Monthly Archives: June 2016

Book Review: “100 Simple Things You Can Do to Prevent Alzheimer’s”

“100 Simple Things You Can Do to Prevent Alzheimer’s and Age-Related Memory Loss” is a nonfiction book written by Jean Carper, a former medical journalist best known for her award-winning 1996 book “Stop Aging Now!” Carper’s most recent book lists and describes 100 tips for reducing your risk of dementia backed up by scientific data. These include having regular eye exams, eating berries every day, and learning a second language.

“100 Simple Things” is written in jargon-free language that any reader can easily understand while also presenting scientific evidence to back each claim without exaggerating the predicted results. Carper demonstrates a deep understanding of the science of Alzheimer’s disease and following even a few of her tips are quite likely to improve the health of your brain as you age. The back of the book provides an excellent guide for creating “Your Anti-Alzheimer’s Plan,” describing how to incorporate these tips into your lifestyle successfully.

One possible conflict of interest with this book is the fact that Jean Carper is the founder of a vitamin and supplement company called Stop Aging Now, best known for the anti-aging multivitamin that Carper designed. Carper sold the company before publishing this book and no longer has any financial connections, but it’s worth keeping this in mind when reading her advice on supplements. Many experts agree it’s best to get nutrients from your diet rather than from a pill whenever possible, although some supplements such as fish oil are still recommended for brain health. My only other criticism is that the book chapters can be a bit redundant. For example, at least five of the tips essentially described the importance of keeping your brain stimulated through mental activity, several others all discussed social interaction, etc. In my opinion, the book could have easily been condensed into 50 or 75 tips.

Overall, I would highly recommend this book to anyone who is experiencing or at risk of dementia, has a loved one with dementia, or simply wants to learn more about brain health. It is easy to follow, scientifically valid, and realistic for anyone to incorporate into their lifestyle.

Rating: 4.5 stars


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The Strange Link Between Alzheimer’s and Cancer

Two of the most common causes of death in America are Alzheimer’s disease and cancer. To most of us, these seem like completely unrelated diseases. However, this intuition is far from the truth. For reasons that puzzle scientists, having Alzheimer’s actually seems to protect you from cancer, while having cancer may protect you from Alzheimer’s.

This counterintuitive relationship was first discovered in 2005 by the Washington University Alzheimer’s Disease Research Center. This study of 882 elderly participants reported that the people with Alzheimer’s disease were significantly less likely to be diagnosed with cancer during the course of the study, and that those who did develop cancer did so at an older age. In 2012, the Framingham Heart Study reported that participants with Alzheimer’s disease were less than half as likely to be diagnosed with cancer during the course of the study compared to dementia-free subjects of the same age, sex, body mass index, and smoking status. A 2014 meta-analysis summarized the results of six independent papers to conclude that Alzheimer’s patients have a 42% reduced risk of cancer in their lifetime, while cancer survivors have a 37% reduced risk of Alzheimer’s. These differences remained statistically significant even after accounting for the effects of reduced life expectancy and demographic factors.

Interestingly, this inverse relationship does not seem to apply to other diseases of the central nervous system, including vascular dementia, Parkinson’s disease, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), or Down’s Syndrome. This suggests that the cancer-protective mechanism is specific to Alzheimer’s disease. Weirdly, the naked mole rat is immune to both cancer and Alzheimer’s, which may help to shed light on this strange connection. (Read more: What Naked Mole Rats Can Teach Us About Alzheimer’s Disease)

Scientists are still unsure as to why cancer and Alzheimer’s are inversely related, although several theories have been suggested. One possibility is that proteins that are needed for cells to divide and reproduce might be under-produced in Alzheimer’s patients, causing a reduction in neurogenesis (the formation of new brain cells, important for learning and memory) while also protecting from cancer by preventing uncontrolled cell division. Another theory is that amyloid beta, the protein that forms toxic clumps in the brains of Alzheimer’s patients, may fight cancer by suppressing the growth of tumors. The APOE4 allele, which increases the risk of Alzheimer’s disease, has also been associated with a reduced risk of certain cancers. Further research is needed to establish a definite mechanism.

One of the main consequences of this relationship applies to clinical trials of drug candidates to treat Alzheimer’s disease (see Where’s our cure to Alzheimer’s disease?). Several trials have had to discontinue prematurely due to an increased risk of cancer among the participants, especially skin cancers. In other words, the drugs that were supposed to be combatting Alzheimer’s disease ended up causing some participants to develop cancer. Though only a subset of trials have reported this problem, it’s worth being aware of the possibility when considering whether to participate in a clinical trial, particularly if your family has a history of skin cancer or other cancers.


Catala-Lopez, F., et al. Inverse and direct cancer comorbidity in people with central nervous system disorders: a meta-analysis of cancer incidence in 577,013 participants of 50 observational studies. Psychother Psychosom. 2014;83(2):89-105. Link
Driver, J.A., et al. Inverse association between cancer and Alzheimer’s disease: results from the Framingham Heart Study. BMJ. 2012;344:e1442. Link
Ma, L.L., et al. Association between cancer and Alzheimer’s disease: systemic review and meta-analysis. J Alzheimer Dis. 2014;42(2):565-573. Link
Roe, C.M., et al. Alzheimer disease and cancer. Neurology. 2005;64(5):895-898. Link
Roe, C.M., et al. Cancer linked to Alzheimer disease but not vascular dementia. Neurology. 2010;74(12):106-112. Link
Slattery, M.L., et al. Associations between apoE genotype and colon and rectal cancer. Carcinogenesis. 2005;26(8):1422-1429. Link


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Book Review: “Your Brain on Food”

“Your Brain on Food” is a nonfiction book written by Dr. Gary Wenk, a professor of Neuroscience and Psychology at the Ohio State University. The book gives a detailed look at how various drugs affect our brains and also touches on what these drugs can teach us about various mental disorders. The chapters are organized by the neurotransmitters (your brain’s chemical signals) that each class of drugs affects.

My first impression of this book is that it would be more aptly named “Your Brain on Psychoactive Drugs.” While there is some mention of food, including cinnamon and coffee, licit and illicit drugs are the primary focus. Though it’s true that the line between “drug” and “food” is often fuzzy (i.e., coffee is a food but also contains psychoactive chemicals), the book’s title implies an emphasis on what we’d typically consider food, which simply is not present. That being said, if you’re looking to learn more about psychoactive drugs, from why allergy meds make you drowsy to why heroin is so addictive, this book provides an excellent overview of that topic.

This book may present something of a challenge for a reader who has not taken a recent class in neuroscience or pharmacology. However, if you’re willing to keep your smartphone handy to occasionally Google unfamiliar words or topics, I believe most people will be able to get the gist of what’s being said. Whether or not you’ve partaken in illicit drug use in the past, you’ll be amazed to learn how and why each drug has such different affects on our behavior, as well as what these highs and lows have helped us to learn about the neurotransmitters that allow our brain to function.

Overall rating: 3.5 stars


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Where’s our cure to Alzheimer’s disease?

(This article was originally written for the Junior Committee of the Central Ohio Alzheimer’s Association’s blog. Click here to view the original on their website.)


Deaths from Alzheimer’s have increased dramatically, while other diseases have reduced death rates. Source

Biomedical research has made great strides in the past several decades. Our death rates for most major diseases have decreased significantly, including heart disease, cancer, stroke, and HIV. However, one conspicuous exception to this trend is Alzheimer’s disease, for which total deaths increased by nearly 70% between 2000 and 2010. Why does research on Alzheimer’s disease seem to be bearing meagre fruits, and when can we expect the next breakthrough?

To answer these questions, we need to have a bit of background on the science of the disease (for more detailed background, see Alzheimer’s Disease: A General Overview). Alzheimer’s disease is differentiated from other types of dementia by the presence of abnormal protein deposits in the brain known as amyloid beta (AB) plaques. Several studies have demonstrated that genetic mutations that increase production of the AB protein increase the risk of developing Alzheimer’s, while a rare mutation that decreases AB production is protective against Alzheimer’s (see The Genetics of Alzheimer’s Disease). This led most researchers to adopt the amyloid cascade hypothesis, which proposes that the gradual accumulation of AB in the brain is the main cause of Alzheimer’s disease. This hypothesis suggested that a cure to Alzheimer’s lay in discovering a drug that could prevent or reverse the buildup of AB plaques.

Between 2002 and 2012, more than 400 drug candidates were discovered that could dissolve AB plaques in mice. However, despite these promising results, the drugs consistently failed in human clinical trials. The patients’ symptoms improved only marginally, if at all. Even worse, many drugs came with a host of severe side effects, including skin cancer (see The Strange Link Between Alzheimer’s and Cancer), gastrointestinal problems, and micro-hemorrhaging, which forced the trials to be canceled prematurely. Hundreds of millions of dollars were spent searching for new ways to destroy the plaques, yet each new drug met the same fate.

Following this torrent of failed clinical trials, some researchers began to wonder if there was a serious problem to the way we were studying Alzheimer’s disease. The long-dogmatic amyloid cascade hypothesis was brought into question when new studies showed that nearly 1 in 3 cognitively normal people have high levels of AB in their brains, suggesting that the plaques could not be the only factor contributing to dementia symptoms.

The scientific community was initially slow to react to criticisms of the amyloid cascade hypothesis. However, in recent years, new areas of research have begun to open up that consider new mechanisms for Alzheimer’s disease development. Many exciting theories have been suggested, including the tau protein, neuroinflammation, microbial infection, mitochondrial dysfunction, and oxidative DNA damage, among others. It’s likely that all of these factors, in conjunction with Ab accumulation, contribute together to this complex disease.

With this new generation of neuroscientists approaching the problem with a fresh perspective, it’s likely that our understanding of Alzheimer’s will be radically transformed in the coming years. Though it’s impossible to predict exactly when the next breakthrough will come, the scientific community’s shift away from the amyloid cascade hypothesis toward more nuanced theories will bring our search for a cure that much closer.


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How to Be a Smart Consumer of Science News

You can hardly turn on the news or look at Facebook’s “trending” list without hearing about the latest results of some scientific study. However, the science news that is reported to the general public is often misleading. Reporters are known for twisting around a study’s results in order to make a catchier headline. If you’ve seen John Oliver’s discussion of this topic on “Last Week Tonight” (click here to watch it, it’s very interesting), you know what a serious problem this can be. Inaccurate or misconstrued scientific results have led to people believing that vaccines cause autism or that global climate change is not caused by human activity. In this article, I will provide you with five questions you should always ask when evaluating the validity of a science news claim. Keeping these questions in mind will help make sure you can tell science from pseudoscience.

Question #1: What news source am I viewing or reading?

As we all know, some news sources are more accurate and unbiased than others. Even seemingly-reputable sources like Scientific American have been guilty of representing the results of scientific studies out of context. Whenever possible, try to find a link to the original science paper, which is often provided in online news articles. This will allow you to view the results in a format that’s less likely to be biased. Pay attention to the journal in which the paper was published. Publications in larger journals like Science, Nature, Neuroscience, or PLoS1 are more likely to be both valid and important than those published in smaller, more specialized journals.

Question #2: How statistically significant were the results?

Statistical significance is the probability that the results of the study arose by random chance, rather than as the result of the experimental conditions. Each study will have a particular threshold that the ratios must be beneath for the results to be declared statistically significant. A common threshold is 0.05, meaning that there is a 5% chance of the results being due to random chance. This may seem small, but it means that there’s a 1 in 20 chance of the results being invalid. For results that are more likely to be valid, look for studies that have a lower significance threshold, such as 0.01 or 0.001.

Question #3: What model organisms were studied?

Clinical trials and other experiments conducted directly on humans are the most likely to have results that generalize to other humans. However, these often require years of supporting data to be authorized, so the majority of neuroscience and biology studies are conducted on animals designed to act as “models” for humans. Common animal models include bacteria, yeast, frogs, fruit flies, zebrafish, mice, and rats. Mice are the most common model for Alzheimer’s disease, though lately their accuracy in representing the disease symptoms has been brought into question. Whenever experiments are conducted on animals, be sure to take their results with a grain of salt.

Question #4: What were the sample size and timeframe?

Sample size is the number of humans or animals observed during the study. For noninvasive research such as online surveys, sample sizes are often hundreds or thousands of people. In contrast, studies that require surgery might have a sample size of only a few dozen. The smaller the sample size, the less likely that the results of the study will generalize to a larger population. On a similar note, you should also pay attention to the timescale of the study. Particularly for age-related diseases like Alzheimer’s, human studies conducted for only a few weeks or months may not be as informative as those conducted for many years.

Question #5: Does the study provide correlational or causational evidence?

This is probably the most important question of all, and it’s also the one that is most often ignored by popular reporting of science news. Correlational evidence (sometimes called epidemiological evidence) is based on observation, while causational evidence is based on random experimental assignment. Let me explain this distinction through an example. A famous 2002 study observed that people who consumed higher levels of caffeine were less likely to be diagnosed with Alzheimer’s disease. This is correlational because it shows that caffeine is correlated with a reduced Alzheimer’s risk, but cannot prove that it necessarily causes a reduced risk. It’s possible that people who consume more caffeine might also be more likely to exercise, have an active social life, or be more educated. In this case, one of these other factors (which are called confounding variables) might be the cause of the reduced risk, rather than the caffeine itself. In contrast, a causational study on this subject was conducted in 2006. The researchers fed lab mice different levels of caffeine and found that those with higher caffeine intake had reduced levels of amyloid plaques in their brains. In this case, the caffeine is more likely to be the cause of this result because all other variables were carefully controlled and the mice were assigned their caffeine intake randomly. An easy way to remember this difference is that correlation typically comes from studies where the subjects have free choice, whereas causation can only be established when the subjects are randomly assigned a condition by the experimenter.


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Monthly Research Update: June 2016

Alzheimer’s disease in men associated with loss of the Y chromosome

A group of Swedish researchers has found evidence that may help explain why some men could be more likely to develop Alzheimer’s than others. The researchers looked at men with lifetime-acquired loss of chromosome Y, or LOY for short. Biological females have two X chromosomes, while males have one X and one Y chromosome. Age-related loss of the Y chromosome is a fairly common condition, affecting at least 15% of men over the age of 70. LOY is associated with a greater risk of mortality (i.e., greater likelihood to die at any given age), as well as higher incidence of certain cancers. It’s not known for sure what causes LOY, though studies have found that it can be induced by smoking.

The researchers in this study looked at the prevalence of LOY in men’s blood cells to see if it was related to their risk of Alzheimer’s. They found that men with Alzheimer’s tended to have greater levels of LOY in their blood, on average nearly three times the levels of the control subjects. The reverse was also true, in that men with LOY were 6.8 times more likely to be diagnosed with Alzheimer’s during the course of the study. These results suggest a possible mechanism for the link between smoking and an increased risk of Alzheimer’s. Further studies with a larger sample size are being planned in order to confirm these results. Click to read more

A possible blood test to detect preclinical Alzheimer’s disease

Researchers from Rowan University have designed a test that may be able to detect the early stages of Alzheimer’s disease. Though these kinds of tests have been suggested before, they’ve often required extraction of cerebrospinal fluid, a painful and potentially dangerous procedure. Other tests that rely on neuroimaging are less invasive but can be expensive and less accurate. The newly-announced test is unique in that it requires only a simple blood draw. The test works by detecting autoantibodies, molecules that can target our own body’s cells for destruction by the immune system, normally as a way of clearing away dead cells and tissues. The levels of these autoantibodies are unique to each person and can be used to detect certain diseases.

The researchers first used the older test to examine cerebrospinal fluid from individuals with mild cognitive impairment. Individuals who the test deemed were likely to develop Alzheimer’s then had their blood analyzed to search for differences in the levels of various autoantibodies. The researchers identified a small set of autoantibodies whose levels in the blood could be used to distinguish people likely to develop Alzheimer’s from healthy control subjects with 100% accuracy. This test might be a faster, easier, and less expensive method than current methods for allowing early diagnosis of Alzheimer’s. However, one possible flaw with the study is that the researchers assumed the cerebrospinal fluid test to which their new blood test was compared is also 100% accurate, which so far has not been definitively proven. The test will need to be further analyzed over a longer period and with a larger sample size before it’s ready to be introduced to clinics. Click to read more

Related reading: How to Be a Smart Consumer of Science News 


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Book Review: “Still Alice”

Lisa Genova’s Still Alice is a fictional novel that tells the story of a successful neuroscientist who is diagnosed with early-onset familial Alzheimer’s disease. Throughout the book, Alice grapples with the frustrations that face anyone affected by Alzheimer’s disease, from becoming disoriented while traveling to the humiliation of incontinence. We follow her from mild cognitive decline over several years to profound dementia in the later stages of her life. The book was made into a movie in 2014.

Being a neuroscientist herself (one who parallels Alice in a variety of ways), Lisa Genova is more than familiar with the science of Alzheimer’s disease. Her discussion of the genetics of familial Alzheimer’s disease, as detailed during Alice’s visits to a genetic counselor, is both informative and interesting to read. We witness the gradual progression of Alice’s symptoms in all its unfiltered rawness. Despite being fictional, Still Alice maintains its scientific accuracy throughout the story.

Despite including discussions of genetics and neuroscience, the information is portrayed in a way that is easily understandable to the average reader. The poignant emotions and vidid imagery throughout the book make it captivating from beginning to end. The story is simultaneously heartbreaking and full of hope and beauty. An abundance of rich detail often made me forget that the story was fictional. I greatly enjoyed reading this book and would highly recommend it to anyone.

Overall Rating: 5 stars


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Alzheimer’s Disease: A General Overview

There’s a lot of misinformation floating around about Alzheimer’s disease, and sometimes it feels like you need to be a neuroscientist to sort through it all. This article will give you a brief primer on this disease and help you to understand the basics.



A portrait of Dr. Alois Alzheimer

In the year 1906, Dr. Alois Alzheimer took the stage at a meeting of German psychiatrists to present his findings on “a peculiar disease.” An fifty-year-old patient named Auguste D. had come to Dr. Alzheimer experiencing memory loss, paranoia, personality changes, and difficulty sleeping. He was baffled by her symptoms and could do little to help her. Following Auguste’s death five years later, Dr. Alzheimer performed an autopsy on her brain and discovered that it was greatly shrunken in volume. Closer inspection revealed that Auguste’s brain was full of abnormal protein deposits located in and around the neurons. Dr. Alzheimer concluded that the pathology of her brain had caused his patient’s symptoms, a revolutionary idea at a time when mind was seen as completely separate from the physical body.

To Dr. Alzheimer’s dismay, the other physicians at the conference seemed uninterested in the findings–it’s said that they were anxious to hear the next speaker, who was to discuss “compulsive masturbation,” and as a result paid little attention to Dr. Alzheimer. When he died in 1915, he had no idea of the enormity of his discovery, or that a century later the disease bearing his name becoming the sixth leading cause of death in the U.S. Amazingly, had his patient Auguste been alive today, we could do no more to slow the progression of her disease than Dr. Alzheimer could more than a hundred years ago (see Where’s our cure to Alzheimer’s disease?).



Alzheimer’s disease has many symptoms aside from the well-known progressive memory loss. Personality and mood changes, such as depression and apathy, are common. Many patients experience reduced executive function, a broad category of cognition which includes attention, self-control, and problem solving. As the disease progresses, motor problems can appear, especially difficulty with speaking, swallowing, and walking. On average, patients with Alzheimer’s pass away within 4 to 8 years of diagnosis. The direct cause of death is often aspiration pneumonia, an infection of the lungs caused by food being improperly swallowed into the windpipe rather than the esophagus. Other common complications include bedsores, falls, urinary tract infection, malnutrition, dehydration, and organ failure.

In Our Brains

Some areas of the brain are affected more than others by this disease. Two areas of the brain that undergo particularly high levels of atrophy (i.e., tissue death) are the hippocampus and the entorhinal cortex. These two regions are most associated with declarative memory. Declarative memories are things that you can describe out loud, such as personal experiences or factual information. Conversely, procedural memory, also known as “muscle memory,” is the unconscious kind of memory that allows you to tie your shoes or play the piano. Interestingly, since procedural memory is handled by different brain systems, it is largely spared by Alzheimer’s disease. In other words, the inability of these patients to do basic tasks like dressing themselves is likely due to disruptions in motor function, and not from forgetting how to do so.


The left panel shows a cross-section of a healthy brain, while the right panels shows a brain with advanced Alzheimer’s disease. The hippocampus and entorhinal cortex are the brain regions most affected by this disease.

In addition to the hippocampus and entorhinal cortex, Alzheimer’s causes atrophy in various other brain regions involved with vision, mood, stress, language, movement, and proprioception (the sense of our body’s position in three dimensions, which is important for movement and coordination).

In Our Cells


Amyloid plaques and tau tangles inside the brain of an Alzheimer’s patient. Source

When Dr. Alzheimer examined his patient’s brain, he characterized the protein deposits into two types: those inside the neurons and those outside the neurons. The protein deposits inside neurons are known today as neurofibrillary tangles. They’re made of a protein called tau. When tau becomes hyperphosphorylated, meaning it has a large number phosphate groups attached to it, it becomes “sticky” and begins to adhere to other tau molecules. The protein deposits outside of neurons are called senile plaques, which are made of the amyloid beta protein. Like tau, amyloid beta can stick to itself to form large clumps in the brain. Both tangles and plaques are toxic to neurons in high concentrations, and are believed to be some of the main drivers of the disease’s progression.

In Our Genes

The genetic factors involved with Alzheimer’s disease is a very complicated topic (see The Genetics of Alzheimer’s Disease for a more detailed look). However, a brief overview will suffice for the purposes of this article. Alzheimer’s is typically classified into two types: familial, a rarer form that usually affects people younger than 65, and sporadic, which affects older patients and accounts for around 95% of Alzheimer’s diagnoses. Familial Alzheimer’s usually results from one of three genetic mutations: APP, which encodes a protein that is the precursor to amyloid beta; and PSEN1 and PSEN2, which encode an enzyme that helps turn APP into amyloid beta. These genes are highly penetrant, meaning that if you have one it’s very likely that you will develop familial Alzheimer’s disease. Additionally, a person who has one of these genes has a 50% chance of passing it on to each of their children.

The causes of of sporadic Alzheimer’s disease are more complicated. One gene that we know to be involved is APOE4. One copy of this gene increases your chances of getting the disease by about 2 to 3 times, while two copies increases your risk by nearly 15 times. This gene is actually fairly common, with 1 in 5 people possessing at least one copy. Many of these people never develop Alzheimer’s, and not all people with sporadic Alzheimer’s have APOE4. This tells us that other factors, which may be genetic or environmental, must also be involved.


Nearly 15% of the U.S. population has two copies of the APOE4 variant. Source

Learn More

Now that you’ve learned some basics about Alzheimer’s disease, here are some more articles for you to read and learn more:


n.a. What APOE means for your health. Alzheimer’s Drug Discovery Foundation. n.d.
Alzheimer’s Association. 2016 Alzheimer’s disease facts and figures. Alzheimer’s & Dementia. 2016;12(4):459-509.
Herrup, K. The  case for rejecting the amyloid cascade hypothesis. Nature Neuroscience. 2-15;18(6):794-799.
Hippius H, Neundörfer G. The discovery of Alzheimer’s disease. Dialogues in Clinical Neuroscience. 2003;5(1):101-108.
Hirono, N., et al. Procedural memory in patients with mild Alzheimer’s disease. Dementia and Geriatric Cognitive Disorders. 1997;8(4):210-216.
Leonard, W. Alzheimer’s Disease Complications. Healthline. 2014.


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