Tag Archives: dementia

Alzheimer’s and Coconut Oil: What Does the Science Say?

Coconut oil has certainly been a health craze over the past few years, with people claiming it can do everything from whiten your teeth to promote weight loss. Recently I’ve had several readers ask me to look into claims that coconut oil could treat or cure Alzheimer’s disease. So let’s dive into the details and figure out whether coconut oil could really be healthy for your brain.

Ketones and Where to Find Them

Most explanations for coconut oil’s supposed miraculous properties focus on its high ketone content. The “ketogenic diet,” sometimes shortened to the “keto diet,” has recently seen a surge in popularity. The idea behind the keto diet is to shift your body’s primary energy source from carbohydrates to ketones. Normally, the carbs in the food you eat are converted into glucose (aka sugar), which your body then uses for energy. However, when your carb intake is very low, a backup mechanisms called ketogenesis kicks in. Your liver starts breaking down fat into ketones, another type of energy-storing molecule similar to glucose but with a different chemical structure.

To induce ketosis, people cut back on their intake of carbs to less than 20 grams per day (equivalent to half a cup of pasta or one slice of bread), compared to the 225 to 335 grams that most people consume daily. To compensate for the reduced calories, they also increase their consumption of fats. Coconut oil is especially popular in keto diets because it is rich in medium-chain triglycerides, a type of fat that your body can easily convert into ketones. By maintaining a low-carb diet for an extended period of time, your body shifts toward utilizing fat as its primary energy source. As a result, your pancreas starts producing lower levels of insulin, the hormone that tells your body to store glucose as fat. The idea then is that less of what you eat gets stored as body fat and more gets burned for energy, and so you lose weight.

An overview of the ketogenic diet. Image Source

How Ketones Affect the Brain

In general, most studies have suggested that the keto diet could be an effective weight loss tool, though research on its longer-term effects remains limited. But what effect does it have on the brain? The idea that coconut oil and other ketogenic foods could help with Alzheimer’s disease comes from studies showing that Alzheimer’s patients have lower glucose metabolism in their brains. This means that their brains have trouble utilizing glucose for energy, which could result in cognitive impairment. This tends to be worse in people with diabetes, perhaps one of the reasons why diabetics are at an increased risk of Alzheimer’s. (See Alzheimer’s Disease: Diabetes of the Brain?)

That’s where coconut oil might come in. Since their brains have trouble metabolizing glucose, perhaps Alzheimer’s patients could substitute ketones as an alternative source of energy. Research shows that ketone metabolism in normal in Alzheimer’s brains, providing hope that this could be a possibility. A recent study also showed that neurons incubated with coconut oil and then exposed to amyloid-beta (a toxic protein associated with Alzheimer’s disease) had increased survival compared to neurons not treated with coconut oil.

Unfortunately, clinical trials in humans are lacking. I was only able to find one small study from Spain, in which 22 Alzheimer’s patients were given 40 mL of coconut oil daily for three weeks. They found that these patients scored better on a memory test than others who did not receive coconut oil. However, the sample size was very small and they also did not include a placebo in the control group, so it’s difficult to say how meaningful these results really are. Other clinical trials studying different types of ketogenic compounds to treat Alzheimer’s disease have seen only limited success in a small subset of participants.

What’s the Verdict?

While it’s possible that it could help you lose weight or provide other health benefits, there’s just not enough evidence to say whether or not coconut oil and other ketogenic foods could reduce the risk of Alzheimer’s disease. On the other hand, there are some possible risks associated with it. Consumption of coconut oil in large quantities can lead to gastrointestinal problems, and its high saturated fat content also makes it a risk factor for heart disease or obesity. However, incorporating a small amount of coconut oil into your diet could be beneficial if you offset those calories with reduced carb intake. That being said, it’s unlikely that coconut oil or any ketogenic diet alone will be enough to dramatically alter your risk of Alzheimer’s disease. (To learn about real ways you can reduce your risk, see How to Reduce your Dementia Risk in 2017)

 

Enjoy this post? Help it to grow by sharing on social media!
Want more? Follow AlzScience via email, Facebook, or Twitter!
Advertisements

Could Young Blood Cure Alzheimer’s Disease?

You may have heard the buzz lately about research surrounding the use of young people’s blood to treat Alzheimer’s disease. The latest findings were presented at the recent Clinical Trials on Alzheimer’s Disease conference, as reported by TIME Magazine. After previous studies showed that injecting an old mouse with the blood of a younger mouse (a process called parabiosis) caused improved memory and cognition, neuroscientists have been curious to see whether the same effect could be true in humans.

A group of researchers from Stanford conducted a small clinical trial to test this idea. They recruited 18 elderly volunteers and injected them weekly with young people’s blood plasma (taken from a local blood bank) or a placebo over the course of four weeks. They found that those receiving the young plasma treatments showed significantly enhanced measures of independence, including ability to shop for themselves or balance their own checkbook. No harmful side effects were noted.

The researchers did not study the subjects’ memory or cognitive ability as part of the trial, but these measures are being planned for future studies with a larger sample size. While still very preliminary, this small trial does suggest that there could be some factors in young people’s blood that could improve cognition in older people. While it’s far too early to start storming the blood banks demanding a transfusion, the link between our brains and our blood suggests that we need to be paying particular attention to our cardiovascular health as we age.

 

Enjoy this post? Help it to grow by sharing on social media!
Want more? Follow AlzScience via email, Facebook, or Twitter!

Spinal Cord Injury May Increase the Risk of Alzheimer’s Disease

It may be surprising to some people to learn that physical injuries can contribute to neurodegenerative diseases. In mice, traumatic brain injuries have been previously shown to induce an Alzheimer’s-like condition, complete with amyloid plaques and neuroinflammation. In a study published this week in the journal Spinal Cord, researchers from the National Taiwan University investigated whether a similar connection exists between spinal cord injuries (SCI) and Alzheimer’s disease.

The researchers utilized medical records from Taiwan’s National Health Insurance Research Database. Their analyses included 9,257 individuals with an SCI and 37,028 non-SCI individuals, with an average age of approximately 63 years. When selecting the subjects for the study, the researchers applied an algorithm that would correct for the effects of other Alzheimer’s disease risk factors, such as age, sex, and cardiovascular health.

Over the course of a three-year period, a total of 25 SCI inviduals and 57 non-SCI individuals were diagnosed with Alzheimer’s. These numbers are quite low, possible due to the difficulty in diagnosing Alzheimer’s with high certainty, since its symptoms are similar to other forms of dementia. Cumulatively, the incidence of an Alzheimer’s diagnosis during the three-year study period was 71% higher in people with a SCI compared to people without a SCI. (I want to emphasize that this does not mean SCI patients are 71% more likely to get Alzheimer’s over their entire lifetime; this number only applies to the three-year period examined in this study.)

This figure from the paper shows the incidence of Alzheimer’s disease over a three-year period. The SCI individuals had an increased risk of Alzheimer’s than the non-SCI individuals.

This study is the first large-scale, longitudinal analysis to demonstrate a correlation between SCI and Alzeimer’s disease. Future research is warranted to determine what might be causing this connection. The authors suggested several possible explanations. It has been previously shown that tau and the amyloid precursor protein are deposited throughout the spinal cord following a SCI. These proteins are both closely linked to the pathogenesis of Alzheimer’s disease, so this could be a possible disease mechanism. Another possibility is that the widespread inflammation triggered by a SCI could perturb the delicate chemistry of molecules within the brain.

There are several important caveats to note with this study. For one thing, while the researchers accounted for health-related Alzheimer’s risk factors, including various medical conditions like diabetes and stroke, their records did not include information about lifestyle-related risk factors, such as smoking or exercise. These factors could have potentially skewed the analysis. Also, since the follow-up period was only three years, the data does not give us information about any longer-term effects of SCI. Finally, while the total sample size was large, only a small subset of subjects were diagnosed with Alzheimer’s, reducing the statistical power of the analysis. Future studies will need to address these problems in order to provide further insight into the emerging connection between SCI and Alzheimer’s disease.

 

Enjoy this post? Help it to grow by sharing on social media!
Want more? Follow AlzScience via email, Facebook, or Twitter!

Study Shows How Alzheimer’s Affects Men’s and Women’s Brains Differently

Women are around twice as likely to develop Alzheimer’s disease during their lifetimes compared to men. This effect is also seen in mouse models of the disease. When mice are genetically engineered to developed Alzheimer’s, the female mice tend to have an earlier diseae onset and more severe pathology compared to hte male mice. The reasons for this discrepancy are unknown. However, a recent study published in Neurobiology of Aging attempted to shed some light on the mystery.

The researchers were interested in studying adult neurogenesis, which is our brains’ ability to create new neurons throughout our lives. Neurogenesis primarily occurs in two areas of the brain: the olfactory bulb, which is involved with the sense of smell, and the hippocampus, which is important for memory. In this study, the scientists wanted to figure out whether neurogenesis in the hippocampus was different for male and female mice with Alzheimer’s disease.

First, they subjected the mice to a test designed to test spatial memory, which is particularly important for the hippocampus. They placed the mice in a container with two objects and allowed them to explore for a few minutes. The next day, they placed the mice back in the container, but now one of the objects had been moved to a new location. We would expect the mice to spend more time sniffing and investigating the object that had been moved, and less time sniffing the object that was in the same place as before.

Screenshot 2017-10-13 12.44.30.png

When one of the cups is moved to a new location, the mouse should spend more time sniffing it compared to the cup that wasn’t moved. This test is used to analyze the mouse’s spatial memory. Image Source

The result was interesting. While the male mice had no trouble rembering which cup had been moved, the female mice did significantly worse, spending the same amount of time sniffing both of the cups. This suggested that the female mice might have some impairment in their spatial memory.

Next, the researches looked at the mice’s brains. They used a technique that caused all newly-born neurons to be labeled bright green, and counted how many neurons were born in the hippocampus during a two-week period. The male mice produced more than four times as many neurons as the female mice. Conversely, the female mice had nearly twice as many astrocytes in their hippocampi compared to the males. Astrocytes are another type of brain cell that is often associated with inflammation. These results suggested that the female mice’s brains were producing many astrocytes but few neurons, perhaps contributing to their impaired spatial memory.

Screenshot 2017-10-13 12.54.35.png

This image from the paper shows astrocytes labeled in red. In the top right panel, you can see that the female Alzheimer’s (APP/PS1) mice have far more red area than the males, indicating a greater number of astrocytes.

The results of this study suggest that the brains of female mice with Alzheimer’s may be devoting so many resources to creating new astrocytes that there’s not enough left to create neurons. However, it opens up many new questions. What is causing this overproliferation of astrocytes in the female mice? The authors of the paper suggest estrogen as a possible cause, since this hormone has been shown to influence memory. Additional studies are needed to determine the true cause.

 

Enjoy this post? Help it to grow by sharing on social media!
Want more? Follow AlzScience via email, Facebook, or Twitter!

New Alzheimer’s Study Sheds Light on the Mysterious Tau Protein

If you’re a regular reader of AlzScience, you know that Alzheimer’s disease is believe to be caused by two toxic proteins that accumulate in the brain: amyloid-beta and tau. (For more background, see Alzheimer’s Disease: A General Overview.) Recently, it’s been shown that tau is actually a better predictor of Alzheimer’s disease progression than amyloid-beta, suggesting that this mysterious protein might have a larger role in the disease than we once thought.

plaque-tanglesRNO

Amyloid-beta plaques and tau tangles form toxic clumps in the brains of Alzheimer’s patients. Source

A study published last week in Nature provided deeper insight into tau. The scientists were interested in studying the ApoE gene, which is considered the strongest genetic risk factor for Alzheimer’s (see The Genetics of Alzheimer’s Disease.) Specifically, having two copies of the ApoE4 allele increases your risk of Alzheimer’s by nearly 15 times, and it’s been shown that people with this allele have greater buildup of amyloid-beta in their brains. However, the researchers in this study wanted to see whether ApoE could also affect tau accumulation.

To test this, they used genetically engineered mice that overexpress the tau gene, causing them to develop many of the symptoms of Alzheimer’s. They then tampered with these mice’s genes so that they would also overexpress ApoE4. (Note: Overexpressing the tau and ApoE4 genes means those genes were more active than they normally would be in the mice. Think of it like a light switch stuck in the “on” position.) They found that these mice had more tau in their brains, and also more severe brain shrinkage due to neuronal death.

Screenshot 2017-09-29 17.29.13

This figure from the paper shows brain slices from different mice. The far left panel shows a healthy mouse brain. The next two (representing the ApoE2 and ApoE3 alleles) have slightly more brain atrophy, while the harmful ApoE4 allele causes very severe atrophy. In contrast, the far right brain, which does not express ApoE at all, has relatively little atrophy.

To figure out how ApoE4 might be causing more tau accumulation, the researchers looked at the mice’s microglia, the immune cells of the brain. The microglia overexpressing ApoE4 tended to overreact to infections, releasing high amounts of pro-inflammatory molecules called cytokines. Neurons and other brains cells are very sensitive to cytokines, and high levels might cause them to produce more tau.

Finally, the researchers turned to human research. They used postmortem brain tissues taken from people who had tauopathies, which are diseases caused by accumulation of tau (but not amyloid-beta) in the brain.  The people possessing the ApoE4 allele had more severe neurodegeneration and greater tau buildup in certain areas of the brain.

Overall, this study demonstrates that ApoE4 does not only act on amyloid-beta, but tau as well. It gives strong support to the notion that tau may be as important as amyloid-beta in understanding the pathology of Alzheimer’s disease. In an interview with Science News, Harvard neurologist Dennis Selkoe described this deadly combination of amyloid-beta and tau as a “double whammy.” Yet this study provides hope that future therapies against ApoE4 could be capable of halting both of these toxic proteins at once.

 

Enjoy this post? Help it to grow by sharing on social media!
Want more? Follow AlzScience via email, Facebook, or Twitter!

Artificial Intelligence Could Help Us Predict Alzheimer’s Disease

Many experts agree that preventing the progression of Alzheimer’s disease is much more effective than trying to reverse it once the damage is done. This makes early diagnosis critical. Unfortunately, most Alzheimer’s patients are not diagnosed until relatively late in disease progression, when toxic amyloid plaques have already accumulated in their brains to potentially irreversable levels. However, this might soon be changing with the recent surge in artificial intelligence technology.

figure1.jpg

This diagram shows the stages of Alzheimer’s disease, which can begin up to 20 years before diagnosis. Most patients are not diagnosed until the mild or moderate stage, since this is when cognitive impairments become more noticeable. Image Source

This research was described in a paper published in Neurobiology of Aging by scientists from McGill University in Canada. Their goal was to create an algorithm to predict whether people with mild cognitive impairment would progress to dementia. They utilized a noninvasive technology called positron emission tomography (PET). PET involves the patient lying inside a donut-shaped machine, similar to a CAT scanner. The machine can measure which areas of the brain have higher or lower activity levels based on how much glucose each brain region is consuming.

20_a

A patient lying inside of a PET machine. Image Source

The researchers used PET scans from 273 patients with mild cognitive impairment. 43 of these patients were diagnosed with probable Alzheimer’s disease at a follow-up appointment two years later. Then the scientists trained an artificial intelligence algorithm to predict which patients would develop Alzheimer’s based on their PET scans.

They used the data to generate the map of the brain that’s shown below. The red-colored areas indicate a higher odds ratio (OR). This means that unusual activity levels in those brain areas are associated with an increased risk of Alzheimer’s disease. For example, an odds ratio of 3 means that a person with unusual activity levels in that brain area is 3 times as likely to develop Alzheimer’s compared to someone with normal activity levels.

gr2.jpg

Figure 2 of the paper shows which brain regions are the most important for predicting the risk of Alzheimer’s disease.

The algorithm was able to predict which patients would progress to Alzheimer’s disease with an accuracy of 84%. This is better than any previously-developed PET algorithms, and comparable to more invasive diagnostic techniques such as spinal taps. This is exciting news because it suggests that a painless, noninvasive technology can be used to predict Alzheimer’s disease with a fairly high degree of accuracy.

As always, we have to point out a few problems with this study. For one thing, it’s impossible to know for sure whether the patients’ Alzheimer’s disease diagnoses performed by doctors at the follow-up appointment were actually correct. This is because many forms of dementia have similar cognitive symptoms, and can be easily confused during diagnosis. Parkinson’s disease, vascular dementia, or even a urinary tract infection can be misdiagnosed as Alzheimer’s disease. (For more info see Is it really Alzheimer’s? 10 common misdiagnoses you should know about). Only a postmortem brain analysis can reveal for sure whether the patients truly had Alzheimer’s. This muddles our ability to judge how accurate the algorithm really was.

Another problem is that PET scans can be quite expensive, costing upwards of $7,000. If a patient is incorrectly diagnosed with Alzheimer’s, this could lead to futher costs for medication to treat a disease they don’t actually have. Finally, while the mild cognitive impairment stage is earlier than most Alzheimer’s patients are diagnosed, it can still be up to ten years after the true beginning of the disease. We still have no reliable way to make diagnoses that early. Nonetheless, this study is at least a step in the right direction. With future advances in artificial intelligence, we might be able to improve our diagnostic accuracy at earlier stages of the disease.

 

Enjoy this post? Help it to grow by sharing on social media!
Want more? Follow AlzScience via email, Facebook, or Twitter!

A Third of Dementia Cases Could Be Preventable

Dementia is caused by a variety of genetic, environmental, and lifestyle factors. A new study published in The Lancet offers hope that many of us could avoid dementia by making healthier choices for our brains. The study was conducted by the International Commission on Dementia Prevention, Intervention, and Care, a panel of 24 experts assembled to conduct a review and meta-analysis of existing dementia research. The scientists concluded that with a cure to Alzheimer’s disease likely to still be years away, the best approach is to focus on prevention.

Among the contents of the report was a series of recommendations for reducing the risk of dementia. They identified nine modifiable risk factors that are responsible for 35% of dementia cases. These factors seem to act primarily at a particular stage of life:

  • Childhood: Low educational attainment
  • Mid life: Hypertension, obesity, hearing loss
  • Late life: Depression, diabetes, physical inactivity, smoking, social isolation

The researchers argue that by addressing these modifiable risk factors, a third of dementia cases could be prevented. They showed that by reducing the prevalence of these risk factors by only 10%, more than 1 million dementia cases could be avoided worldwide. The report also included several recommendations for dementia management and care. These included pharmacological treatment of dementia patients at all disease stages, individualized care tailored to each patient, managing neuropsychiatric symptoms with social or environmental interventions, and providing support for caregivers, who are at an increased risk of depression and other health problems.

A press release of the data presented at the Alzheimer’s Association International Conference noted that there are many other likely risk factors associated with dementia, including diet, air pollution, and sleep. These were not mentioned in the report due to a lack of conclusive research, but it is likely that even more dementia cases could be preventable with these other factors considered. For more information on brain health and dementia prevention, see How to Reduce Your Dementia Risk in 2017.

170720094907_1_540x360

Image Source: Keck Medicine of USC

 

Enjoy this post? Help it to grow by sharing on social media!
Want more? Follow AlzScience via email, Facebook, or Twitter!