Interview with a Dementia Researcher: Dr. Aida Suarez Gonzalez, Clinical Neuropsychologist

What areas of research are you currently pursuing?

I am a clinical neuroscientist with a strong translational focus. I have a passion for non-pharmacological interventions and evidence-based services to help people to live well with dementia.

What are the big questions or theories currently being debated in your field?

The development of new multicomponent functional interventions in dementia (such as disease education, counselling, goal-setting, goal-oriented cognitive rehabilitation, coping strategies training, etc.) is a hot topic. These interventions have the potential to increase autonomy, quality of life, and mental health in patients and families.

Another big concept is the need to develop more suitable methods to produce high quality evidence in support of non-pharmacological interventions. The traditional methods used in classic drug trials do not always makes sense when applied to non-pharmacological approaches.

I am also interested in the introduction of a new generation of purpose-built assistive technologies (such as specific communication aids, adapted e-readers, memory aids, etc.). These tools are revolutionizing the way we provide support, so people can remain independent for longer. IDEAL and GREAT are two examples of programs that support the concept of living well with dementia.

What is a common misconception related to dementia that you often encounter?

There are two big misunderstandings that particularly trouble me because they produce undesirable consequences when a diagnosis of dementia is provided.

First, we always highlight that dementia is not a natural part of aging, that it is a disease. However, we usually forget to add that this is a very common disease in old age and that we, as longer-living societies, have lived with age-related diseases for centuries (and hey, here we are after all).

I don’t mean we should belittle the seriousness of dementia, but rather encourage more acceptance and reconciliation with life and trust in the resilience of what we human beings are capable of. I think this way of thinking moves the focus from the frustration of the current absence of a treatment to reflecting on what we can do to live well with the disease. And of course this way of seeing things is not incompatible with increasing research efforts towards finding a cure.

Secondly, calling the dementias “dementias” contributes the stigma and misunderstanding of the disease. In many societies across the world, the word dementia means losing yourself, your reasoning, judgement, understanding and contact with reality. And this is not true. This is a false and unfair misconception that every day strips millions of people around the world from their social roles and right to decide about their lives, and exposes them to patronization.

Of course, advanced stages of the disease do impair your thinking skills severely, but this is not the case in the early and even moderate stages (that can last for many years) and it also depends a lot on the dementia subtype that you have. With the right support, many people with progressive cognitive impairment can lead fairly independent lives for a long time.

Look for example at the UK Network of Dementia Voices, which is a community of 100 groups of people living with dementia that seeks to magnify their own views, make their voices being heard and pressure the public administration to include their advice in matters that affect them.

The same applies to the 3 Nations Dementia Working Group, who are a powerful group of people living with dementia transforming the way we perceive dementia and progressive cognitive impairment by making an extraordinary contribution to society through education and raising awareness. They do public speaking, provide input to public policy bodies and bring value, advice and information about what is like the experience of living with dementia. They have dementiayes, and also they are inspiring, powerful and they are transforming the world.

What recommendations would you give to people wanting to reduce their risk of Alzheimer’s disease?

There is quite a lot of scientific consensus around the main preventive measures: healthy diet, good control of vascular risk factors such as cholesterol, diabetes and hypertension, regular physical exercise, remaining mentally active, and maintaining strong and good quality social bonds and social networks.

How can non-scientists contribute to the fight against Alzheimer’s?

The lay public can make a powerful contribution by trying to educate themselves about dementia, understanding better the changes experienced by a person with the disease, and committing to contribute towards a more dementia-friendly society.

For example, if you run a fruit shop in a neighborhood with an aged population, it’s very likely that some of your clients may be living with memory problems. You can seek information to educate yourself to understand better what that means and place a sign in your shop window explaining that this is a “memory problems friendly shop” and that people can come and speak to you about how to better support them to continue doing their shopping safely and independently.

When do you believe a viable Alzheimer’s treatment will be available?

I wish I had a response for that and I wish that response was “soon.” However, it is possible that we still have to live with Alzheimer’s in our lives for a long time, so I would encourage researchers and policy-makers to double efforts on finding a treatment, but also on helping us having good, purposeful, meaningful and fulfilling lives even if carrying a diagnosis of Alzheimer’s. There is a lot of life beyond the diagnosis, let’s also embrace that and make the best of it.

Is there any other information you’d like to add?

I would like to encourage other scientists to join a movement for change that focuses more on people and less on the disease, at least in the case of the diseases for which a cure has not been found yet. We hardly have any relevant tools to use in clinical studies to measure the impact of non-pharmacological interventions on people’s real lives and this needs to change. Current methods in this area are so quantitatively constrained and disease-oriented that allow little flexibility and, their resulting scientific outputs are usually difficult to translate into clinically practice.

 

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Dr. Aida Suarez Gonzalez is a clinical neuropsychologist at University College London’s Dementia Research Centre. She earned her Masters degrees in Gerontology and Clinical Neuropsychology, as well as her PhD in Neuropsychology, from the University of Salmanca in Spain.

 

 

 

 

 

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The New Definition of Alzheimer’s Disease Raises Ethical Dilemmas

A redefinition of Alzheimer’s disease could be a boon for clinical trials, but some warn that it could put patients at risk.

The current guidelines for diagnosing Alzheimer’s disease were established in 2011 by the National Institute on Aging and the Alzheimer’s Association. The guidelines, originally published in the journal Alzheimer’s and Dementia, focus on observable symptoms such as memory impairments, language problems, and personality changes.

However, the same group recently proposed a new set of guidelines based on biomarkers rather than symptoms. Biomarkers are physiological changes that can be easily measured and may be associated with a disease. For Alzheimer’s disease, the most widely-recognized biomarkers are amyloid-beta and tau, two toxic proteins that accumulate in the brains of people with this disease. The new guidelines propose that Alzheimer’s disease should be defined based on the presence of amyloid-beta and tau in the brain, without regard to cognitive symptoms.

This new way of defining Alzheimer’s disease brings with it both advantages and potential risks. In a recent Perspectives article published in Neural Regeneration Research, my colleagues and I discussed what the new guidelines could mean for the future of Alzheimer’s disease research and brought up some of the ethical dilemmas that it could pose.

Positive Aspects of the New Definition

The new way of defining Alzheimer’s disease offers several advantages, particularly for pharmaceutical companies. Most drug candidates for Alzheimer’s disease work by trying to get rid of amyloid-beta from the brain. Unfortunately, Alzheimer’s clinical trials have been a resounding failure for the past 30 years (see Where’s our cure to Alzheimer’s disease?). As a result, several pharma companies including Pfizer have shut down their Alzheimer’s research programs entirely.

Many pharma researchers believe that the reason these drugs failed is because they were administered too late in the disease’s progression. By the time Alzheimer’s disease is diagnosed, the patient’s brain is already full of large amyloid-beta deposits. But perhaps if we could administer the drugs to people in their 30s or 40s, when amyloid-beta has started to accumulate but cognitive symptoms are not yet apparent, they might be more effective.

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Clumps of amyloid-beta (shown in this illustration) can appear in the brain decades before the appearance of Alzheimer’s disease symptoms. Image Source

Under the current guidelines, these younger people who have amyloid-beta in their brains but no memory problems would not be considered to have Alzheimer’s disease. As a result, pharma companies would have to overcome steep legal issues in order to administer an experimental drug to people without a diagnosed disease. However, the new guidelines would allow these people to be diagnosed with Alzheimer’s, and thus they could be included in clinical trials.

This change would be great news for pharma companies, and possibly for the rest of us too. If they discover new drugs that can stop Alzheimer’s disease when administered at an earlier stage, it would be a huge breakthrough in preventing people from getting the disease. However, despite these advantages, there are some risks that we need to consider as well.

Ethical Issues with the New Guidelines

One of the biggest problems with this new definition is that many people who have amyloid-beta in their brains do not go on to develop the symptoms of Alzheimer’s disease. In fact, some studies suggest that as many as 1 in 3 seniors have enough amyloid-beta in their brains to meet the diagnostic criteria, yet they show no cognitive issues.

This discrepancy means that if we start diagnosing Alzheimer’s disease based on amyloid-beta alone, some people who receive the diagnosis in their 30s or 40s will never go on to experience any symptoms. Being diagnosed with a disease (particularly one that is currently incurable) can cause a substantial degree of anxiety and depression. There are ethical issues to be considered when we start diagnosing people with a disease they may never actually experience, causing undue stress for the patients and their families.

Another problem is that these asymptomatic individuals could be subjected to unnecessary treatments. In addition to the financial costs of such treatments, many Alzheimer’s clinical trials report adverse side effects, including increased rates of re-emergent infections and certain kinds of cancer. Treatments targeting amyloid-beta also increase the risk of ARIA (amyloid-related imaging abnormalities) by five-fold. ARIA is caused by tiny micro-bleeds in the brain’s blood vessels, which can result in confusion, headaches, and difficulty walking.

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Cerebral micro-bleeds from ARIA appear as abnormal white regions on this brain scan. Image Source

In redefining Alzheimer’s disease based on amyloid-beta, rather than the symptoms that actually affect patients’ lives, we will be subjecting many patients to unnecessary emotional hardship and potentially-harmful treatments. Whether the benefits to clinical trails are worth this sacrifice is a question worth careful consideration.

Does Amyloid-Beta Actually Cause Alzheimer’s?

In addition to the ethical problems that I’ve discussed, there’s a darker possibility that this new definition could severely derail Alzheimer’s disease research. For decades, the “amyloid cascade hypothesis” was widely accepted among neuroscientists. This hypothesis states that amyloid-beta is the initial cause of Alzheimer’s disease, and therefore we must get rid of it in order to cure the disease.

However, a growing body of evidence suggests that the amyloid cascade hypothesis could be wrong. For one thing, many people with amyloid-beta never develop this symptoms of Alzheimer’s disease, as I mentioned earlier. In addition, several studies suggest that amyloid-beta actually serves important roles in the brain and body (see The Villain of Alzheimer’s Disease Could Actually Be a Hero). For example, it may help the immune system to fight off infections by clumping around microbes and preventing them from spreading.

It’s possible that getting rid of amyloid-beta is the wrong strategy for fighting Alzheimer’s. And if that’s the case, then redefining Alzheimer’s in terms of amyloid-beta will only distract future research efforts away from the real path to a cure.

Concluding Thoughts

The advantages of the new definition for aiding future clinical trials are important, and they could help us discover treatments that are effective before the development of symptoms. However, we need to weigh this against the ethical risks of diagnosing asymptomatic people with Alzheimer’s, as well as the questionable validity of the hypothesis the guidelines are based on.

This debate should not be only left up to researchers and clinicians; I believe it is important that patients and their families also discuss this important issue and make their voices heard by the scientific community.

 

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Saliva Test for Alzheimer’s Disease Shows Encouraging Results

A small study suggests that saliva tests for amyloid-beta could be a useful method for diagnosing Alzheimer’s disease.

As we discussed in last week’s article, Alzheimer’s disease is notoriously difficult to diagnose, particularly in its early stages. Some estimates suggest that up to half of all Alzheimer’s diagnoses are incorrect. Currently-available tests for Alzheimer’s are often expensive and invasive, and in many cases they still can’t offer a completely accurate diagnosis.

In a recent study published in BMC Neurology, researchers investigated whether saliva could be used to detect the hallmarks of Alzheimer’s disease. The test quantifies levels of amyloid-beta, a toxic protein that accumulates in the brains of Alzheimer’s disease patients. Since detecting amyloid-beta inside the brain can be difficult, its levels in the saliva could be a useful proxy to aid in diagnosis.

The study included 15 patients with mild to moderate Alzheimer’s disease and 8 patients with normal cognition. The researchers collected saliva samples and used a highly sensitive protein test called an ELISA to quantify how much amyloid-beta each sample contained. They found that the saliva of Alzheimer’s patients contained more than twice as much amyloid-beta than that of the healthy patients.

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This figure from the paper shows that Alzheimer’s disease patients (represented as diamonds) all had higher salivary amyloid-beta levels than the normal patients (represented as squares). This relationship held true regardless of the patients’ age.

The results of this study suggest that the levels of amyloid-beta in the saliva could be a cheap and easy method for improving the accuracy of Alzheimer’s disease diagnoses. Since the current diagnostic methods require a spinal tap or blood sample, a saliva test could help encourage people to get tested for Alzheimer’s, considering an estimated 3-10% of individuals have a phobia of needles.

Due to the small sample size, this study needs to be repeated and expanded before we can draw broader conclusions. However, the preliminary results are encouraging and help to corroborate previous studies that have shown similar accuracy for these saliva tests. Perhaps in the future, diagnosing Alzheimer’s disease will be as simple as spitting into a tube.

 

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Computer Algorithm Diagnoses Alzheimer’s Disease from Brain Scans

Alzheimer’s disease is notoriously difficult to diagnose. Its symptoms are very similar to other conditions like Parkinson’s disease and vascular dementia (and may even occur simultaneously in some patients), making the task of diagnosing a patient’s condition challenging for physicians. An even more difficult task is predicting whether an individual with mild cognitive impairment will later progress to Alzheimer’s disease. Even advanced techniques have poor predictive power. Positron emission tomography (PET), a type of brain scan that measures the energy consumption of different brain regions, has only a 57.2% rate of accuracy.

To address this dilemma, a team of Canadian and South Korean scientists tested five different computer algorithms for their accuracy in diagnosing or predicting Alzheimer’s disease. Their results were published this week in Scientific Reports.

The researchers used a database of PET scans from the Alzheimer’s Disease Neuroimaging Initiative to train the computer models. Their study included 94 patients with Alzheimer’s disease and 111 age-matched healthy patients. They found that one model, called the Support Vector Machine with Iterative Single Data Algorithm (SVM-ISDA), could distinguish the Alzheimer’s patients from healthy controls with 80% accuracy.

The researchers then tested the performance of the computer models on three different PET scan databases. This time, rather than distinguishing Alzheimer’s disease from healthy patients, they wanted to see whether the models could predict whether individuals with mild cognitive impairment would develop Alzheimer’s disease within the next 3 years. Here the SVM-ISDA once again came out on top, though its predictive power was lower than for the previous task. The model predicted which patients would develop Alzheimer’s disease with an overall accuracy of around 51-59%. The other algorithms all had less than 50% accuracy.

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PET scanners like this one measure how much energy is consumed by different brain regions.

They next wanted to see whether the computer models could distinguish Alzheimer’s disease from two other types of dementia: Lewy body disease and Parkinson’s disease. These conditions are both frequency misdiagnosed as Alzheimer’s disease. They found that in patients who had Parkinson’s disease but had not yet developed dementia, the computer models could distinguish between Alzheimer’s and Parkinson’s. However, for patients with Lewy body disease or Parkinson’s disease dementia, the models could not distinguish them from Alzheimer’s disease.

The conclusion for this study was that the SVM-ISDA is the most accurate computer model for diagnosing and predicting dementia based on PET scans. However, while the model performed fairly well in diagnosis, its ability to predict Alzheimer’s disease in patients with mild cognitive impairment was barely more than 50%, and it couldn’t distinguish Alzheimer’s from other forms of dementia.

This highlights how much research is still needed to be able to predict patients’ prognosis. Earlier diagnosis could mean earlier administration of treatments, which might make them more effective in slowing or preventing the onset of Alzheimer’s disease. It would also allow patients and their families more time to plan for the future.

 

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What “Childhood Alzheimer’s Disease” Can Teach Us About the Brain

Niemann-Pick disease type C (NPC) is a condition you’ve probably never heard of. It’s an extremely rare disease, occurring in approximately 1 in 100,000 live births. But despite its rarity, the strange connections between NPC and a much more common condition, Alzheimer’s disease, are now leading researchers to consider how the connected mechanisms of these two diseases may help us in our search for a cure.

What Is Niemann-Pick Disease?

Children with NPC, including Addison and Cassidy Hempel shown in this article’s top image, typically appear normal until reaching middle to late childhood. Around that age, they begin experiencing subtle symptoms such as clumsiness, poor handwriting, and impaired speech. Some children lose the ability to move their eyes up and down or side to side. These problems gradually worsen over time, with affected children eventually losing the ability to speak or swallow. They may also develop seizures, involuntary muscle contractions, or other movement disorders.

Perhaps even more tragic than the physical symptoms are the effects of NPC on the brain. Children with this condition experience a progressive loss of memory and cognition, which has led to the disease’s unofficial name of “childhood Alzheimer’s disease.” Eventually, after a decline that can last many years, these children succumb due to respiratory failure or severe seizures. There is currently no effective cure or treatment.

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These images from the National Niemann-Pick Disease Foundation show the tragic progression of this disease in a child.

The Cholesterol Connection

NPC is caused by a mutation in one of two genes, known as NPC1 and NPC2. These genes are necessary for cells to be able to process and transport cholesterol. While cholesterol is often seen as something to avoid in our diets, we actually require a small amount of it to survive. Our cells need cholesterol to create new membranes or synthesize steroid hormones. When we consume cholesterol, it gets engulfed in cellular compartments called lysosomes, where it is processed and later released into the cell membrane. In people with NPC, cholesterol can’t be properly processed, so it gradually accumulates inside their lysosomes, especially within neurons. With all their cholesterol trapped, the neurons eventually begin to degenerate and die.

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This image shows the spleen of a patient with NPC. The white blobs are large accumulations of cholesterol. Image Source

NPC is an extreme example of what can happen when cholesterol metabolism goes awry. However, it’s not the only neurological disease that cholesterol plays a role in. People with Alzheimer’s disease, the most common form of dementia, tend to have higher levels of cholesterol in their brains than healthy controls. This may result in increased production of amyloid-beta, a toxic protein that’s considered one of the main causes of Alzheimer’s disease. Interestingly, patients with NPC also show increased levels of amyloid-beta in their cerebrospinal fluid, as well as the accumulation of tau (another toxic protein related to Alzheimer’s disease) inside their brains.

The connections between NPC and Alzheimer’s disease don’t stop there. Studies have found that mutations in NPC1 and other genes involved with cholesterol metabolism lead to an increased risk of Alzheimer’s disease. This suggests that cholesterol could be a key contributor to the neurodegeneration that occurs in both Alzheimer’s disease and NPC.

Where We Go From Here

Rare diseases like NPC are largely ignored by pharmaceutical companies, simply because they aren’t common enough for the research and development of a drug to turn a profit. While each of these diseases by itself is extremely uncommon, because there are thousands of different conditions out there, it’s estimated that 25 million Americans suffer from a rare disease. Most of these have no effective treatment.

Studying rare diseases may not be profitable, but they’re still incredibly important. As previously discussed in a fantastic SciShow video, rare diseases can often provide insight into the causes of more common conditions that share the same underlying mechanism. NPC and Alzheimer’s disease provide just one example of how researching cures for a disease that affects only a few thousand people worldwide could help us to learn about another condition that kills millions every year.

 

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How Music Impacts Alzheimer’s Patients

This article is a guest post by Carolyn Ridland, the founder of CaregiverConnection. You can read more about Carolyn at the bottom of this page.

It is challenging to watch a loved one go through problems with memory and thinking and exhibit behavioral changes that are characteristic of Alzheimer’s disease. Even more challenging is the fact that the condition develops very gradually until a point reaches where the patient cannot coordinate the normal day to day activities. While it might be impossible to treat the condition, there is a spectrum of therapies that have been suggested and deemed very useful in reversing the progression of the disease. One of these therapies is the use of music. Many people who have a loved one with the condition are glad to try anything that might work, but the important question is, how does music affect the function of the brain, and what impact will it have on a patient with Alzheimer’s?

How does Alzheimer’s affect the brain?

Most people think that Alzheimer’s and dementia, in general, are a regular component of the aging process. However, it is not a normal part of aging, despite that its greatest risk factor is age. There are people who start exhibiting symptoms of Alzheimer’s disease before they reach 65, which is known as early-onset. It is known that the brain typically shrinks with age, but it does not typically lose its neurons; this is not the case with Alzheimer’s patients. In fact, as they age, the neurons get destroyed, and this widespread damage makes most neurons lose their connections with each other, impairing metabolism, communication and repair (Jacobsen et al., 2015). The disease eats away at the brain function until the person can hardly function. While there is no known cure for Alzheimer’s, early detection and the use of the right therapies can help in slowing down the effects of the disease.

Music therapy for Alzheimer’s patients

Studies have shown that when patients who suffer from Alzheimer’s are led through songs that they recognize, their cognitive abilities are boosted, and they are able to recall memories and emotions tied to the songs. When participants with Alzheimer’s took a test on cognitive ability and life satisfaction, those that listened or sang during the test scored better in the test. Here are ways in which music could be beneficial to your loved one with Alzheimer’s.

Music evokes emotions that are attached to memories

Everyone has music pieces which are attached to very specific memories. These tied connections stay in the brain for decades, and the moment that the song is played, the attached emotions come flowing back, bringing with them the attached memories. Since a patient with Alzheimer’s is already having a hard time dealing with their memories, there is no better ways to trigger them than to play their favourite songs.

Musical aptitude and appreciation is the brain ability that stays the longest

As mentioned, people who suffer from Alzheimer go through a gradual loss of their cognitive abilities until their brain function completely deteriorates. However, the great news is that as the other abilities fade away, the ability to remember and appreciate music and the attached memories remains much longer than many others. This means that you can use music as a way of connecting with your loved one when they can no longer discuss their childhood or the memories which you made together. In addition, by playing music, you will make the person feel that they are still good at something, which makes them feel good.

Singing becomes a hobby

There is nothing that is more frustrating to a person with Alzheimer’s than the knowledge that they knew how to do something such as playing chess, but for some reason, they no longer can do it. Well, if your loved one’s condition has gotten to the point where they no longer remember these activities which they once used to enjoy, think about introducing music because it brings along fun games such as karaoke, sing along, and dancing games. Research shows that a simple act of watching music stimulates certain areas of the brain, which helps the patients exercise and polish their mind-power.

Music as a mood booster

People who have dementia tend to have a constant feeling of the blues and lots of episodes of stress induced agitation. Music has the ability to calm the listener’s nerves, elevate their mood and stimulate positive interactions with others. The good thing about music and especially the instrumental part of it is that it does not need a lot of cognitive processing, which means that it will not need a person with dementia to use their cognitive function to enjoy.

How to select the right music

The mental health and cognitive benefits that patients with Alzheimer’s get from listening to music are endless. It is therefore important to make sure that you include it in their daily routine. When choosing music for a loved one, always consider the following factors:

  • Consider the preferences that your loved one used to have. Using music as a mood booster will only work when the music is something the person can relate with.
  • To set the mood using music, play slow and mellow tunes when you want them to wind down and sleep. On the other hand, when you want them to get active, play faster beats.
  • Encourage movement when playing the music by inviting the person to dance with you or asking them to sing along.
  • When you are playing the music, try your best to cancel out all other sources of noise as you do not want to overstimulate their brain and agitate them.
  • Pay attention to the response which they give to each type of music. The response is what will guide you towards ticking the songs they like and eliminating those that they do not.

Those are a few important things to know about the use of music to help Alzheimer’s patients cope better with their condition and enjoy life. Keep looking for creative ways to incorporate music into their day to day life, and this may even help them hold on to their memories for an even longer time.

 

Middle Aged Woman Smiling With Hands On CheeksThis article is a guest post by Carolyn Ridland, the founder of CaregiverConnection. About 10 years ago, her parents began reaching the point where they could not be self-sufficient anymore. She was just married with two toddlers, so she felt like she couldn’t take them in, yet she wanted to make sure they were taken care of. Carolyn wanted to share her story, and to let others know that they are not alone if they are in a similar position. Children are expected to take care of their elderly parents when the time comes, but it’s not always that easy. Caregiver Connection emerged from a place of real love and compassion. They understand the struggle that exists when you care deeply about your loved ones, but you’re faced with decisions you never wanted to make. Their main message is that nobody should have to face these times alone.

 

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Ketogenic Drug Shows Promise in Early Clinical Trials for Alzheimer’s Disease

There’s a lot of hype surrounding the ketogenic diet, but unlike many other fads, this one may actually have the potential for real benefits. In a study published this week in Experimental Gerontology, researchers tested a recently-developed drug called caprylidene that can simulate the effects of the ketogenic diet.

A small cohort of sixteen Alzheimer’s disease patients was recruited for the study. Fourteen of them were randomly assigned to take caprylidene for 45 days, while the other two took a placebo. The researchers administered brains scans before and after the 45-day period to monitor any changes in the patients’ cerebral blood flow.

They found that most of the subjects who took the caprylidene had higher blood flow in several regions of the brain. This suggests that the drug enhanced the patients’ abilities to metabolize energy in these specific regions. However, the drug seemed to have no effect on patients who possessed the APOE4 allele, a genetic variant that is associated with a greater risk of Alzheimer’s disease.

This small study provides some evidence in favor of the ketogenic diet as a possible treatment for neurodegeneration. As I’ve discussed in one of my previous articles (see Alzheimer’s and Coconut Oil: What does the science say?), the ketogenic diet is based on shifting your body’s primary energy source from carbohydrates to fats. When you deprive your body of glucose, this induces a state of “ketosis,” in which your liver begins breaking down fat stores to form another type of energy-storing molecule called ketones.

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An overview of the ketogenic diet. Image Source

Recently, evidence began to emerge that suggested the ketogenic diet could be useful for people with Alzheimer’s disease. Studies show that the brains of Alzheimer’s patients have a harder time metabolizing glucose, which causes their neurons to be starved for energy. This has led some to suggest that by providing neurons with ketones, the ketogenic diet might allow the brain to access an alternative energy source and perhaps restore some function.

Those of you who have cared for a loved one with Alzheimer’s disease may recognize that implementing a strict dietary plan like the ketogenic diet is next to impossible. This makes drugs like caprylidene, which induces ketosis artificially, a useful alternative.  While the small number of subjects used in this study is cause for caution, it suggests possible merit to this hypothesis and a need to replicate these intriguing findings with a larger sample size.

 

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