My personal journey with Alzheimer’s began in 2005 when my wife, Valerie, was diagnosed with this terrible disease that is mind-boggling and forcing family and friends to watch in horror as their loved one slowly disappears.
Stunned by the news, I was overwhelmed by grief for my life partner and the loss of our future together. Valerie was a spirited, energetic person with a passion for education that we shared. Once diagnosed, I began to better understand the cause of the disease and to find new approaches and therapies that could prevent, delay, or reverse its spread in others.
There is so much we still do not understand about Alzheimer’s disease, but its devastating effects are increasing. There are 6.2 million patients in the US, a number that is expected to more than double by 2050. In 2018, more than 120,000 Americans died from the disease, making it the sixth leading cause of death in the country. Almost two thirds of the patients are women, but there is no explanation for this gender gap. In the United States, the cost of treating these patients is estimated to be more than $ 300 billion in 2020. The total costs, taking into account loss of income, life savings and productivity, are many times higher.
Scientists have conducted more than 400 clinical drug trials in the past 14 years to look for a pharmaceutical cure. All failed. This month the Food and Drug Administration approved a Biogen drug, aducanumab, as a treatment to slow cognitive decline in Alzheimer’s patients. However, the FDA’s advisory committee overwhelmingly recommended against approval because there is so little evidence in clinical trials that the drug works. Three members of the committee resigned from the committee in protest at the agency’s decision.
The lack of progress in developing an effective drug or combination of drugs that will treat the disease as it occurs suggests that we have looked at this problem incorrectly. Instead, effective therapies may require systemic approaches based on the principles of science-based wellbeing. In my own search for answers, I have learned that some important discoveries are being made.
For example, Michael Phelps, a UCLA biophysicist and inventor of PET scanning (the technology that creates images of disease changes in the body) found that some of the chemical changes in the brain when a person goes from wellbeing to Alzheimer’s disease 4 to 4 Occur 10 years before a clinical diagnosis could be made. It should be possible through clinical trials to develop a blood test that can detect blood biomarkers that reflect these brain changes at a very early stage in the transition to disease. With such information, patients could begin treatment long before the disease has reached its traditional diagnosable stage.
But what kind of treatment would that be?
Just as we have long known that exercise, eating a healthy diet, and avoiding harmful habits like smoking can prevent heart disease, studies have shown that a person’s lifestyle can play a large role in whether and how quickly the disease progresses.
For example, one researcher, Dale Bredesen, has focused on a systemic approach to stabilize the synaptic connections between nerve cells that are lost in this disease. He has begun studies to validate the idea that treatment should be “multimodal” – based on correcting a patient’s unique deficiencies as assessed by analyzing their blood and other factors such as environmental toxins, diet, exercise and sleep become.
In a groundbreaking study, a team of Finnish and Swedish researchers found that non-drug approaches can work as interventions for older adults at increased risk of dementia.
The Finnish Geriatric Interventional Study for the Prevention of Cognitive Impairment and Disability, also known as FINGER, was a two-year, double-blind, randomized controlled study of 1,260 people. Participants were enrolled in a program that included nutritional counseling, exercise, cognitive training, and social activities, along with intensive monitoring and control of metabolic and vascular health.
Essentially, the participants selected for the interventions went through something like a science-based approach to wellness. When the FINGER study was announced, there was some skepticism. Many of the interventions have previously been tried on dementia patients, often with disappointing results. However, the researchers were not convinced that these approaches were all dead ends. Exercise alone cannot move the needle much. Cognitive training alone can be relatively fruitless. Socialization in and of itself cannot do much. But the whole could be more than the sum of its parts – and it was.
At the end of the study, the patients who received the multiple interventions were much more likely than the control group to maintain their cognitive functions – and even improve them. Her memories were stronger. Her ability to pay attention and maintain that attention was better. The relationship between her thoughts and physical movements was sharper.
To maintain brain health, we need to intervene with multimodal therapies as early as possible. The key will be to identify each individual’s particular vulnerabilities and design a combination of interventions specific to that person.
The Institute for Systems Biology has carried out several clinical studies on multimodal therapies and is now setting up a clinical study with 1,000 people at high Alzheimer’s risk. The study will run genomic and other tests (including quantifying 1,000 blood analytes and gut microbiomes) on each participant twice a year while tracking their digital health measurements using wearable technology like Fitbits.
With this data, we should be able to identify transitions from wellness to Alzheimer’s at the earliest stages. In similar studies in healthy adults, years before clinical diagnosis, we were able to identify runaway blood analytes that are biomarkers for the early detection of various types of cancer.
With increasing evidence of the effectiveness of multimodal therapies, families with a history of Alzheimer’s disease will have good reasons to undergo genetic testing to assess their risk. Everyone has two copies of the APOE gene. A defective form of this gene, APOE4, has been linked to Alzheimer’s disease. With a copy of APOE4, a person aged 65 and over has a 12% higher chance of developing the disease. With two copies that is 65%.
Based on Valerie’s diagnosis, my children and I decided to get tested. It turned out that Valerie and I each have a copy of the APOE4 gene. My daughter was relieved to learn that both of her APOE genes are normal. However, my son has two defective copies of the gene, which makes him more likely to develop Alzheimer’s later in life. This sobering news led him to adopt a personalized multimodal plan of lifestyle, environment, and blood chemistry changes that could potentially prevent the onset of the disease.
Although there is still a lot of research to be done, multimodal therapies could play a central role in the fight against Alzheimer’s disease. And new blood tests could help people at high risk of Alzheimer’s to introduce preventive therapies at an early stage. If these advances are successful, perhaps we can envision a world where far fewer families will experience the pain of this terrible disease.
Leroy Hood, a member of the National Academies of Sciences, Engineering and Medicine, is Professor and Co-Founder of the Institute of Systems Biology and Senior Vice President and Chief Science Officer of the Providence St. Joseph Health Systems.
source https://dailyhealthynews.ca/second-opinion-the-key-to-treating-alzheimers-disease-may-not-be-a-drug/
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