Wednesday, May 23, 2018

Keep those with dementia safe by following these tips

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two

Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition]

The Alzheimer’s Disease Education and Referral (ADEAR) Center, a service of the National Institute on Aging, part of the National Institutes of Health.

Here are 20 ways to make your home a safer place for a loved one with dementia. 




While some Alzheimer's behaviors can be managed medically, many, such as wandering and agitation, cannot. It is more effective to change the person's surroundings—for example, to remove dangerous items—than to try to change behaviors. Changing the home environment can give the person more freedom to move around independently and safely. 

Minimize Danger

People with Alzheimer's disease may not see, smell, touch, hear, and/or taste things as they used to. You can do things around the house to make life safer and easier for the person. For example: 
  1. Check all rooms for adequate lighting. Use nightlights in bathrooms, bedrooms, and hallways.
  2. Be careful about small pets. The person may not see the pet and trip over it.
  3. Reset the water heater to 120 degrees Fahrenheit to prevent burns.
  4. Label hot-water faucets red and cold-water faucets blue, or write the words "hot" and "cold" near them.
  5. Install grab bars in the tub/shower and beside the toilet.
  6. Put signs near the oven, toaster, and other things that get hot. The sign could say, "Stop!" or "Don't Touch—Very Hot!"
You can also try these tips: 
  • Check foods in the refrigerator often. Throw out any that have gone bad.
  • Put away or lock up things like toothpaste, lotions, shampoos, rubbing alcohol, soap, or perfume. They may look and smell like food to a person with Alzheimer's.
  • If the person wears a hearing aid, check the batteries and settings often.

Basic Safety for Every Room

Add the following items to the person's home if they are not already in place: 
  • Smoke and carbon monoxide detectors in or near the kitchen and in all bedrooms
  • Emergency phone numbers and the person's address near all phones
  • Safety knobs and an automatic shut-off switch on the stove
  • Childproof plugs for unused electrical outlets and childproof latches on cabinet doors
You can buy home safety products at stores carrying hardware, electronics, medical supplies, and children's items. 

Lock up or remove these potentially dangerous items from the home: 

  1. Medicines
  2. Alcohol
  3. Cleaning and household products, such as paint thinner and matches
  4. Poisonous plants—contact the National Poison Control Center at 1-800-222-1222 or www.poison.org to find out which houseplants are poisonous.
  5. Guns and other weapons, scissors, knives, power tools, and machinery
  6. Gasoline cans and other dangerous items in the garage

Moving Around the House

Try these tips to prevent falls and injuries:
  1. Simplify the home. Too much furniture can make it hard to move around freely.
  2. Get rid of clutter, such as piles of newspapers and magazines.
  3. Have a sturdy handrail on stairways.
  4. Put carpet on stairs, or mark the edges of steps with brightly colored tape so the person can see them more easily.
  5. Put a gate across the stairs if the person has balance problems.
  6. Remove small throw rugs. Use rugs with nonskid backing instead.
  7. Make sure cords to electrical outlets are out of the way or tacked to baseboards.
  8. Clean up spills right away.
Make sure the person with Alzheimer's has good floor traction for walking. To make floors less slippery, leave floors unpolished or install nonskid strips. Shoes and slippers with good traction also help the person move around safely.

You may want to re-evaluate the safety of the person's home as behavior and abilities change.

For more home safety tips, see the NIH / National Institute on Aging's checklist: 

Monday, May 21, 2018

Dementia:Do NOT do theses things

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two

Follow alzheimersideas on twitter



BIGJOURNEYsmallsteps

Whether caregiving for someone with Alzheimer's or just visiting, be wise & avoid these phrases. 





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Saturday, May 19, 2018

What is HS-AGING?

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two

Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition]

University of Kentucky Sanders-Brown Center on Aging

3 important dementia studies focus on HS-AGING. It's a type of dementia almost as common as Alzheimer's in the 85+ group. Yet few people have heard of it. Why? What makes it different? 




In those who live to a very advanced age (beyond the age of 85) HS-AGING (hippocampal sclerosis in the elderly) is almost as prevalent as Alzheimer's. Remarkably, HS-Aging appears to be a completely separate disease from Alzheimer's, although it is almost always diagnosed as Alzheimer's disease while people are alive.

Three important papers authored by Dr. Peter Nelson and others at the University of Kentucky Sanders-Brown Center on Aging, explore the neuropathology behind this little-understood brain disease.

HS-AGING, much like Alzheimer's disease, causes symptoms of dementia, such as cognitive decline and impaired memory. Although Alzheimer's disease is probably the most recognized cause of dementia, HS-AGING also causes serious cognitive impairment in many older adults.

Overview of 3 New Studies on HS-AGING:

  1. The first paper, published in the Journal of Alzheimer's Disease, draws from a very large sample population and shows that presently, around 20% of all dementia cases are diagnosed as HS-AGING at autopsy, although almost none are given that diagnosis during life. That means that the presence of this disease is currently almost unknown by the health care providers who are seeing patients.
  2. A second study, "Arteriolosclerosis that affects multiple brain regions," appears in a recent issue of the journal Brain, and looks at small blood vessels in patients with HS-Aging and describes a specific change, called "arteriolosclerosis," which is present in patients with HS-Aging. This small blood vessel change may provide a new therapeutic target to alter the progression of the disease.
  3. Finally, the third paper, "Hippocampal sclerosis of aging, a prevalent and high morbidity brain disease," appears in Acta Neuropathologica and offers an overview of HS-AGING for patients and researchers. This paper reviews the relevant scientific literature and also presses home the point that HS-AGING is a very common disease that exerts a strongly adverse impact on public health.
It is important for physicians and scientists to understand the unique pathology of HS-AGING, and to be able to differentiate it from other diseases, as it is only by making an accurate diagnosis that clinicians can hope to treat people who present with signs of cognitive decline. These current studies represent a leap forward in the knowledge base about HS-AGING, and represent potential new paths to explore for diagnosis and treatment of this serious, but under-appreciated brain disease.

In people over 95, a type of dementia called HS-Aging is about as common as Alzheimer's. Yet few people have heard of it. Why? What makes it different?

What is HS-Aging?

HS-Aging stands for "Hippocampal Sclerosis in Aging People".

Alzheimer's and HS-Aging are types of dementia. In people over 95, their prevalence is about equal.

HS-Aging is Not Well Known. Everyone Has Heard of Alzheimer's. Why?

There are hundreds of types of dementia. In people aged 65 to 95, 60% of dementia cases are Alzheimer's. That is why Alzheimer's is so well-known.

At age 95, the balance shifts and HS-Aging becomes about as common as Alzheimer's.

Few people have heard of HS-Aging. The main reason is because it is often mis-diagnosed as Alzheimer's. Why?

When dementia is seen in the elderly, the default diagnosis is Alzheimer's. This is caused by many factors, among them:

  • Patients often do not want to go through extensive testing for a variety of reasons.
  • There is no simple test. The differences between dementias can be subtle. Therefore, distinguishing between dementias is often technically challenging.
  • Cost comes into play. For example, F18 dementia scans can run thousands of dollars. Therefore, many a diagnosis is made based on incomplete information.

With these realities, it is common for a diagnosis to default to the most common dementia, which is Alzheimer's.

As a result, people with dementias such as HS-Aging often live out their lives thinking they have Alzheimer's.

How does HS-Aging differ from Alzheimer's?

Alzheimer's and HS-Aging both damage the hippocampus. It seems that HS-Aging hits harder than Alzheimer's, causing greater disturbances to memory.

HS-Aging describes a brain under attack from a protein called TDP-43. It causes sclerosis, or the hardening of tissues. In the case of HS-Aging, TDP-43 proteins harden brain tissue in the hippocampus (sometimes called the memory-processing center), causing the loss of a large number of crucial brain cells. It is called Hippocampal Sclerosis because the brain's hippocampus is the focus of the attack.

Alzheimer's, on the other hand, is an attack on the brain by plaques (made from beta-amyloid) and tangles (made of tau proteins). Researchers speculate that the plaques clump together and "choke" brain cells, while the tangles strangle them from within.

How does HS-Aging differ from regular HS?

Regular Hippocampal Sclerosis (HS) occurs in younger people where brain tissue hardening is associated with epilepsy. HS-Aging is a similar hardening, but it occurs in the elderly with different consequences. It is caused by a long life of physical wear-and-tear on the brain, similar to vascular dementia. As a matter of fact, once people hit 95, the combined occurrences of HS-Aging PLUS vascular dementia actually outstrip Alzheimer's.

Why does the type of dementia matter?

As explained above, the biochemistry of each dementia differs significantly. This implies different medications are required to fight the chemicals causing the dementia. A person's response to medicines and supplements will be entirely different, depending on the disease.

Importantly, new F18 imaging techniques have recently been introduced that let doctors see if a person with dementia has the plaques associated with Alzheimer's. Using this technique helps doctors tell the difference between Alzheimer's and HS-Aging. This is particularly crucial in the world of clinical trials, where participants must closely match the experimental drugs they are testing.

CTE Research Leading to Rapid Improvements in HS-Aging Treatments

When we talk about dementia in aging athletes, it is usually the type of dementia called CTE (Chronic Traumatic Encephalopathy). Recent studies showed athletes in contact sports like football are 19 times more likely than average to develop dementia. As a result, there has been a huge burst of research on CTE treatment.

CTE treatment has a lot in common with HS-Aging treatment. With the new attention both of these dementias are now receiving, there is good reason to hope for effective new treatments in the immediate future.


MORE INFORMATION: 
Study #1 above was done with the collaboration of the National Alzheimer's Coordinating Center (or "NACC"; the first author of this study, Willa Brenowitz, is based in Washington state and works with NACC), enabling Nelson and colleagues to incorporate data from dozens of federally funded Alzheimer's Disease Centers around the country. These centers are funded by the National Institute on Aging, part of the National Institutes of Health. The research was supported by NIA grant numbers U01 AG016976 and P30 AG028383.

Study #2 above was based on analyses that were boosted through collaboration with the larger NACC-based dataset. Further, the first author, Dr. Janna Neltner, provided critical expertise in digital pathologic measurement of the brain. 

SOURCE:
University of Kentucky Sanders-Brown Center on Aging


Thursday, May 17, 2018

Is caffeine good for dementia?

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two

Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition]



Years of good research suggested caffeine lowers the risk of getting dementia. Now, top researchers uncovered a subtle twist - evidence that AFTER dementia kicks in, continuing to drink caffeine may exert opposite effects. Get the details. 




A pattern-breaking study provides evidence that a long-term consumption of caffeine has negative effects for Alzheimer's disease, worsening the neuropsychiatric symptoms appearing in the majority of those affected by the disorder. 

The study was coordinated by the Institute of Neuroscience of the Universitat Autònoma de Barcelona (Inc-UAB) and in collaboration with the Karolinska Institutet (KI) in Sweden. The research was recently published in Frontiers in Pharmacology.

Memory Problems VS. Behavioural Problems

It is well known that memory problems are the hallmarks of Alzheimer's disease. However, this dementia is also characterised by neuropsychiatric symptoms, which may be strongly present already in the first stages of the disorder. Known as Behavioural and Psychological Symptoms of Dementia (BPSD), anxiety, apathy, depression, hallucinations, paranoid, sundowning, etc. are part of an array of symptoms which are manifested in different manners depending on the individual patient. They are considered the strongest source of distress for patients and caregivers. 

Preventor or Agitator?

Coffee or caffeine has recently been suggested as a strategy to prevent dementia, both in patients with Alzheimer's disease and in normal ageing processes, due to its action in blocking molecules -- adenosine receptors -- which may cause dysfunctions and diseases in old age. However, there is some evidence that once the cognitive but also the NPS symptoms are developed, caffeine may exert opposite effects. 

To address these issues, the study was conducted with normal ageing mice and familial Alzheimer's models. "The mice develop Alzheimer's disease in a very close manner to the human patients with early-onset form of the disease. They not only exhibit the typical cognitive problems but also a number of BPSD-like symptoms, so it is a valuable model to address whether the benefits of caffeine will be able to compensate its putative negative effects," explains Raquel Baeta-Corral, first author of the research. 

"We had previously demonstrated the importance of the adenosine A1 receptor as the cause of some of caffeine's adverse effects. Now, we simulated a long oral treatment with a very low dose of caffeine (0.3 mg/mL) equivalent to three cups for a human coffee-drinker to answer a question which is relevant for patients with Alzheimer's, but also for the ageing population in general, and that in humans would take years to be solved since we should wait until the patients were aged' -- explains Dr Björn Johansson, researcher and physician at the Karolinska University Hospital. The research was conducted from the onset of the disease up to more advanced stages, as well as in healthy age-matched mice.

Caffeine Alters Behaviour

The results indicate that caffeine alters the behaviour of healthy mice and worsens the neuropsychiatric symptoms of mice with Alzheimer's disease. The researchers discovered significant effects in the majority of variables studies, especially in relation to neophobia, a fear of everything new, anxiety-related behaviours, and emotional and cognitive flexibility. 

In mice with Alzheimer's disease, the increase in neophobia and anxiety-related behaviours exacerbates their BPSD-like profile. Learning and memory, strongly influenced by anxiety, got little benefit from caffeine. 

"Our observations of adverse caffeine effects in an Alzheimer´s disease model together with previous clinical observations suggest that an exacerbation of BPSD-like symptoms may partly interfere with the beneficial cognitive effects of caffeine. These results are relevant when coffee-derived new potential treatments for dementia are to be devised and tested," says Dr Lydia Giménez-Llort, researcher from the INc-UAB Department of Psychiatry and Legal Medicine and lead researcher of the project. 


SCIENTISTS' RESEARCH ARTICLE:
MORE INFORMATION:
  • The results of the study form part of the PhD thesis of Raquel Baeta-Corral, first author of the article, and are the product of a research led by Lydia Giménez-Llort, Director of the Medical Psychology Unit, Department of Psychiatry and Legal Medicine and researcher at the UAB Institute of Neuroscience, together with Dr Björn Johansson, Researcher at the Department of Molecular Medicine and Surgery, Karolinska Institutet and the Department of Geriatrics, Karolinska University Hospital, Sweden, under the framework of the Health Research Fund project of the Institute of Health Carlos III*.
  • FIS Project at the Institute of Health Carlos III -- General Subdirector of Research Evaluation and Promotion (AES-PI10/00283), co-funded by the European Regional Development Fund (ERDF), the Åhlén Foundation and the Stockholm County Council (ALF 20170190)
SOURCE:

Tuesday, May 15, 2018

Can Alzheimer's gene be fixed?

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two

Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition]




Experimenting with ApoE4, the best known "Alzheimer's Gene", The Gladstone Institute developed compounds to change the gene's structure - eliminating certain signs of Alzheimer's, restoring normal cell function, and improving survival. Learn all about this giant step forward. 




Using human brain cells, scientists at the Gladstone Institutes discovered the cause of -- and a potential solution for -- the primary genetic risk factor for Alzheimer's disease, a gene called apoE4. 

Having one copy of the apoE4 gene more than doubles a person's likelihood of developing Alzheimer's disease, and having two copies of the gene increases the risk by 12-fold, as compared to the most common version of the gene, apoE3. 


The apoE4 gene creates a protein of the same name. The apoE4 protein differs from the apoE3 protein at only one point, but that single change is enough to alter its main structure and, thus, its function. Scientists have been unclear about why apoE4 is so much more damaging to brain cells than other versions of the protein. 

In a new study published in Nature Medicine, researchers revealed how apoE4 confers its risk for Alzheimer's disease in human brain cells. What's more, they were able to erase the damage caused by apoE4 by changing it, with a small molecule, into a harmless apoE3-like version.

A Better Model

Most Alzheimer's research and drug development are done in mouse models of the disease. However, a succession of clinical trial failures has spurred scientists to turn to other models. 

"Drug development for Alzheimer's disease has been largely a disappointment over the past 10 years," says lead author Yadong Huang, MD, PhD, a senior investigator and director of the Center for Translational Advancement at Gladstone. "Many drugs work beautifully in a mouse model, but so far they've all failed in clinical trials. One concern within the field has been how poorly these mouse models really mimic human disease."

Instead, Huang decided to use human cells to model the disease and test new drugs. Thanks to induced pluripotent stem cell technology, his team was able to examine, for the first time, the effect of apoE4 on human brain cells. To do so, the researchers created neurons from skin cells donated by Alzheimer's patients with two copies of the apoE4 gene, as well as from healthy individuals who had two copies of the apoE3 gene. 

The researchers confirmed that, in human neurons, the misshapen apoE4 protein cannot function properly and is broken down into disease-causing fragments in the cells. This process results in a number of problems commonly found in Alzheimer's disease, including the accumulation of the protein tau and of amyloid peptides. 

Notably, the presence of apoE4 does not change the production of amyloid beta in mouse neurons. But in human cells, scientists noticed apoE4 has a very clear effect on increasing amyloid beta production, which highlights the species difference in the way apoE4 controls amyloid beta metabolism. 

"There's an important species difference in the effect of apoE4 on amyloid beta," says Chengzhong Wang, PhD, the first author on the paper and former research scientist at Gladstone. "Increased amyloid beta production is not seen in mouse neurons and could potentially explain some of the discrepancies between mice and humans regarding drug efficacy. This will be very important information for future drug development."

Fixing a Toxic Protein

Once the scientists confirmed that apoE4 does, indeed, cause damage in human cells related to Alzheimer's disease, a key question remained: how does the presence of apoE4 lead to cell damage? Is the presence of apoE4 resulting in a loss of normal apoE3 function, or does the addition of apoE4 cause the toxic effects? 

"It's fundamentally important to address this question because it changes how you treat the problem," explains Huang, who is also a professor of neurology and pathology at UC San Francisco. "If the damage is caused due to the loss of a protein's function, you would want to increase protein levels to supplement those functions. But if the accumulation of a protein leads to a toxic function, you want to lower production of the protein to block its detrimental effect." 

To answer this question, the researchers examined brain cells that did not produce either form of the apoE protein, and the neurons looked and functioned just like cells with apoE3. However, if the researchers added apoE4, the cells became riddled with pathologies related to Alzheimer's disease. This discovery indicates that the presence of apoE4 -- and not the absence of apoE3 -- promotes the disease. 

Finally, the researchers looked for ways to repair the abnormalities caused by apoE4. In earlier work, Huang and his collaborators developed a class of compounds that can change the structure of the harmful apoE4 protein so it resembles the innocuous apoE3 protein, referred to as apoE4 "structure correctors." 

Treating human apoE4 neurons with a structure corrector eliminated the signs of Alzheimer's disease, restored normal function to the cells, and improved cell survival. Huang is now working with his collaborators in academia and the pharmaceutical industry to improve the compounds so they can be tested in human patients in the future. 

Their work suggests the real feasibility of a drug that could have a significant impact at the early stage of Alzheimer's development, exactly where most investigators are focused these days, before Alzheimer’s wipes out memory.


MORE INFORMATION:
  • Other scientists on the study include Ramsey Najm, Qin Xu, Dah-eun Jeong, David Walker, Maureen Balestra, Seo Yeon Yoon, Heidi Yuan, and Gang Li from the Gladstone Institutes. Zachary Miller, Bruce Miller, and Mary Malloy from UCSF also took part in the research. This research was funded by the National Institute on Aging, the California Institute of Regenerative Medicine, and the Roddenberry Foundation.
SOURCE:


Sunday, May 13, 2018

Supplements that do not help Alzheimer's

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two

Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition]

Live Science


Dr. Gisele Wolf-Klein is program director for the geriatric fellowship and director of geriatric education for the North Shore-LIJ Health System, where for more than 30 years she has guided seniors on falls, healthy aging, and memory and medication challenges. Dr. Liron Sinvani is a geriatric hospitalist at North Shore University Hospital in Manhasset, N.Y., where she is conducting a study on improving geriatric care. She has published widely on the dietary supplement controversy. The authors contributed this article to Live Science's Expert Voices: Op-Ed & Insights
The Latin axiom "caveat emptor," let the buyer beware, applies to people of all ages. But in our medical practices, we have witnessed the incredible dependence elderly patients have on herbal supplements to help them (in their minds, at least) prevent and manage chronic illness.

That is why we breathed a sigh of relief at the recent action that may spur consumers, especially those in vulnerable age groups, to exercise more caution in purchasing products with no proven health benefits. On Feb. 3, the New York State attorney general's office demanded that four major retailers — GNC, Target, Walmart and Walgreens — remove certain store-brand herbal supplements from their shelves pending further quality-control measures. DNA testing on the supplements showed that a whopping 79 percent contained none of the herbs listed on their labels. Just as bad, the tests indicated the supplements often contained cheap fillers such as powdered rice, pine, citrus, houseplants and wheat — the latter despite claims on some labels that a product was wheat- and gluten-free.
Old story, new ending
Were we surprised to hear about these allegedly fraudulent and potentially dangerous supplements? Sadly, no. Copious research has delved into the dietary supplement industry, which boasts a global market of $68 billion, showing either fraudulent ingredients or tainted supplements packed with hidden ingredients. Recent research by Dr. Sinvani and colleagues also details how the vitamin and dietary supplement industry is a poorly regulated multibillion-dollar business, with the widespread use of supplements raising medical, social and ethical concerns, given the unclear benefits and the associations with health risks. 
But the U.S. Food and Drug Administration (FDA) doesn't regulate supplements, since these products are not "drugs." So the New York State action marks the first time a law enforcement agency has cracked down on retailers for selling what appear to be deliberately deceptive products.
When we see patients, we ask them to bring along all their medications and supplements. Too often, we note that these seniors are taking up to 20 pills each day, but only a handful of these pills are actually prescribed drugs. Why are seniors spending so steeply on herbal supplements, often hundreds of dollars each month, despite living on limited budgets? For most, the main reason is fear — not just of becoming ill, but of losing their minds.
Can supplements save your mind?
Dementia is the biggest specter among the elderly. Seniors can accept heart disease, diabetes or slowly diminishing mobility, but they cannot accept the idea of developing Alzheimer's disease. Unfortunately, modern medicine has yet to come up with an effective treatment to truly alter the course of this scourge, which affects more than 5 million Americans. Given that void, the herbal supplement industry has attempted to prey on seniors hoping and banking on the idea that readily available products containing "natural" substances such as seaweed, coral or coconut oil can help them dodge dementia. [What's the Difference Between Alzheimer's Disease and Dementia?]
Here are some of the worst offenders among herbal supplements purporting to prevent or treat dementia:
  • Gingko biloba: This Chinese plant, long promoted as a memory booster, is so popular that the U.S. National Institutes of Health (NIH) analyzed the supplement's effectiveness in a large clinical trial. Known as the GEM (Ginkgo biloba for the Evaluation of Memory) study, 3,000 participants over age 75 were randomly assigned to receive two daily doses of either the extract or a placebo, and were tracked every six months for six years. The results? A slightly higher percentage of Ginkgorecipients actually developed dementia over time, and the supplement was proven ineffective at reducing the overall rate of Alzheimer's.
  • Coconut oil: Also wildly popular as a food additive and skin balm, coconut oil has been touted as a less-expensive, over-the-counter source of caprylic acid, which is claimed to treat Alzheimer's disease. The catch? There has never been any clinical testing of coconut oil for Alzheimer's and no scientific evidence supporting positive outcomes. Caprylic acid itself would be ineffective in treating the disease, anyway, since the organic compounds called ketones that comprise this fatty acid could never cross the blood-brain barrier — glucose is the only energy the brain can use.
  • Tramiprostate: This modified form of taurine, an amino acid found naturally in seaweed, is marketed as a "medical food" known as ViviMind. Tramiprostate was tested in a large clinical trial as a possible Alzheimer's treatment, but after results proved inconclusive, the manufacturer decided to market the product as a "medical food." This "food," however, offers no proven benefits. 
  • Coenzyme Q10: This is an antioxidant occurring naturally in the body. A synthetic version of coenzyme Q10 was tested for Alzheimer's disease use but showed no benefit in a clinical trial. Beyond that, little is known about what dosage of this compound is safe. 
  • Coral calcium: A form of calcium carbonate claimed to be derived from the shells of formerly living organisms in coral reefs — which are illegal to harvest — these supplements have been heavily marketed as a cure for not only Alzheimer's, but also cancer and other serious illnesses. Both the FDA and the U.S. Federal Trade Commission (FTC), which have filed formal complaints against the distributors of coral calcium, have stated they are unaware of competent or reliable scientific evidence supporting the exaggerated health claims.
Unlisted ingredients

If you're a topical expert — researcher, business leader, author or innovator — and would like to contribute an op-ed piece, <a href=mailto:expertvoices@techmedianetwork.com>email us here</a>.
If you're a topical expert — researcher, business leader, author or innovator — and would like to contribute an op-ed piece, email us here.

It's one thing to lure consumers into buying dietary supplements with false promises of preventing or managing illness. It's quite another to include ingredients in these supplements that aren't even listed on the labels. 
Because seniors often take multiple prescribed medications for chronic conditions, they are most prone to dangerous drug interactions with, and allergies to, these unmentioned ingredients in supplements. We truly hope the actions of the New York State attorney general's office lead seniors, and those who care for them, to abandon the use of all supplements unless specifically directed to use supplements by their doctors.
"It's fairly outrageous that little can be done to impede the exploitative marketing of unproven and unlikely [to be beneficial] substances to vulnerable Alzheimer's patients and their desperate caregivers." That decade-old statement by Dr. Sam Gandy, chair of Alzheimer's research at Mount Sinai School of Medicine, has remained true — until now. Finally, something has been done to help protect the most vulnerable members of society.

Fitness is important in dementia prevention. Click below for more info