A few years ago, Lori Weiss, a high school math and engineering teacher, noticed it was taking her longer to do her lesson plans and grading. She also repeatedly needed to ask for help using spreadsheets she\u2019d once mastered and she struggled to answer her students\u2019 questions.<\/p>\n
The symptoms were all too familiar to Weiss. Not only had she cared for her grandfather with Alzheimer\u2019s disease when she was a teenager, she\u2019d also watched her mother slowly lose her memory to the disease for nearly two decades. She had aunts, uncles, and a cousin as well who were diagnosed with the neurological disorder, which gradually steals a person\u2019s memory and cognitive abilities.<\/p>\n
\u201cIt\u2019s rampant in my family,\u201d Weiss says.<\/p>\n
Weiss decided to speak with her primary care physician, who referred her to a neurologist for testing. In 2020, at the age of 62, Weiss was diagnosed with mild cognitive impairment. Two years after that, a PET scan revealed amyloid plaques, a buildup of toxic proteins in the brain that disrupt neural function and are a hallmark of Alzheimer\u2019s disease.<\/p>\n
Soon, Weiss began to lose her sense of direction, which prompted fears that she might be forced into a full-time care facility at a young age.<\/p>\n
\u201cLosing my freedom was just more than I could handle,\u201d she says. Around that time, a friend saw a TV advertisement for a clinical trial for a drug that would attempt to slow progression of the disease using manmade monoclonal antibodies to attack and remove the amyloid plaques in the brain.<\/p>\n
\u201cI don\u2019t even think that I thought twice about\u201d enrolling in the trial, says Weiss, who has been receiving monthly infusions of the drug, called donanemab<\/a>, near her home in Portland, Oregon, for about a year. \u201cI just said, \u2018Yeah, sign me up!\u2019\u201d<\/p>\n Although donanemab is not approved by the Food and Drug Administration (FDA), it uses a similar approach to the drug lecanemab, which received accelerated FDA approval on Jan. 6, and which showed biological and clinical benefits for patients in trials. In November, drugmaker Eli Lilly and Company announced promising results<\/a> for donanemab, but last week, the FDA denied<\/u><\/a> the company\u2019s request for accelerated approval, saying it needed more data for participants receiving the drug for at least 12 months.<\/p>\n Nonetheless, this recent progress has given people like Weiss hope that previous generations have not had.<\/p>\n \u201cAlzheimer\u2019s research is getting to a place where cancer research was maybe 30, 40 years ago.\u201d<\/p>\n Anton Porsteinsson, MD, University of Rochester Medical Center in New York<\/p>\n<\/blockquote>\n Participating in the clinical trial \u201chas had a huge impact,\u201d Weiss says. \u201cIt\u2019s given me the drive to do things while I can; it\u2019s given me the desire to talk to more people about getting treatment, getting diagnosed early, and getting in drug trials.\u201d<\/p>\n Weiss says that since she\u2019s begun taking donanemab, she\u2019s regained her sense of direction and has not noticed significant cognitive decline. For her, even the hope that the trial has given her has made all the difference.<\/p>\n \u201cFor my husband and I, it\u2019s totally changed our lives. Instead of living in fear \u2026 we treat each day like it\u2019s Valentine\u2019s Day,\u201d Weiss says. Getting diagnosed early has \u201cgiven me so much more life. [I thought] getting the disease was a death sentence for me, but I\u2019m taking a water painting class, I\u2019m in a walking group and a music group. I thrive on my relationships with my Alzheimer\u2019s friends and other friends, and I\u2019m connected with my family. I feel like I\u2019m living my life. It\u2019s so much better than I imagined.\u201d<\/p>\n And while Alzheimer\u2019s researchers are careful to emphasize that they are still a long way from a cure, many say the hope is not a false one. The field has had several breakthroughs in recent years, from identifying easier and cheaper ways to diagnose the disease early to better understanding how individuals with the disease might require a variety of interventions.<\/p>\n \u201cAlzheimer\u2019s research is getting to a place where cancer research was maybe 30, 40 years ago,\u201d says Anton Porsteinsson, MD, director of the Alzheimer\u2019s Disease Care, Research and Education Program at the University of Rochester Medical Center in New York. \u201cI think we\u2019re at a point where we\u2019re going to see a logarithmic increase in discovery.\u201d<\/p>\n Alzheimer\u2019s disease, which was discovered in 1906 and is now the seventh leading cause of death in the United States, has long boggled the scientific community. Though research over the decades<\/a> has identified characteristics of the disease \u2014 such as the presence of amyloid plaques between neurons and the buildup, known as tangles, of another toxic protein, tau, inside neurons \u2014 questions remain about what causes the disease and how best to treat it in a clinically meaningful way.<\/p>\n \u201cIt\u2019s a complex disease. It\u2019s not just a single molecule that\u2019s gone awry. It\u2019s not an infection that has a viral particle,\u201d says Ronald C. Petersen, MD, PhD, director of the Mayo Clinic Alzheimer\u2019s Disease Research Center in Rochester, Minnesota. \u201cWe\u2019ve defined it by the presence of amyloid, neuritic plaques<\/a>, and neurofibrillary tangles<\/a>, but that\u2019s just the tip of the iceberg.\u201d<\/p>\n Many researchers now believe that the precursors to developing Alzheimer\u2019s begin to accumulate in the brain 10 or more years before symptoms begin to show.<\/p>\n Alzheimer\u2019s disease progression affects the brain much like a forest fire, with many factors affecting how it spreads, says Rudolph E. Tanzi, PhD, director of the Genetics and Aging Research Unit at Massachusetts General Hospital in Boston.<\/p>\n Amyloid plaques and tau tangles can build up over years, at some point triggering an inflammatory response that can quickly destroy brain cells. These conditions can be influenced by a range of factors, from genetic predisposition to environmental exposures to lifestyle, he explains.<\/p>\n That\u2019s why the solution to treating \u2014 or ideally, preventing \u2014 Alzheimer\u2019s disease will likely require a combination of interventions, Petersen says.<\/p>\n One important part of the puzzle \u2014 and a part that has been the focus of much pharmaceutical development \u2014 is targeting the amyloid plaques.<\/p>\n This approach has been controversial. In 2021, the FDA granted accelerated approval to the anti-amyloid drug aducanumab, sold as Aduhelm, despite objections from an advisory committee and outcry from the scientific community that the lack of clinical benefit made the drug\u2019s high cost, initially set at $56,000 a year and later reduced to $28,000 a year, unjustifiable. A Congressional investigation<\/a> found numerous flaws and irregularities in the process the FDA used when approving the drug.<\/p>\n Lecanemab, on the other hand, has been met with more optimism in the Alzheimer\u2019s research community because its clinical trials demonstrated an actual clinical benefit to patients early in the disease progression.<\/p>\n \u201cThe field is feeling that, finally, we have a drug that didn\u2019t have the controversy aducanumab had,\u201d Petersen says. \u201cIt looks like it does what it\u2019s supposed to do biologically [and] this looks like it could be meaningful for patients.\u201d<\/p>\n In clinical trials, lecanemab showed<\/a> a modest but tangible decrease in cognitive decline (of 27%) over 18 months in Alzheimer\u2019s patients who were early in the disease\u2019s progression, compared with patients who were given a placebo. Though it\u2019s far from a cure, experts say it could give patients months of retaining memory and cognition that they might otherwise lose, a prospect that could be meaningful for patients and their families who have no other options.<\/p>\n But this drug, too, has stirred some controversy because of its high price tag and potentially deadly side effects, including swelling and bleeding in the brain. The pharmaceutical company Eisai has priced lecanemab, sold as Leqembi, at $26,000 a year, and the Centers for Medicare and Medicaid Services has yet to decide<\/a> if it will cover the drug.<\/p>\n \u201cIt\u2019s very expensive,\u201d Tanzi says, explaining that patients who take the drug will also need several MRIs to check for brain bleeds on top of the cost of the infusions. \u201cThere is a health care disparity this could create; those who want to remove amyloid can pay out of pocket [but] the average person can\u2019t afford that. The wealthy can protect themselves.\u201d<\/p>\n The high costs of treatment could also exacerbate existing racial disparities when it comes to Alzheimer\u2019s outcomes. Although Black Americans are about twice as likely<\/a> as White Americans to have Alzheimer\u2019s, and Hispanics are about 1.5 times as likely<\/a> to have it, White people make up a disproportionate majority of clinical trial participants and non-White people report greater barriers to diagnosis and access to care, according to the Alzheimer\u2019s Association<\/a>.<\/p>\n \u201cMost of the research operations are either based at large academic institutions or private professional research sites,\u201d Porsteinsson explains about pharmaceutical company trials. \u201cThe temptation [for researchers] is to go where the treatment is \u2018easiest\u2019; where you\u2019ve recruited before.\u201d<\/p>\n In its clinical trial recruitment for lecanemab, the University of Rochester succeeded in increasing the representation of Hispanic participants, but struggled to include a representative number of Black patients.<\/p>\n \u201cWe can\u2019t just wait until the brain deteriorates.\u201d<\/p>\n Rudolph E. Tanzi, PhD, Massachusetts General Hospital in Boston<\/p>\n<\/blockquote>\n \u201cIf we want to go after historically underrepresented groups in research, first we need to recognize they\u2019re underrepresented for a reason,\u201d Porsteinsson says. \u201cThere might have been a poor experience with researchers coming [into their community], doing a study [the researchers] needed, and then basically leaving. There isn\u2019t an ongoing commitment.\u201d<\/p>\n He says that if Alzheimer\u2019s treatments are going to be meaningful to all people affected by the disease, it will take a concerted effort to include more diversity in clinical trial participants, not only in race and ethnicity, but in health status and inclusion of people with comorbidities. Often, trials tend to select for the healthiest patients possible, he explains.<\/p>\n \u201c[We must] secure making our research more representative of the American population,\u201d Porsteinsson says. \u201cIt\u2019s going to take an investment in infrastructure and it\u2019s going to take an investment of time.\u201d<\/p>\n Alzheimer\u2019s disease already affects more than six million people living in the United States, and that number is projected to grow to 13 million by 2050. It\u2019s also an incredibly financially costly disease, with an economic impact of $321 billion in health care costs in 2022, expected to rise to $1 trillion by 2050, according to the Alzheimer\u2019s Association.<\/a> That prospect prompted the U.S. Congress to approve an additional $226 million to the National Institutes of Health for Alzheimer\u2019s research in December, bringing the annual federal funding outlay to more than $3.7 billion<\/a>.<\/p>\n Experts say it is not in vain. Research efforts, particularly those at teaching hospitals, have helped unlock mysteries about the genetic underpinnings of the disease, ways to identify biomarkers in the blood that can more easily diagnose the disease in its earliest states, and complex treatment approaches that use lifestyle interventions and a combination of drug therapies.<\/p>\n Tanzi believes that the future of Alzheimer\u2019s treatment and prevention will be similar to current management of heart disease and diabetes. It could mean more regular screenings and early interventions, such as taking anti-amyloid drugs and incorporating lifestyle and diet changes before the disease gets out of control. And for those already diagnosed, it means using a combination of therapies that target different aspects of the disease, such as neuroinflammation and plaque buildup.<\/p>\n \u201cWe can\u2019t just wait until the brain deteriorates,\u201d he says.<\/p>\n With the current momentum, Porsteinsson hopes that young and aspiring physician-scientists will be inspired to join the field and continue the research for generations to come.<\/p>\n \u201cWhat many medical students and young doctors have historically been hesitant about is that dementia is very nebulous, there is a lot of gray there. \u2026 They felt things were pretty bleak, too uncertain, and there was too little you could offer,\u201d he says. \u201cNow, I think we are at the dawn of a very different era.\u201d<\/p>\n<\/p><\/div>\n\n A few years ago, Lori Weiss, a high school math and engineering teacher, noticed it was taking her longer to do her lesson plans and grading. She also repeatedly needed to ask for help using spreadsheets she\u2019d once mastered and she struggled to answer her students\u2019 questions. The symptoms were all too familiar to Weiss. …<\/p>\n","protected":false},"author":1,"featured_media":48407,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":[],"categories":[161],"tags":[],"_links":{"self":[{"href":"http:\/\/www.brandon.ddtest.info\/multisite-test\/wp-json\/wp\/v2\/posts\/48406"}],"collection":[{"href":"http:\/\/www.brandon.ddtest.info\/multisite-test\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"http:\/\/www.brandon.ddtest.info\/multisite-test\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"http:\/\/www.brandon.ddtest.info\/multisite-test\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"http:\/\/www.brandon.ddtest.info\/multisite-test\/wp-json\/wp\/v2\/comments?post=48406"}],"version-history":[{"count":0,"href":"http:\/\/www.brandon.ddtest.info\/multisite-test\/wp-json\/wp\/v2\/posts\/48406\/revisions"}],"wp:featuredmedia":[{"embeddable":true,"href":"http:\/\/www.brandon.ddtest.info\/multisite-test\/wp-json\/wp\/v2\/media\/48407"}],"wp:attachment":[{"href":"http:\/\/www.brandon.ddtest.info\/multisite-test\/wp-json\/wp\/v2\/media?parent=48406"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"http:\/\/www.brandon.ddtest.info\/multisite-test\/wp-json\/wp\/v2\/categories?post=48406"},{"taxonomy":"post_tag","embeddable":true,"href":"http:\/\/www.brandon.ddtest.info\/multisite-test\/wp-json\/wp\/v2\/tags?post=48406"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}\n
Fighting a complex disease<\/h2>\n
Equity starting in research<\/h2>\n
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A stage set for discovery<\/h2>\n
Source link <\/a><\/p>\n","protected":false},"excerpt":{"rendered":"