FDA Cites 17 Companies For Illegally Marketing Dietary Supplements as Treatments For Dementia

For many ailments and conditions, over-the-counter products are readily available to help consumers find relief or treat various medical symptoms. When it comes to the relief and treatment of Alzheimer’s disease, there are many false claims being advertised about products that can “cure” the disease. This form of deceptive advertising is misleading vulnerable consumers to purchase fake treatments, and encouraging them to waste money on treatments that have not been properly reviewed by the FDA. “Brain health supplements make up more than $3 billion of the global market, and are predicted to reach $5.8 billion by 2032” (ALZFORUM, 2019).  Why? Because consumers are fearful of developing dementia and experiencing cognitive decline, while others are looking for ways to increase cognitive performance at work or school.

According to ALZFORUM, the press release made by the FDA on February 11, 2019 accused 17 companies of illegally marketing their products as dementia treatments. The supplements included vitamins, minerals, and herbal products. These products are unapproved or misbranded new drugs that claim to prevent, treat or cure Alzheimer’s disease and other serious health conditions. Selling them with this misbranding is in violation of the Federal Food, Drug, and Cosmetic Act. The FDA press release can be found here. The full ALZFORUM article can be read here. 

Several prescription drugs have been approved by the FDA for the treatment of people with an Alzheimer’s disease diagnosis such as: donepezil (Aricept®), rivastigmine (Exelon®), galantamine (Razadyne®), and memantine (Namenda®) (National Institute on Aging, 2016).  None of these drugs can cure or reverse the disease, but may provide symptom relief.

Clinical trials research is required for the FDA approval of new drugs to make sure they are effective and safe. To see what research opportunities are currently being offered at the Center for Cognitive Health, please fill out the How Can We Help You section at the bottom of this page or call (503) 548-0809. You may meet the criteria needed to help us test the efficacy of new drugs. 

To learn more about protecting yourself from fake treatments, take a look at this article provided by the FDA for consumers.

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Sources:
Alzheimer’s Disease Fact Sheet [Internet]. National Institute on Aging. U.S. Department of Health and Human Services; [cited 2019Mar15]. Available from: https://www.nia.nih.gov/health/alzheimers-disease-fact-sheet
 
Dementia Researchers Commend FDA Crackdown on Supplement Hype [Internet]. ALZFORUM. [cited 2019Mar15]. Available from: https://www.alzforum.org/news/community-news/dementia-researchers-commend-fda-crackdown-supplement-hype
 
Office of the Commissioner. Press Announcements – FDA takes action against 17 companies for illegally selling products claiming to treat Alzheimer’s disease [Internet]. U S Food and Drug Administration Home Page. Office of the Commissioner; [cited 2019Mar15]. Available from: https://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/ucm631064.htm
 
Office of the Commissioner. Consumer Updates – Watch Out for False Promises About So-Called Alzheimer’s Cures [Internet]. U S Food and Drug Administration Home Page. Office of the Commissioner; [cited 2019Mar15]. Available from: https://www.fda.gov/ForConsumers/ConsumerUpdates/ucm631046.htm

Amyloid PET Identifies Those At Risk For Alzheimer’s Disease

Michael Mega, MD, PhD Director, Center for Cognitive Health

        The definition of Alzheimer’s disease is changing. With the ability to visualize beta amyloid, the predominate protein that makes up the plaques in Alzheimer patient’s brains, physicians now can tell who is at risk for the disease. Prior to the advent of amyloid PET scans, and spinal fluid analysis of beta amyloid, the certain diagnosis of Alzheimer’s disease was only made at death by microscopic evaluation of amyloid plaque burden. Now with the ability to visualize amyloid burden in life we have a window on how the disease evolves.

Alzheimer’s disease was once defined as a clinical presentation of a memory disorder with a decline in another domain of thinking (either language, visual-spatial processing, or problem solving) that is severe enough to interfere with daily functioning. Although many brain diseases can interfere with daily functioning to cause “dementia,” Alzheimer’s disease is the number one cause of dementia. Using this old definition of Alzheimer’s disease, investigators found that 15-20% of patients had o amyloid deposited in their brains on Amyloid PET scans. These patients may have diluted the findings in clinical trials testing amyloid lowering agents that hoped to slow or stop the disease. For this reason the definition of Alzheimer’s disease has moved from the old clinical description to a biological diagnosis. Now a person can only have Alzheimer’s disease when they are found to have an abnormally high amount of amyloid in their brain.

We all produce beta amyloid in our brains. Those of us who develop Alzheimer’s disease either make too much amyloid or do not clear it properly. Amyloid PET scans have shown the beginnings of amyloid accumulation in people as young as 30 to 40 years old. When a cognitively normal person has an abnormally high amount of amyloid in their brain they are now said to have preclinical Alzheimer’s disease; if they have a slight memory problem they meet the definition of prodromal Alzheimer’s disease, when their memory and thinking dysfunction is severe enough to interfere with daily life they are said to have full-blown Alzheimer’s dementia.

Selective amyloid lowering agents appear not to work in full-blown Alzheimer’s dementia. Can these new drugs work in the earlier stages of the disease in people with positive Amyloid PET scans? That is a question that our aging society is waiting to answer.  

Photo Caption:

Amyloid PET scans show amyloid deposits in red in the brains of people with Alzheimer’s disease. A&B) Patients scanned at screening and after 78 weeks of treatment with the selective amyloid lowering agent: bapineuzumab, note the reduction in amyloid deposition. C&D) Patients given placebo in the same study, note increased accumulation of amyloid in their brains.

How to Lower Your Risk for Alzheimer’s Disease

Michael Mega, MD, PhD Director, Center for Cognitive Health

Do you have a family history of Alzheimer’s disease? If you do there is much you can do now to reduce the chances of developing the disease even if you are carrying genes that increase your risk. Your lifestyle can turn on genes that fight disease and turn off those that increase the risk for disease. We are just beginning to understand that the foods we eat, our physical activity, how we deal with stress, and the cognitive stimulation we receive from our work or pastimes can influence our risk for developing Alzheimer’s disease.

Reducing many of the risks for cardiovascular disease also reduce the risk for Alzheimer’s disease. The food we eat can be medicine, or poison. The most harmful “food” we consume is refined sugar. The higher our daily dose of this manmade poison the greater our risk for developing obesity, diabetes, stroke, heart attack, and Alzheimer’s disease. Embracing a Mediterranean diet low in simple carbohydrates and high in fruits, vegetables, nuts, olive oil, and seafood is associated with a reduction of Beta-amyloid, the protein thought to cause Alzheimer’s disease (see figure below.)

Increasing our physical activity with aerobic exercise by as little as 20 minutes every other day has been associated with improvements in cognitive testing in patients with Mild Cognitive Impairment (MCI), a condition thought to be prodromal Alzheimer’s disease when Beta-amyloid is abnormally high in the brain. Stress, or administration of the stress hormone glucocorticoid, increases Beta-amyloid and the protein that makes up the microscopic tangles in the brain involved in synaptic dysfunction and neuronal death associated with Alzheimer’s disease. Thus, stress reduction through mindfulness, biofeedback, and yoga can reduce disease risk.

Learning new information increases the density of the connections, or synapses, between brain cells; these synapses are pruned early in the disease. Increased synaptic density, occurring through cognitive stimulation increases our cognitive reserve. The higher our cognitive reserve the lower our risk for developing Alzheimer’s disease. So if you don’t use it you will loose it. Now is the time to modify your lifestyle to prevent Alzheimer’s even if you have a history of the disease.

Photo Caption:  Amyloid PET scans showing two-year increase in amyloid deposits in the brains of 36 cognitively healthy people who did not adhere to a Mediterranean diet compared to 34 who did adhere to the diet. These data support a 1.5-3.5 year protection against Alzheimer’s disease when people follow a Mediterranean diet for only 2-3 years. (Berti, V et al. Neurol 2018; 90:e1798) 

Our Research

In the quest to conquer Alzheimer’s disease, new drugs that can be used long before the effects of the disease take hold are being tested. These drugs can target and diminish production of a specific protein found in the brain – Beta-amyloid – that’s thought to cause Alzheimer’s.

“The field of Alzheimer’s care has changed significantly in recent years,” says Michael Mega, M.D., Ph.D. Mega is a Cognitive Neurologist and founder of the Center for Cognitive Health in Portland. “Science is no longer testing people with full-blown Alzheimer’s, because it’s known that anti-amyloid drugs don’t work when the disease is that advanced.

The Center for Cognitive Health is participating in clinical trials testing new drugs to treat the early stages of memory problems associated with Alzheimer’s.

It’s long been hypothesized that Beta-amyloid plaques, the sticky buildup surrounding neurons in the brain, are the cause of Alzheimer’s.

“The emergence of Amyloid-PET (Positron Emission Tomography) enables the amyloid plaque to be visualized in the living brain,” says Mega. “It allows us to select people who are at risk to develop Alzheimers disease, and then administer these anti-amyloid compounds to see if we can slow cognitive decline.”

The biological purpose of amyloid protein is not well understood. “Some data indicate that a byproduct of its production helps the “pruning” process during the first year of life,” says Mega, who’s worked in the cognitive health field for 27 years. “That’s a time when neurons not being used for sensory perception are “pruned” to allow others being used to become stronger.”

Amyloid, and other misfolded proteins, appears to be cleared from the brain during REM sleep as a form of daily de-toxing. Hence, there’s a theory that REM sleep abnormalities are a precursor to Alzheimer’s, Parkinson’s and other degenerative diseases.

Because amyloid deposits in the brain appear to peak about 10 years before memory symptoms occur, scientists are committed to determining when anti-amyloids should best be administered.

Keep an eye out for new research opportunities being offered at the Center for Cognitive Health!

Welcome!

On top of providing top notch care to patients with memory impairment and cognitive decline, we are committed to increasing awareness of Alzheimer’s disease causes, treatments, and current topics in research. Here you will find posts with articles related to Alzheimer’s disease, Mild Cognitive Impairment (MCI), and various brain health tips. Keep checking back for new posts! We encourage you to share our blogs with family and friends as the first step towards fighting Alzheimer’s is understanding the disorder itself and it’s impacts on those who suffer from it!