid for many years now," says Malú Gámez Tansey, co-director of the Center for Translational Research in Neurodegenerative Disease at the University of Florida. Tansey and a number of other researchers offered a wide range of alternative strategies at the Alzheimer's Association International Conference in Denver last month. Here are three of the most promising: © 2021 npr

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27940 - Posted: 08.11.2021

Jason Ulrich and David M. Holtzman In 1907 German psychiatrist Alois Alzheimer published a case report of an unusual illness affecting the cerebral cortex. A 51-year-old woman living in an asylum in Frankfurt am Main exhibited symptoms that are all too familiar to the millions of families affected by what is now known as Alzheimer’s disease. There was memory loss, confusion and disorientation. After the patient died, Alzheimer examined her brain and made a few key observations. First, it was smaller than average, or atrophic, with a corresponding loss of neurons. Next, there were tangles of protein fibers within neurons and deposits of a different protein outside brain cells. For the next 100 years, these two pathological proteins—known as tau and amyloid—were the focus of research into the causes of the disease. But there was an additional, often forgotten clue that Alzheimer noted in the autopsy. Under the microscope lens, he saw clear changes in the structural makeup of certain nonneuronal cells. Called glia, they constitute roughly half of the brain’s cells. After being studied by only a small number of scientists since Alzheimer’s discovery, glia have now entered the spotlight. One type, called microglia, is the main kind of immune cell in the brain and may influence the progression of the disease in different ways during both early and later stages. Microglia might also explain the complex relation between amyloid and tau, the aberrant proteins that lead to neuron degeneration and memory loss. © 2021 Scientific American

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27927 - Posted: 07.28.2021

By Pam Belluck, Sheila Kaplan and Rebecca Robbins Two months before the Food and Drug Administration’s deadline to decide whether to approve Biogen’s controversial Alzheimer’s drug, aducanumab, a council of senior agency officials resoundingly agreed that there wasn’t enough evidence it worked. The council, a group of 15 officials who review complex issues, concluded that another clinical trial was necessary before approving the drug. Otherwise, one council member noted, approval could “result in millions of patients taking aducanumab without any indication of actually receiving any benefit, or worse, cause harm,” according to minutes of the meeting, obtained by The New York Times. “It is critical that the decision be made from a place of certainty,” the minutes said. The session, whose details have not been reported before, represented at least the third time that proponents of approving aducanumab in the F.D.A. had received a clear message that the evidence did not convincingly show the drug could slow cognitive decline. On June 7, the F.D.A. greenlighted the drug anyway — a decision that has been met with scathing rebuke from many Alzheimer’s experts and other scientists and calls for investigations into how the agency approved a treatment that has little evidence it helps patients. How and why the F.D.A. went ahead and approved the drug — an intravenous infusion, marketed as Aduhelm, that the company has since priced at $56,000 a year — has become the subject of intense scrutiny. Two congressional committees are investigating the approval and the price. Much is still unknown, but an examination by The Times has found that the process leading to approval took several unusual turns, including a decision for the F.D.A. to work far more closely with Biogen than is typical in a regulatory review. Allegations about the collaboration prompted the F.D.A. to conduct an internal inquiry after a consumer advocacy group called for an inspector general’s investigation, according to documents reviewed by The Times. The agency has not disclosed the inquiry. © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27919 - Posted: 07.21.2021

By Linda Searing Keeping your brain active later in life may delay by as much as five years the onset of Alzheimer’s disease, the most common type of dementia. Research published in the journal Neurology found that cognitively stimulating activities that involve seeking or processing information — such as reading books, magazines or newspapers, writing letters, playing card games, board games or checkers, and doing puzzles — seemed to add dementia-free time to older people’s lives. The research involved 1,903 people (average age was 80), none of whom had dementia at the start of the study and who were tracked and tested for up to 22 years. In that time, 457 participants developed Alzheimer’s. That occurred on average at age 94 for people who did the most brain-stimulating activities later in life, compared with developing Alzheimer’s at age 89 for those with the least amount of cognitive activity. Alzheimer’s, considered a degenerative brain disease, affects memory, thinking and behavior, with symptoms eventually becoming severe enough to interfere with once-routine daily tasks. Today, about 6.2 million Americans 65 and older have the disease, two-thirds of them women, according to the Alzheimer’s Association. That number is expected to reach nearly 13 million by 2050, unless ways are discovered to prevent, cure or slow the disease. The researchers found that neither education nor cognitive activity early in life were associated with the age at which a person developed Alzheimer’s. Rather, it’s what you do later in life that seems to make a difference. And, as the lead author of the story said, “It’s never too late to start doing the kinds of inexpensive, accessible activities” tracked in the study, “even in your 80s.”

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 27914 - Posted: 07.21.2021

By Rebecca Robbins The Food and Drug Administration on Friday called for a federal investigation of the process that led to the approval of a new drug for Alzheimer’s disease that has spurred sharp criticism from lawmakers and the medical community. In a letter to the Department of Health and Human Services’ independent Office of the Inspector General, the F.D.A.’s acting commissioner, Dr. Janet Woodcock, acknowledged the scrutiny the agency has faced about the approval process for the drug, which is known as Aduhelm and has a $56,000 annual price tag. She pointed to interactions between representatives from the drug’s developer, Biogen, and the agency, saying some “may have occurred outside of the formal correspondence process.” “To the extent these concerns could undermine the public’s confidence in F.D.A.’s decision, I believe it is critical that the events at issue be reviewed by an independent body,” Dr. Woodcock wrote. She noted that the review should look at whether any of the communication between the agency’s staff and Biogen’s representatives violated F.D.A. rules. Dana Conti, a spokesman for Biogen, said the company “will, of course, cooperate with any inquiry in connection with a possible review of the regulatory process.” It is unusual for the agency to request an investigation into its own staff’s decision-making process for an individual drug approval. The move is likely to intensify the controversy that has surrounded Aduhelm. The F.D.A. approved it a month ago, overriding the fierce objections of its own independent advisers and many other scientists, who said there was insufficient evidence to know whether the drug was effective. On Thursday, the F.D.A. moved to narrow its recommendation about who should receive the drug. After originally recommending it for all Alzheimer’s patients, the agency’s new guidelines say it should be prescribed only to people with mild cognitive problems. © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27900 - Posted: 07.10.2021

By Paula Span Dr. Kenneth Koncilja, a geriatrician at the Cleveland Clinic, saw the announcement from the Food and Drug Administration on June 7, on Twitter: The agency had approved Aduhelm (aducanumab), the first drug to treat Alzheimer’s disease to be approved in nearly 20 years. The calls from patients’ spouses and family members began within the hour, and have not stopped. “I was shocked at how fast the word spread — ‘Hey, is this something we can use? When can we get it?’” Dr. Koncilja recalled. “There’s a mix of excitement, anxiety and desperation.” His first call that morning came from Joan Morehouse, 78, who has been caring for her 71-year-old husband, James, in their home in North Perry, Ohio, since his Alzheimer’s diagnosis four years ago. She has watched him get lost on familiar drives and forget their grandchildren’s names. When her brother and her son both emailed her a news article about the F.D.A. action, she recalled, “I said, ‘Oh, my God, my prayers have been answered.’” It fell to Dr. Koncilja to explain the complexities: That Aduhelm is not yet widely available. That protocols determining which patients qualify have yet to be developed. That the clinical trial data was ambiguous and that the drug might bring no noticeable improvements in daily life. That its side effects include brain swelling and bleeding. And that its maker, Biogen, estimates the annual cost of monthly intravenous infusions at $56,000, plus expensive scans and tests. “It’s a more difficult question than I’ve ever had before,” Dr. Koncilja said. Patients ask him how their lives will change, “and I don’t know how to answer.” © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27894 - Posted: 07.08.2021

By Laurie McGinley Neurologist Matthew S. Schrag was surprised when he heard the Food and Drug Administration had approved a controversial Alzheimer’s drug. There was scant evidence the treatment worked, in his view. Even more concerning to Schrag: the FDA’s apparent embrace of a long-debated theory about Alzheimer’s disease, which afflicts more than 6 million Americans. The amyloid hypothesis, which has dominated the field for decades, holds that toxic clumps in the brain, called amyloid beta, are the main driver of the disease and that removing them will slow cognitive decline. But years of testing drugs that target amyloid had yielded a string of failures, and Schrag and others had been pushing the field to focus on other possible factors, including inflammation in the brain or damage to tiny blood vessels. Anti-amyloid efforts, they said, had squeezed out other approaches that might be more promising. “We had been hoping for a recalibration of the field,” said Schrag, a researcher at Vanderbilt University Medical Center. Now, he’s worried drug companies will double down on an approach he thinks is a dead end. The role of the sticky clumps of protein in the brain has long divided researchers and is at the forefront again amid the FDA’s recent clearance of the first drug to treat the disease in almost two decades. It is one of many controversies that has erupted since the FDA approved the drug, called Aduhelm, on June 7. Members of Congress have vowed to conduct hearings on the relationship between the FDA and the drug’s maker, Massachusetts-based Biogen. Analysts worry the drug’s list price — $56,000 a year per patient — could wreck Medicare’s finances. Doctors are scrambling to decide who should take it, complaining that the FDA-approved label, which includes all Alzheimer’s patients, is far too broad.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27890 - Posted: 07.06.2021

Asher Mullard The recent controversial approval of the Alzheimer’s drug aducanumab by the US Food and Drug Administration (FDA) has raised the possibility that the agency could now be more willing to fast-track treatments for a swathe of neurodegenerative diseases — illnesses that have so far thwarted drug developers. But an independent advisory panel fiercely questioned the new drug’s effectiveness, and researchers are divided on whether the potentially smoother approval path that aducanumab has paved will really deliver useful therapies for people with conditions such as amyotrophic lateral sclerosis (ALS), Huntington’s disease and Parkinson’s disease. Drug developers including Amgen, in Thousand Oaks, California, and Pfizer, based in New York City, have shut down their neuroscience programmes in recent years because of the difficulties of finding successful treatments for brain diseases. So Eric Siemers, a drug-development consultant in Zionsville, Indiana, thinks aducanumab’s approval could bring renewed investment and innovation. On the basis of conversations he has had with investors and clients, he says the tide is already turning. “There’s a lot more interest now in research in neurodegenerative diseases,” says Siemers, who is also chief medical officer of the Alzheimer’s disease company Acumen Pharmaceuticals in Charlottesville, Virginia. Acumen filed paperwork for an initial public offering just days after the approval of aducanumab. Some advocacy groups are also encouraged, on behalf of desperate patients with few or no therapeutic options. “If the FDA can find a way to be flexible for Alzheimer’s, maybe they can find a way to be flexible for ALS,” says Neil Thakur, chief mission officer at the ALS Association. © 2021 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27884 - Posted: 07.03.2021

By Pam Belluck and Rebecca Robbins In a powerful statement of disagreement with the Food and Drug Administration’s approval of Biogen’s controversial Alzheimer’s drug, three scientists have resigned from the independent committee that advised the agency on the treatment. “This might be the worst approval decision that the F.D.A. has made that I can remember,” said Dr. Aaron Kesselheim, a professor of medicine at Harvard Medical School and Brigham and Women’s Hospital, who submitted his resignation Thursday after six years on the committee. He said the agency’s approval of the drug, aducanumab, which is being marketed as Aduhelm, a monthly intravenous infusion that Biogen has priced at $56,000 per year, was wrong “because of so many different factors, starting from the fact that there’s no good evidence that the drug works.” Two other members of the committee resigned earlier this week, expressing dismay at the approval of the drug despite the committee’s overwhelming rejection of it after reviewing clinical trial data in November. The committee had found that the evidence did not convincingly show that Aduhelm could slow cognitive decline in people in the early stages of the disease — and that the drug could cause potentially serious side effects of brain swelling and brain bleeding. None of the 11 members of the committee considered the drug ready for approval: Ten voted against and one was uncertain. “Approval of a drug that is not effective has serious potential to impair future research into new treatments that may be effective,” said Dr. Joel Perlmutter, a neurologist at Washington University School of Medicine in St. Louis, who was the first to resign from the committee. © 2021 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27849 - Posted: 06.11.2021

By Laurie McGinley The Food and Drug Administration on Monday approved the first Alzheimer’s treatment intended to slow cognitive decline, a move hailed by patients and advocates but sharply criticized by others who argued there was not sufficient evidence that the drug works. The medication, called aducanumab, is the first drug cleared for Alzheimer’s that is designed to alter the course of the disease by slowing the deterioration of brain function — not just to ease symptoms. No Alzheimer’s treatment has been approved since 2003, reflecting the extraordinarily high failure rate of drugs developed for the illness. But in an explicit acknowledgment of the uncertainties about the effectiveness of the drug, the FDA did not grant the medication full approval. Instead, the agency cleared the drug — its brand name will be Aduhelm — based on its ability to reduce clumps of amyloid beta in the brain, a hallmark of the disease. It ordered the drug’s maker, the biotech giant Biogen, to conduct a post-approval study confirming the medicine actually slows cognitive deterioration. If the medication does not provide such a clinical benefit, the FDA’s approval could be withdrawn. Patrizia Cavazzoni, director of the FDA’s Center for Drug Evaluation and Research, said officials believe it is “reasonably likely” that the reduction in amyloid clumps will confer “important benefits to patients.” Monday’s FDA decision was the most contentious in years and followed prolonged debate among researchers, doctors, patients and advocates about whether the medication works — a consequence of the drug’s complicated history. One of the biggest points of disagreement is whether a reduction in amyloid beta, a sticky compound that many scientists believe damages communication between brain cells and eventually kills them, results in a slowdown in cognitive decline. © 1996-2021 The Washington Post

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27846 - Posted: 06.08.2021

Laurie McGinley When Phil Gutis was diagnosed with early-stage Alzheimer’s disease at 54, he immediately enrolled in a clinical trial for an experimental drug but had little hope of being helped. Over time, though, he started feeling better, his brain less cloudy. “There was just a fogginess I remember having a couple of years ago that I don’t really feel I have now,” said Gutis, who has received monthly infusions of a medication called aducanumab for five years, except for a short interruption. Now, he is hoping others with the disease will have a chance to try the drug. But he is worried that the Food and Drug Administration, which is weighing whether to approve the drug, will reject it, derailing the medication and jeopardizing his ability to get the treatment. “Would my world become fuzzy again?” said Gutis, who lives in New Hope, Pa., with his husband and is a former reporter. “I don’t want to go backward.” By June 7, the FDA is expected to make one of its most important decisions in years: whether to approve the drug for mild cognitive impairment or early-stage dementia caused by Alzheimer’s. It would be the first treatment ever sold to slow the deterioration in brain function caused by the disease, not just to ease symptoms. And it would be the first new Alzheimer’s treatment since 2003. The medication is a monoclonal antibody, a protein made in the laboratory that can bind to substances — in this case, clumps of amyloid beta, a sticky plaque compound that many scientists believe damages communication between brain cells and eventually kills them. The treatment is designed to trigger an immune response that removes the plaques.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27839 - Posted: 06.02.2021

Amanda Heidt A damaged drainage system in the brain might be behind the spotty performance of some Alzheimer’s therapies, according to a study published April 28 in Nature. Mice modeling the neurodegenerative disorder that received plaque-busting antibodies along with a treatment to stimulate the growth of lymphatic vessels in the brain saw many of their symptoms reversed. Mice with damaged lymphatics, on the other hand, didn’t respond as well to the antibodies. This suggests that dysfunctional lymphatics might hinder the performance of antibody-based immunotherapy, an approach that has had mixed results in clinical trials among Alzheimer’s patients. “Whenever a paper provides us with a novel way to look at Alzheimer’s, such as this one does . . . it opens up a world of possibilities,” says Gabrielle Britton, a neuroscientist at the Instituto de Investigaciones Científicas y Servicios de Alta Tecnología in Panama who was not involved in the research. “The methods are sound, and [the fact] that they use several different approaches that converge on the same findings suggests a very strong paper.” The buildup of amyloid-β plaques in the brain is a hallmark of the disease, and one of the most promising immunotherapies has been a monoclonal antibody called aducanumab that breaks them up. But two clinical trials were discontinued after they yielded contradictory results, and scientists have been working ever since to figure out why as the companies continue to move forward with new trials of the therapy. The working hypothesis, Britton tells The Scientist, is that the discrepancy stems from some unexplained variation among participants. © 1986–2021 The Scientist.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27835 - Posted: 05.29.2021