Tau, Amyloid Detection Could Improve Diagnostic Capabilities
Researchers from Aberdeen have identified changes in the brains of those suffering early signs of Alzheimer’s disease.
A University of Aberdeen study confirmed for the first time that two proteins, assumed to contribute to the disease process, are both present at very early stages of Alzheimer’s disease. Both are present in an area of the brain that is involved in memory formation and information processing–the hippocampus.
The Alzheimer’s Research UK funded the research, which will have implications for the development of new drugs, but may also provide important information for diagnosis of the disease.
The team, led by Dr Koss and Professor Bettina Platt, used human brain samples provided by the Brains for Dementia Research platform to investigate changes in the brain at different stages of the disease. The researchers developed novel ways to study two proteins (tau and amyloid), both associated with Alzheimer’s disease, and determined how each one contributed to the onset, progression and symptoms of the disease.
“The entire research community is in agreement that it’s important to diagnose Alzheimer’s disease early,” said Dr. Koss. “Our findings will go some way to help achieve this. These early-stage changes in the brains of people with Alzheimer’s disease highlight key biochemical processes that may not only enable improved diagnostic procedures but may also inform drug development.”
Early diagnosis also can help protect caregivers and others from the transmission of Alzheimer’s disease. It’s likely spreading through the bodily fluids of victims. Items exposed, including drinking glasses, utensils are impossible to sterilize.
“There is now real evidence of the potential transmissibility of Alzheimer’s,” says Thomas Wiesniewski M.D. a prion and Alzheimer’s researcher at New York University School of Medicine. “In fact, this ability to transmit an abnormal conformation is probably a universal property of amyloid-forming proteins.”
A new drug that can treat Alzheimer’s disease is finally on the horizon after scientists proved they can clear the sticky plaques from the brain which cause dementia and halt mental decline. Hailed as the best news in dementia research for 25 years, the breakthrough is said to be a potential game changer for people with Alzheimer’s disease.
Scientists said they were amazed to find that patients treated with the highest dose of the antibody drug aducanumab experienced an almost complete clearance of the amyloid plaques that prevent brain cells communicating, leading to irreversible memory loss and cognitive decline.
Crucially they also found that after six months of the treatment, patients stopped deteriorating compared with those taking a placebo, suggesting that their dementia had been halted.
If shown to be effective in larger trials, the first drug to treat dementia could be available in just a few years.
“The results of this clinical study make us optimistic that we can potentially make a great step forward in treating Alzheimer’s disease,” said Prof Roger Nitsch, at the Institute for Regenerative Medicine at the University of Zurich. “In the high dose group the amyloid has almost completely disappeared. The effect size of this drug is unprecedented. Despite it being a small sample, there appeared to be a slowing of cognitive decline and functional decline. The group with a high degree of amyloid removal were basically stable. If we could reproduce this, it would be terrific.”
Dr. Alfred Sandrock, from the Massachusetts-based biotech company Biogen, which is hoping to bring the drug to market, said: “This is the best news that we have had in 25 years and it brings new hope to patients with this disease.”
There are currently 850,000 people living with dementia in Britain, a figure that is expected to rise to one million by 2025 and two million by 2050. There are more than 50 million people battling the disease today. Despite a high death rate, the population of those afflicted with the disease is expected to soar over the next decade.
The most common kind of neurodegenerative disease is Alzheimer’s disease, but scientists have been unable to reach consensus about the cause of the condition, and despite more than 400 drug trials, nothing has been effective. Current treatments can reduce symptoms to some extent but doctors have nothing that can halt or slow progression of the disease.
Aducanumab is a treatment made up of antibodies, tiny y-shaped proteins that latch on to dangerous substances in the body, acting like flags, showing the immune system what to clear away.
Scientists tested various human immune cells with amyloid in a laboratory until they found one which produced an antibody that broke up the plaques. They then cloned it in large numbers for the new therapy, which is given intravenously just once a month.
In the trial, which was reported in the journal Nature, scientists tested varying levels of the drug over a year, as well as giving one group a placebo. They found that more amyloid was removed as the dose increased. Brain scans of those given the highest dose shown virtually no amyloid left at all.
The drug is likely to be most effective for patients in the very earliest stages of Alzheimer’s disease, or those who have not yet begun to show symptoms. Several universities are working on early blood tests for dementia which could pick the disease up a decade or more before the first physical signs appear.
Dementia experts and charities said that the breakthrough offered real hope for the future treatment of Alzheimer’s disease. There are now two large phase-three clinical studies taking place to further evaluate safety and efficacy on a total of 2,700 patients with early-stage Alzheimer’s disease and researchers are currently recruiting British participants.
“These results provide tantalizing evidence that a new class of drug to treat the disease may be on the horizon,” said Dr David Reynolds, chief scientific officer at Alzheimer’s Research UK.
“The findings suggest that aducanumab may slow memory and thinking decline in people with early Alzheimer’s and, although the analysis is only exploratory in this early trial, it paints a positive picture for ongoing trials with the drug.”
Encouragingly, this treatment also appeared to slow memory decline, demonstrating that amyloid formation is a direct or indirect cause of memory loss. This has been suspected for some time, but has never been proven in humans.
“These findings could be a game changer if the effects on memory decline can be confirmed in more extensive follow-on studies.”
The Alzheimer’s Society said the “most compelling” evidence from the trial was the fact that more amyloid was cleared when patients took higher doses of the drug.
Dr James Pickett, head of research at the charity, said: “No existing treatments for Alzheimer’s directly interfere with the disease process, and so a drug that actually slows the progress of the disease by clearing amyloid would be a significant step.
“While there were hints that it might have an effect on the symptoms of the disease, we need to see the results from further, larger research trials to understand whether this is the case. These larger trials are now under way, including in the UK, and due to finish in 2020.”
Prof Richard Morris, Professor of Neuroscience at the University of Edinburgh, said: “We cannot yet say we have a cure for Alzheimer’s, as this is only a first step … but the importance of this first step cannot be understated.
“Let’s keep our fingers crossed for success in the next steps.”
Editor’s Note: Congratulations to Julianne Moore. Her performance in Still Alice just earned her an Oscar for Best Actress at the 2015 Academy Awards. The movie and her role could change the face of Alzheimer’s disease forever. Please join us as we advocate for the truth and reforms that can help contain many areas of mismanagement that are contributing to the reckless spread of the disease.
Still Alice Explores Alzheimer’s Disease
Julianne Moore is on a roll. Her latest film Still Alice premiered in Toronto in September with little hype and emerged as one of the biggest hits of the festival thanks to her powerful performance. The role earned her a Golden Globe Award and now an Oscar for Best Actress.
Moore plays a Columbia professor diagnosed with early onset Alzheimer’s disease in the new movie, which is based on Lisa Genova’s 2007 novel by the same name. The movie profiles a renowned linguistics professor struggling with the symptoms of Alzheimer’s disease–a real-life scenario playing itself out millions of times around the world every year.
Moore has already netted multiple awards for Still Alice including Best Actress at the Gotham and Hollywood Film Awards, the Golden Globes and the Academy Awards for her work in Still Alice.
Moore spoke with Indiewire a few months ago about the work that went into her portrayal of the disease and about working with co-star Kristen Stewart, who plays her daughter in the film. The interview follows below:
I caught this film back at the Toronto International Film Festival, and it totally floored me. I don’t think I’ve cried that much in my entire life, let alone in two hours.
“Oh, thanks for that. That’s one of the things about this movie is how touched people are by it, and I do feel like it’s genuine. It’s not forced in terms of peoples’ reactions. It’s not like the movie is trying to make you cry, it’s just people really connect to it. Which is nice,” said Moore.
I’m sure you’ve encountered people who know or have known people with Alzheimer’s disease. What’s that been like to hear real stories and how the film touched those people?
“I got a note from a friend of mine’s wife saying she’d had a family member with Alzheimer’s too, and she suddenly felt close to her. And felt like she understood something about the experience. For me, all the research that I did — people have this notion that with Alzheimer’s, somehow the “self” disappears. They’re like, “That’s not the person I knew,” and “Somehow the self has gone away, somehow they’re not present anymore.” But in all my research and dealings with people, I’ve found the opposite. The people, they were changed, certainly, but their personality somehow remained. That was really, tremendously moving to me.”
Do you know anyone personally who suffered with Alzheimer’s in your life?
I don’t know anyone impacted by Alzheimer’s disease, yet. I’m really, really very lucky — that hasn’t been something that’s affected my family.
One of the film’s two directors, Richard [Glatzer] has ALS. And I’m curious what that lent to your process — to work with somebody who’s going through that struggle every day, who went through that struggle on set with you.
How did you approach portraying the scope of the disease in such a compressed amount of time?
It was completely dependent on the amount of research I did. I couldn’t have done this movie — there was no way I was going to be able to figure out what to do with this movie — unless I’d had the proper amount of time to do research. Thankfully, I worked on it for about four months. I started research while I was doing [“The Hunger Games”] “Mockingjay.” I started watching every doc I could get my hands on. Every film, every documentary, every interview. So, there, once I got back to the city, I started with the head of the national Alzheimer’s Association, Elizabeth Gelfand Stearns, to talk about her experiences. And then they set up these Skype calls with three women across the country — all who had been diagnosed with early onset, or what they call “younger onset,” which means before the age of 65. And the youngest person I spoke to was a woman named Sandy Oltz, who was diagnosed at 45, which was was astonishing. From there, I went to Mount Sinai and spoke to Dr. Mary Sano, who is head the Alzheimer’s research there — and some of the other researches and clinicians. And I had a neuropsychiatrist administer the cognitive tests, which are extensive and shockingly difficult [laughs]. Then I went to the New York Alzheimer’s Association and met with the support group there, and spoke to the women in the groups about their feelings and experiences. And then from there, went to a long-term care facility and met people who were really pretty declined. So it was four months.
How did you map out Alice’s gradual loss of memory? It’s so expertly modulated in the film, but that must have posed such a huge challenge for you.
Thank you, it did! As I was saying before, if I hadn’t done the research — not that I understand what it’s like to have Alzheimer’s, anything I had any question about, I asked. I wouldn’t do any behavior I hadn’t witnessed. There would be times Rich, and Wash and I were talking about something. I remember there was something in the movie where I’d be looking and something and think, “I don’t understand that behavior. I don’t know what I’m looking at.” And we came up with the thing about tying her shoe, working really hard to tie her shoe. And I did see people working very hard to complete actions that seemed to be simple actions. So, it was always about that. Trying to be really specific, and just think about what I wanted to do in each scene. I went to the script a gazillion times, so that when we were shooting it, there was no question about what I would be doing. So I just kind of kept in my head that way.
Sara Schupp hasn’t seen her mother in a while. She hopes to someday soon, but for now, it’s the difference between crying on the way to work every day for a week and functioning like a normal 34-year-old. Her mother, Bernadette LandiVittori, was diagnosed with early onset Alzheimer’s disease in 2001. The family decided to move her to the Morton Terrace Care Center in January 2013. Schupp visited many times at first, but a little more than a year later, it’s been too much for her to take.
Her mother weighs 100 pounds. She doesn’t know who her daughter is, even when they are in the same room. Thirty-four years of Schupp’s life have vanished from her mother’s memory.
“I want to be that courageous person. I want to be that person who goes to see her, and I have a lot of guilt because of it,” Schupp said. “I cannot physically bring myself to drive there right now. I’m hoping that will change, and I’ll be that strong person. But right now, I can’t do it.”
Schupp’s experience with the disease was unusual in that her mother was diagnosed at age 54, when her daughter was just a senior in college. However, according to a report released in March by the Alzheimer’s Association national office, her experience may become more common as increasing numbers of seniors are being diagnosed with Alzheimer’s, and there is currently still no cure.
Alzheimer’s is the sixth-deadliest disease in the United States, but even that’s a naive statistic, said central Illinois Alzheimer’s Association Executive Director Nikki Vulgaris-Rodriguez. It’s more likely the third-deadliest disease nationally when causes of death, like pneumonia, are viewed as the results of Alzheimer’s degenerative nature, she said.
For women age 65 and older, the numbers are more alarming as two-thirds of the cases are women. One in six women in their 60s is likely to be diagnosed with Alzheimer’s, according to the report.
The financial toll of the disease is also burdening the nation, the report states. It estimates that Alzheimer’s will cost Medicare and Medicaid a combined $150 billion in 2014 for the 5 million Americans living with the disease. The Association predicts that once the Baby Boomer generation reaches the age of greatest risk for dementia in the coming decade, an astronomical rise in these numbers will occur.
Alzheimer’s advocacy groups say they want to impart on the public and politicians that the disease costs billions of dollars and is underfunded by the U.S. government when compared to HIV/AIDS, cancer and heart disease.
“We have a very active advocacy program for both the federal and state levels,” Vulgaris-Rodriguez said. “We’re constantly out there with our volunteer ambassadors to help be a voice for our population in the Alzheimer’s community.”
Schupp recently stepped into that volunteer ambassador role for the 18th Congressional District in Illinois. She has met with aides of U.S. Rep. Aaron Schock and hopes to meet Schock in person this summer to discuss the increasing need for more funding and better research of Alzheimer’s.
Becoming an advocate was difficult for Schupp after watching her mother lose herself to the disease over the course of nearly 13 years. Fresh off of graduation from Southern Illinois University when her parents informed her of her mother’s diagnosis, Schupp experienced denial and took the approach that everything was normal.
And her caregiving role was minor as her father, Lamonte LandiVittori, assumed daily care for his wife. Schupp was allowed to devote herself to her career and starting her own family while her father cared for her mother.
For three weeks in 2010, Schupp stepped into her father’s shoes while he was recovering from heart surgery, taking both parents into her home. She couldn’t believe the stress, strain and emotion of those three weeks.
“I don’t know how my dad did it for so long,” Schupp said. “I think it’s taken an extreme physical and emotional toll on him.”
Lamonte LandiVittori now has stage four colon cancer. Schupp can’t prove it, but she believes the stress of the past decade contributed to his condition.
The struggle with Alzheimer’s greatly affects caregivers, said Vulgaris-Rodriguez, who recommends anyone taking on that role to take advantage of the support groups offered by the local Alzheimer’s Association.
“It does happen,” Vulgaris-Rodriguez said. “Our support programs give the caregiver an understanding of the stress level so they can manage their own stress.”
Looking back from what is now the final chapter in her mother’s struggle with Alzheimer’s, Schupp urges those dealing with the disease to seek out those support groups — something she did not do. Those groups might have told her what she knows now 13 years later.
“In that first year, spend as much quality time with that person as possible,” Schupp said.
Daiichi Sankyo Co. Ltd. and University of California, San Francisco (UCSF) announced that they have established a drug discovery collaboration focused on developing novel therapeutics and molecular diagnostics for multiple neurodegenerative diseases.
Under the terms of the agreement, Daiichi Sankyo will provide its compound library to the UCSF Institute for Neurodegenerative Diseases (IND), and both parties will perform high-throughput compound screening and optimization together. The project will bring together the drug development capabilities of Daiichi Sankyo with the expertise of world-renowned neuroscientists at UCSF, in a collaborative effort to create multiple drug discovery programs in debilitating disease areas such as Alzheimer’s, Parkinson’s, Creutzfeldt-Jakob disease and fronto-temporal dementias– all conditions for which there currently are no effective therapeutics available.
Daiichi Sankyo will provide research funding and milestone payments and royalties for successful clinical progression and commercialization of new products. Daiichi Sankyo will receive the option to enter into an exclusive license agreement to develop and commercialize promising compounds.
“This is a golden opportunity. These diseases require a big-picture approach, and that’s what Daiichi Sankyo is taking,” said Stanley Prusiner, who received the 1997 Nobel Prize in Physiology or Medicine for his discovery of prions, a new biological principle of infection.
Prions are alternatively folded proteins that undergo replication– some prions perform critical cellular functions but others cause neurodegenerative diseases. Initially, Prusiner studied prions causing “mad cow” disease and Creutzfeldt-Jakob disease (CJD), but recently, he and many others have focused their work on other replicating, misfolded proteins— which Prusiner and others argue are prions—that are thought to cause the more common neurodegenerative disorders, including Alzheimer’s and Parkinson’s diseases.
“Alzheimer’s alone kills as many people every year as cancer does, but it only receives one-tenth of the funding that we dedicate to cancer research,” Prusiner said. “This collaboration won’t fill that funding gap, but it will offer the tremendous value of Daiichi Sankyo’s scientific expertise to make progress on these diseases.”
“Daiichi Sankyo is committed to identifying potential new therapies to help fuel our passion to find medicines for the patients who need them. Using the compound screening technology at UCSF, along with their expertise in prion research, will give us an opportunity to explore the potential. I am excited about this collaboration and look forward to seeing results of this partnership.” said Glenn Gormley, senior executive officer and global head of research and development, Daiichi Sankyo Co. Ltd.
Founded in 1999, the IND is one of the top academic laboratories focused on discovering causes and developing cures for neurodegenerative diseases. As the leader of the IND, which is based at UCSF and includes neuroscience research at several other UC campuses, Prusiner is committed to creating therapeutics and diagnostics that will halt neuronal diseases with his extraordinary experiences in prion research.
Daiichi Sankyo will send scientists from Venture Science Laboratories (VSL) to work on site at the UCSF institute and will jointly establish the drug discovery programs. VSL was established internally, as a biotech-like organization, in Daiichi Sankyo R&D Division in April 2013 in order to further strengthen Daiichi Sankyo’s drug discovery capabilities. With innovation and entrepreneurial spirit, VSL is engaged in drug discovery and early development for treatment of neurodegenerative diseases and other high unmet medical needs in age-associated diseases for growing aging population in the world.
Researchers have developed a new cognitive test that can better determine whether memory impairments are due to very mild Alzheimer’s disease or the normal aging process. The simple test asks subjects to determine if circles containing certain designs match each other, which exercises the hippocampus portion of their brain.
Memory impairments and other early symptoms of Alzheimer’s are often difficult to differentiate from the effects of normal aging, which makes it hard for doctors to recommend treatment for those affected until the disease has progressed substantially.
Previous studies have shown that a part of the brain called the hippocampus is important to relational memory – the “ability to bind together various items of an event,” said Jim Monti, a University of Illinois postdoctoral research associate who led the work with psychology professor Neal Cohen, who is affiliated with the Beckman Institute at Illinois.
Being able to connect a person’s name with his or her face is one example of relational memory. These two pieces of information are stored in different parts of the brain, but the hippocampus “binds” them so that the next time you see that person, you remember his or her name, Monti said.
Previous research has shown that people with Alzheimer’s disease often have impairments in hippocampal function. So the team designed a task that tested the relational memory abilities of the participants, according to their study report in the journal Neuropsychologia.
Participants were shown a circle divided into three parts, each having a unique design. Similar to the process of name-and-face binding, the hippocampus works to bind these three pieces of the circle together. After the participants studied a circle, they would pick its exact match from a series of 10 circles, presented one at a time.
People with very mild Alzheimer’s disease did worse overall on the task than those in the healthy aging group, who, in turn, did worse than a group of young adults.
The test also revealed an additional memory impairment unique to those with very mild Alzheimer’s disease, indicating the changes in cognition that result from Alzheimer’s are qualitatively different than healthy aging. This unique impairment allows researchers to statistically differentiate between those who did and those who did not have Alzheimer’s more accurately than some of the classical tests used for Alzheimer’s diagnosis, Monti said.“That was illuminating and will serve to inform future work aimed at understanding and detecting the earliest cognitive manifestations of Alzheimer’s disease,” Monti said.
Although this new tool could eventually be used in clinical practice, more studies need to be done to refine the test, he said.
“We’d like to eventually study populations with fewer impairments and bring in neuroimaging techniques to better understand the initial changes in brain and cognition that are due to Alzheimer’s disease,” Monti said.
The Alzheimer’s Association estimates that the number of Americans living with Alzheimer’s disease will increase from 5 million in 2014 to as many as 16 million by 2050.
Managing, Coping With Alzheimer’s Disease Symptoms
Many years ago, I worked as a psychologist for the Navy’s Military Sealift Command. Toward the end of my last tour of duty, I visited Ryoanji, the famous Buddhist monastery and meditation rock garden in Kyoto, Japan. Although I found the rock garden cultivated a sense of calm stillness within me, I gained the greatest spiritual insight as I left.
Along the path there was a small sign reading “The Usual Path.” It was meant to direct tourists back to their destination. The sign did not read “The Right Path” or “The Only Path,” just “The Usual Path.”
Most tourists opted for the usual path. It was safe and predictable, while the unusual path was unfamiliar and filled with challenges. But ultimately both paths led to the same place. That small, unbiased sign in the Buddhist monastery garden has given me inspiration and courage on my alternative path as a person living with Alzheimer’s disease.
When first diagnosed with younger-onset Alzheimer’s disease, it became crystal clear to me that I was no longer on “The Usual Path.” My journey now is unusual, unfamiliar and full of challenges — for both me and my loved ones. When first diagnosed, my life as I knew it, and the plans I had for it, changed. I have no idea how long my memory and cognitive functions will serve me.
My experience coping with Alzheimer’s disease is similar to others who have been diagnosed with this disease. Suddenly, I had to navigate life-insurance policies, trusts, wills, financial and long-term-care planning, early retirement, Social Security disability, state disability insurance, medical directives and compromised health — all at the same time. This journey has been nothing short of overwhelming and confounding.
The longer I am on this journey, the more I have a sense of urgency to live life to the fullest. I am “seizing the moment.” Ironically, I am happier now than I ever have been, mindful of the present moment rather than worrying about the future or brooding about the past. Prior to my Alzheimer’s diagnosis, much of my life was about striving for this or that and not really paying attention to the things I value most — my primary and secondary relationships, spirituality and health.
Being mindful of the present moment is a beneficial way to deal with the daily health and emotional challenges of this disease. The capability to live in the present moment deepens, develops and matures when there is an intention to pay attention. Daily walking (or some sort of exercise) also helps, because it is a deliberate exercise to strengthen body, mind and spirit.
My choice is to be a fighter and not a victim of Alzheimer’s disease. To have the energy to fight a good fight, I need to renew, rekindle and rediscover my inner spirit. And the only way I know to do this is by seizing the moment, cultivating stillness and quiet, avoiding stimuli and distractions and embracing the value and meaning of life. Because of Alzheimer’s, not in spite of it.
Early Alzheimer’s Disease Diagnosis Can Improve Treatment
A small study shows promising results that in the near future doctors will be able to predict Alzheimer’s disease accurately using only a simple blood test. As of now this is only a short-term test—it predicts Alzheimer’s disease or other kinds of cognitive decline within the next three years or so. Nonetheless, within these parameters the blood test results maintain a high degree of accuracy for predicting the development of Alzheimer’s disease. Such a diagnostic test could be used to catch at-risk patients before their diseases have had much chance to progress.
The study in question was conducted over a period of five years by researchers from the University of Georgetown. They monitored 525 men and women all 70 years old or older. The researchers regularly collected blood from these patients and monitored who developed Alzheimer’s disease and who remained healthy. The collection of blood samples over the course of these five years revealed that persons that developed Alzheimer’s disease or other cognitive declines had higher levels of 10 different kinds of cell membrane lipids. Looking for these indicative cell membrane lipids allowed researchers to accurately predict whether or not a patient would develop Alzheimer’s disease with up to 90 percent accuracy.
Over the years scientists have sought a way to easily and accurately identify Alzheimer’s disease while it is still in its early stages. This has led to a number of unique diagnostic tests, including examining the thickness of a patient’s retina, and even testing patients to see whether or not they can smell peanut butter in both nostrils.
Alzheimer’s Diagnosis Not An Exact Science
Although successful thus far, research is still in its early stages with regards to determining the accuracy with which blood tests can predict the onset of Alzheimer’s disease. A larger study with even more patients will be required to further examine this diagnostic strategy.
If indeed successful, this research comes at a critical time for elderly patients. Currently it is estimated that one in three senior citizens will die with some sort of dementia. Of all the different kinds of mental illnesses that cause dementia, Alzheimer’s is the most prevalent, and the problem is not going away. America is currently aging. This is in part due to increases in overall health that result in greater longevity. It is also due to how the Baby-Boomer generation is fast reaching retirement age. With these factors in mind, one study estimates that the incidence of Alzheimer’s disease may triple by 2050.
Currently there is no cure of Alzheimer’s disease. However early treatment can help patients delay the disease onset and thus maintain more independence and a higher quality of life. Current medication options include a range of cholinesterase drugs that help mitigate problems with reasoning, lapses in memory, and confusion. Vitamin E is also sometimes prescribed to patients. Finally, patients with Alzheimer’s disease can initiate their own treatment by engaging in mentally-stimulating activities such as puzzles, games, and other learning activities. Of course the sooner a patient becomes aware of his/her condition, the faster these treatments can be administered and the more effective they are. Therefore the newly-developed blood tests which can accurately predict Alzheimer’s disease years in advance could greatly better the prognosis for millions of people.
Usually we think of Alzheimer’s disease (AD) as affecting seniors who are on up in years. It’s less well-known that 10 percent of people with Alzheimer’s have the early-onset variety. Early-onset Alzheimer’s can strike before 65 years of age. Of the more than 5 million people in the United States, almost 4 percent have early-onset Alzheimer’s.
Adults who have Down syndrome are prone to early-onset Alzheimer’s, with symptoms beginning to show in the middle or late 40s, or early 50s. Less commonly, early-onset AD can be seen in people who are only 30-40 years old. Other people who get early-onset Alzheimer’s disease often also have a genetic defect on chromosome 14. This is not the case for people with late-onset Alzheimer’s disease.
It can run in families. If either of your parents, or any of your grandparents, for instance, had early-onset Alzheimer’s disease, you may be at risk. Mutations in three genes can be involved. The three genes are the APP, PSEN 1, and PSEN 2. Early-onset Alzheimer’s is also often linked with myoclonus, which is a form of spasm and muscle twitching.
A diagnosis of early-onset Alzheimer’s disease can be difficult to determine since each person is affected differently, and can have a variety of symptoms. Symptoms can be wrongly believed to be stress-related, for instance.
It appears at a time of life when things are busy and responsibilities are heavy, with work, raising children and possibly caring for parents with health problems. Because early-onset Alzheimer’s is often misdiagnosed, people suffering from AD can run into added troubles. They may lose their jobs, relationships may be damaged, since their medical condition has not been properly identified.
Loss of income because of not being able to function at work compounds the difficulties. Family may not be understanding or supportive about what is going on. Medical benefits and programs for social support are less available for someone with early-onset Alzheimers.
Do you think you or someone you love may have early-onset Alzheimer’s? You can see a doctor who specializes in AD for a medical exam, brain imaging, cognitive tests, and a neurological exam. Diagnosis is far from a science. Diagnoses are basically a process of elimination and somewhat of a guessing game.