Tag Archives: neuroscience

Amyloid-Beta: Villain or Hero in Alzheimer’s Disease? (Podcast)

Last week I was interviewed on Straight from a Scientist, a podcast series where scientists talk about their research for a general audience. In Part 1, which you can listen to here, we had an informal conversation about my research and background. You can now listen to Part 2, a roundtable segment where the host, Connor Wander, and I discuss current topics in Alzheimer’s disease research, including a new look at the physiological roles of amyloid-beta. Enjoy!


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AlzScience Interview on Straight from a Scientist Podcast

Straight from a Scientist is a podcast series where scientists talk about their research for a general audience. I recently had the amazing opportunity to be interviewed on the show, and I’ve pasted the link below where you can listen to it. It was a great discussion about Alzheimer’s disease, axon guidance, and life as an undergraduate researcher. Be sure to stay tuned for the show’s Alzheimer’s Disease Roundtable episode, which should be coming out within the next week.


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Vascular Damage May Affect Progression to Alzheimer’s Dementia


Guest author: Rachana Tank has a master’s degree in Neuropsychology from Maastricht University in the Netherlands. Her goal is to pursue a PhD in psychology exploring cognitive ageing, where her research interests lie.

As we grow older, we tend to become a little forgetful which is thought to be a normal part of ageing, but when does forgetfulness turn into abnormal ageing? Sometimes even slight but noticeable changes in thinking skills can be symptoms of an underlying issue. Alzheimer’s dementia is a continuous process, a progression taking place over many years, during which individuals experience considerable deficits before reaching clinical dementia. Stages leading up to Alzheimer’s dementia are referred to as predementia stages and are considered to be on the spectrum of Alzheimer’s dementia. In such stages, cognitive deficits are typically experienced as deterioration of memory, attention, and language skills.

Predementia stages can include individuals who self-report a decline in cognitive abilities (subjective cognitive impairments), or experience cognitive impairments that can be diagnosed by standardised testing (mild cognitive impairments). Both of these can, but not always, indicate an initial phase of neurodegeneration that may suggest they are in an early stage of Alzheimer’s dementia.


The difference between normal brain ageing (purple line) and stages of cognitive decline experienced as part of abnormal brain ageing in dementia. Image source

Individuals with subjective or mild cognitive impairments tend to have a higher incidence of future cognitive decline than the general population and more often show Alzheimer related pathology. However, it is still difficult to predict which individuals in these stages will progress to Alzheimer’s dementia.

Differentiating between those who will progress and who will not is a difficult task. However, biomarkers can be utilised to indicate the presence of Alzheimer’s pathology to detect and diagnose predementia stages. Namely, amyloid protein plaques and neurofibrillary tau tangles are the hallmarks of Alzheimer’s disease, with amyloid pathology being the earliest identifiable change in the brain. Although amyloid and tau have both been fundamental to understanding and estimating the pathological cascade, there is a lot of emerging evidence to suggest that it is not just tau and amyloid in isolation that contribute to progression of Alzheimer’s pathology and subsequent cognitive symptoms.

As evidence indicates there is more to consider than amyloid and tau, recent research, including my master’s research, investigates mixed Alzheimer’s pathology in early stages. Mixed pathology refers to hallmark Alzheimer pathology, such as amyloid and tau, that coexist with additional abnormalities such as vascular disease. Vascular disease is of particular interest in predementia stages as it is the most common disease to coexist with typical Alzheimer pathology early in the disease process.

Vascular disease can be defined as any condition that affects the arteries, veins, and capillaries responsible for carrying blood to and from the heart. Vascular damage can compromise brain health by reducing blood flow to vital areas, leading to loss of neurons. Such damage to the brain affects how well certain areas function, sometimes leading to decreased cognitive abilities such as language difficulties, attention problems or memory issues. There is evidence that vascular disease shortens time to progression when coexisting with traditional Alzheimer pathology. However, the mechanisms by which they may interact is not known.


Arterial plaques are one example of vascular disease. Image source

My research investigated mixed pathology in 269 memory clinic patients aged 39 or older with subjective or objective cognitive impairments. Levels of amyloid burden and vascular damage were recorded at baseline and at follow-up between 1 and 5 years later. Those who progressed to Alzheimer’s dementia were then compared to those who did not. Vascular damage was assessed using MRI scans, and level of amyloid pathology was determined via cerebrospinal fluid samples.

The results of my research found that Alzheimer’s disease patients with vascular damage had less amyloid in their brains than Alzheimer’s patients who did not have vascular damage. This suggests that vascular damage may worsen the effects of amyloid plaques on cognitive decline and Alzheimer’s. These findings are compatible with other studies that investigated vascular damage in relation to amyloid burden.

Different amounts of amyloid in patients did not show any direct relationship with vascular damage, suggesting that the presence or absence of vascular disease does not influence the presence of Abeta. However, both vascular damage and amyloid pathology increased the risk of progressing to Alzheimer’s dementia significantly, and 93% of individuals who progressed to Alzheimer’s dementia showed abnormal levels of both amyloid and vascular pathology, indicating that both contribute to the development of Alzheimer’s dementia. These research insights help us to better understand early stages and the influencing factors involved. This allows us to develop interventions, for example, promoting cardiovascular health in those at risk by encouraging memory clinic patients to participate in exercise programs.

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Macular Degeneration: Alzheimer’s Disease of the Eye?

Macular degeneration affects more than 10 million Americans, making it the leading cause of vision loss. It occurs when, for reasons that aren’t entirely understood, the central region of the retina (known as the “macula”) begins to deteriorate. The disease is considered incurable and usually occurs in people over the age of 55. Smokers and individuals of Caucasian decent are at an increased risk, as well as anyone with a family history of the disease.


This animation from the American Macular Degeneration Foundation shows the loss of central vision that occurs with this disease.

Surprisingly, there are many parallels between macular degeneration and Alzheimer’s disease. Though the two conditions may seem unrelated, both are believed to be caused by the buildup of a toxic protein called amyloid-beta. In Alzheimer’s disease, amyloid-beta plaques accumulate in the brain, while in macular degeneration, amyloid-beta forms fatty deposits behind the retina called “drusen.” Plaques and drusen appear to have similar composition of proteins and fats, and utilize the same mechanisms to damage surrounding tissue.


Diagram of a normal eye and an eye with macular degeneration. Image Source

The similarities between these two diseases don’t end there. Older people with macular degeneration are three times as likely to have cognitive impairment, suggesting that the same processes leading to amyloid-beta accumulation in the retina could also be occurring in the brain. This makes sense, since the retina and the brain are both part of the central nervous system. Additionally, several mouse models of Alzheimer’s disease exhibit amyloid-beta buildup in both the brain and the retina, further cementing the link between the two conditions.

The emerging connection between Alzheimer’s and macular degeneration has several important consequences. If amyloid-beta buildup in the retina could be a sign of a similar process happening in the brain, it raises the possibility that eye exams could serve as a non-invasive method to screen people for Alzheimer’s disease. Clinical trials for this idea are still ongoing, but the early results seem encouraging. These eye exams could potentially allow for earlier Alzheimer’s diagnosis or a lower risk of misdiagnosis.

This relationship also suggests that people with Alzheimer’s disease could be at a greater risk of macular degeneration, or vice versa. If you or a loved one is experiencing dementia, it’s recommended to minimize the risk of macular degeneration by receiving regular eye exams, protecting the eyes from sunlight, and maintaining a healthy diet.


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Anxiety and Depression May Be Early Signs of Alzheimer’s Disease

Though most people with Alzheimer’s disease aren’t diagnosed until after age 65, the disease can begin in their brains years or even decades before that. For this reason, scientists have been trying to identifying biomarkers that will allow us to diagnose Alzheimer’s at an earlier stage, prior to the onset of cognitive symptoms.

In a study published last week in The American Journal of Psychiatry, researchers from Harvard University examined 270 subjects aged 62 to 90, all of whom lived in a retirement community and initially showed no signs of cognitive impairment or mental illness. The subjects were given a test for geriatric depression and a PET scan of their brains annually for five years.


Researchers used a PET scanner like this one to examine amyloid-beta levels in the subjects’ brains.

At the beginning of the study, participants who had depression had higher levels of amyloid-beta, a toxic protein linked to Alzheimer’s disease, in their brains. Furthermore, participants with higher amyloid-beta levels at baseline had steeper increases in their geriatric depression scores after five years. These results suggest that a sudden development or worsening of depressive symptoms could be a sign of early Alzheimer’s disease.

Next, the researchers looked at the participants’ subscores for different sections of the depression test. They found that only the anxiety subscore was correlated with amyloid-beta levels. The other two subscores, which relate to apathy and unhappiness, had no relationship to amyloid-beta. This suggests that anxious-depressive symptoms are the strongest predictor of early Alzheimer’s disease.

It’s difficult to determine from this study whether anxiety or depression could lead to Alzheimer’s disease, or if instead preclinical Alzheimer’s causes anxiety/depression. It’s likely that there are many other factors at play, such as social interaction, diet, and exercise levels. Additionally, the small sample size prevents us from drawing broad conclusions. However, the authors of the study are currently working on a follow-up analysis of these subjects, which should illuminate whether the people with higher amyloid-beta levels went on to be diagnosed with Alzheimer’s disease.

In the meantime, if you or a loved one notices a sudden increase in anxious-depressive symptoms, this should be taken seriously and brought up with a doctor. An earlier Alzheimer’s disease diagnosis, prior to the development of dementia, may allow our drugs to act more effectively and slow the rate of cognitive decline.


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What Naked Mole Rats Can Teach Us About Alzheimer’s Disease

Yes, you read that title correctly. I’m talking about naked mole rats, the burrowing hairless rodents with a face only a mother could love. You might just know them for their strange appearance, but naked mole rats have fascinated scientists for decades due to their extreme longevity. They are by far the longest-lived rodent species, with a maximum lifespan of more than 30 years, compared to only 2 years for your typical mouse. They also are practically immune to cancer, for reasons we don’t entirely understand.

So what does this have to do with Alzheimer’s? Well, another one of the naked mole rat’s strange quirks is that is possesses extremely high levels of amyloid-beta, the toxic protein that is believed to cause Alzheimer’s disease. In humans, amyloid-beta aggregates into sticky plaques in the brain, which can cause a whole host of problems. Amazingly, naked mole rats have even higher amyloid-beta levels than 3xTg-AD mice, which are an Alzheimer’s mouse model genetically engineered to over-produce amyloid-beta. However, the amyloid-beta found in naked mole rats is less sticky and does not tend to form plaques, despite being just as toxic to neurons. Additionally, while amyloid-beta in humans increases as we age, its levels remain constant in naked mole rats. This suggests that amyloid-beta could be harmless (or possibly even beneficial) when it’s present in its non-sticky form. A 2015 report also found that the brains of old naked mole rats look more like what you’d expect to see in a baby animal’s brain, with high numbers of new neurons constantly being formed.

The fact that naked mole rats possess exceedingly high levels of amyloid-beta throughout their lifespan, yet do not develop Alzheimer’s disease, makes them an extremely useful research subject. If scientists can unravel what makes these rodents so resistant to amyloid-beta, we might be able to apply this finding to humans in the form of a treatment for Alzheimer’s disease. So even though they may not be the cutest creatures, you might someday have the naked mole rat to thank for keeping your brain healthy!

Here are some more fun facts about naked mole rats! They have no sense of pain and are nearly blind. They are almost entirely cold-blooded, relying on their environment to regulate body temperature. In order to live underground, naked mole rats have evolved very low rates of breathing and metabolism, and can survive for up to 5 hours in low-oxygen conditions. They live in eusocial colonies similar to ants or bees, with a single queen that produces all the colony’s offspring.


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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)


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