Dementia is a growing problem worldwide, affecting millions of people and their families. Traditional nursing homes and memory care facilities aim to provide safety and medical care, but they often struggle to offer a sense of normalcy and independence. That’s where dementia villages are designed to excel.

Dementia villages are specially designed communities that allow residents with dementia to live as independently as possible while receiving the care they need. Unlike conventional nursing homes, these villages mimic real-life neighborhoods, complete with grocery stores, cafes, parks, and communal spaces. Caregivers and medical professionals are embedded within the community, often dressed as shopkeepers or fellow residents, to ensure a seamless and familiar environment.

How Dementia Villages Got Started

Dementia villages originated in the Netherlands with Hogeweyk, a groundbreaking care facility in Weesp, Netherlands. Opened in 2009, Hogeweyk is home to around 150 residents, all of whom have advanced dementia. The village operates on the philosophy that maintaining a sense of routine, autonomy, and social interaction can significantly enhance the quality of life for individuals with dementia.

The Hogeweyk dementia village in Weesp, Netherlands, is designed to provide residents with a familiar and engaging environment that mirrors everyday life. The village features amenities such as a restaurant, café, supermarket, theater, office, various club rooms, a physiotherapist, and a hair and beauty salon.

These facilities enable residents to participate in routine activities like shopping, dining, and attending performances, fostering a sense of normalcy and independence.

The village comprises 27 houses, each accommodating six or seven residents. These homes are tailored to reflect four distinct lifestyles—traditional, urban, formal, and cosmopolitan—ensuring that residents live in settings that resonate with their personal backgrounds and preferences.

Each house includes a living room, kitchen, private bedrooms, bathrooms, and outdoor spaces like terraces or balconies, promoting a homely atmosphere.

To learn more about The Hogeweyk and its innovative approach to dementia care, you can visit their official website: hogeweyk.dementiavillage.com

For a visual overview of how dementia villages operate, you might find the following video informative:

How Dementia Villages Work

Dementia villages function like small, enclosed towns. Residents can walk freely within the village, shop at a supermarket, dine at a restaurant, or enjoy outdoor activities—all within a safe and secure environment. The goal is to minimize confusion and distress while encouraging social engagement and personal choice. Caregivers, who double as community staff, provide support in a way that feels natural rather than clinical. The setting also includes quite a bit of nostalgia in many cases, harking back to the days of their youth.

The Benefits of Dementia Villages

1. Enhanced Quality of Life: By living in a familiar, home-like setting, residents experience less stress and anxiety compared to traditional care facilities.

2. Greater Independence: Residents can make choices about their daily routines, fostering a sense of control and dignity.

3. Increased Social Interaction: The design encourages interaction with caregivers and other residents, reducing isolation and loneliness.

4. Personalized Care: The environment allows staff to tailor care to each individual's needs without a rigid, institutionalized approach.

The Future of Dementia Care

Dementia villages are gaining global attention, with similar models being adopted in countries like Denmark, Canada, and Australia. As the demand for dementia care rises, these villages offer a promising alternative to traditional memory care settings. They represent a shift from institutionalized care to a more compassionate, community-driven approach.

Why Not?

Dementia villages challenge the conventional way of thinking about memory care, prioritizing dignity, autonomy, and a sense of normalcy. While they may not be a one-size-fits-all solution, they offer an inspiring glimpse into the future of dementia care—one that places humanity at its core.

An open-access study was just published in Alzheimer’s Research and Therapy, giving evidence that statins (cholesterol-reducing medications) can actually reduce cognitive decline in Alzheimer’s patients.

How does it work?

The concept behind this slowing of Alzheimer’s disease progression is that excess cholesterol in the brain may be part of the problem for Alzheimer’s patients. According to prior research cited by the authors of this study, excess cholesterol could (a) impede blood flow in the brain and (b) increase the build-up of harmful amyloid plaques. If so, reducing brain cholesterol should, in theory, help reduce Alzheimer’s symptoms.

What is the evidence?

The study looked at a dataset of 15,568 Swedish patients with Alzheimer’s disease or mixed dementia and hyperlipidemia (elevated cholesterol and triglycerides), two-thirds of whom were on statin medication. The analysis showed that taking statins on a daily basis was associated with 0.63 more points on the MMSE (Mini-Mental State Examination) after 3 years compared to not using statins.

Note that a correlational study of Humana insurance claims data also showed a reduction in the incidence of neurodegenerative diseases like Alzheimer’s in statin users.

A few cautions

According to one of the authors of the paper, this result doesn’t mean doctors should start prescribing statins for dementia, but they shouldn’t let a dementia diagnosis stop them from prescribing statins. The difference in cognitive decline between statin users and non-users (.21 points per year) does not reach a clinically meaningful threshold (1 to 3 points per year) that scientists tend to want to see before recommending physicians prescribe medications.

Every study has limitations. One prominent limitation of this study is that it is correlational, meaning that they can’t infer causality the way they could in an experiment where neither researchers nor participants know who is in the placebo or treatment groups. We can see from this study that statin use and decreased cognitive decline co-occur, but we can’t know for sure why that is. A 2015 article explained the problem of inferring causality from correlational research better than I can. A second limitation is that the study's outcome depends on a series of statistical choices by the authors. This is always the case with large survey datasets, and it helps explain why scientists often come to different conclusions with the same or similar data. Consider, for example, that scientists have been going back and forth for years about whether statins help or hurt Parkinson’s patients (another neurodegenerative disease), and to this day, there is no solid consensus.

None of this is meant to say the study is bad. I’m only saying that I agree with the authors that more research in this area is needed. This is a great early step.

About the author

Aaron Charlton, PhD is a health, medical and science blogger who works for Neurology Associates Neuroscience Center and other medical clients.

My rough translation:

I noticed a great writeup by Michael Simpson, CEO of Skeptical Raptor, on this topic. Simpson does a great job of addressing the primary issues that come up when scientists attempt to do research in this area:

First of all, the studies rely on self-reported measures. The scientists don’t follow people around 24/7. They just ask them “how much do you smoke,” “what do you eat,” etc. The problem with this is that someone who has poor health outcomes will assume they did something wrong and focus on what it is they did wrong. They will be ungenerous about their past “I smoked too much,” “ate too much,” “slept to little,” etc. So it’s a lot of speculation. Someone with the same diet and behavior who had good health outcomes will likely react in the opposite way, speculating why they’ve done so well. In either case it does become sort of speculative and not super informative.

Secondly, the studies are correlational, meaning they don’t know what causes what. Did you stay married because you’re religious, or are you religious because you stayed married? It’s hard to know. Also, it could be a third variable that we haven’t thought about that causes both the religiosity and the commitment to marriage. It can be very hard to parse out.

Here is a quick example more closely related to nutrition: In the U.S. we’ve been told for decades that eggs are bad for us. Now we notice that healthy people eat fewer eggs. Are they healthy *because* they eat fewer eggs? Or do they eat fewer eggs because they want to be healthy and they’re generally told that’s what they need to do? Gets confusing, right?

In the case of the actual study that Simpson looks at, there are six healthy habits that can stave off mental decline. They are listed in order from the largest effect to the smallest. This may be true but consider the study limitations:

1. Healthy diet, β =0.016

2. Active cognitive activity, β=0.010

3. Regular physical exercise, β=.007

4. Active social contact, β=0.004

5. Never/former smoker, β=0.004

6. Never alcohol, β=0.002.

The good thing is that we have nothing to lose by adopting these habits since they can help in whole host of areas.

Article is written for Neurology Associates Neuroscience Center.

Teddy Mac was a professional singer for his entire adult life. At age 80 he was diagnosed with Alzheimer’s disease and he started to decline and become withdrawn.

His son noticed that he came back to life when music was playing and he was singing along so the son recorded it and turned it into a social media phenomenon. The pair were able to create and sell albums and raise funds for charity.

Teddy’s condition has continued to decline but he is still at home being cared for by those he loves.

Learn more »

Early symptoms of Alzheimer's disease include difficulty remembering recent events, problems solving problems or completing familiar tasks, difficulty with language, disorientation in time and place, poor or decreased judgment, problems with abstract thinking, misplacing things, changes in mood or behavior, and loss of initiative. These symptoms can also be caused by other conditions besides Alzheimer’s. A proper diagnosis can only be made by a qualified healthcare professional (typically a neurologist).

Read this story about how one couple discovered the presence of Alzheimer’s disease:

Julia, when did you first realize there was something "off" with Mike? How did you respond to this? Julia: Two things stand out. I found a paycheck in a cookbook. This was odd because Mike had always been so on-top of everything. Also, his driving abilities seemed to be declining. Honestly, I panicked at first and then I was definitely in denial. We ended up getting help through the Alzheimer's Association much later on; looking back, we should've reached out earlier, but I was scared and felt helpless and isolated.

Mike, what about you? When did you first start noticing things? What did you notice? Mike: Things just weren't right, but I couldn't figure out exactly what wasn't right. And, I don't think I could accept it. I kept asking for directions to go to work), and it once took 20 minutes to do a bank deposit which was unusual because I always had a keen mind.

What did you do when you noticed these behaviors? Can you take us through the time you began to notice problems, through getting the diagnosis? Julia: We didn't do anything at first. Eventually, we realized we needed to get help because Mike was struggling with day-to-day tasks. Initially, Mike was diagnosed with Mild Cognitive Impairment (MCI). We later got the diagnosis of Alzheimer's disease.

What did they notice? Misplacing things, difficulty in completing basic tasks, forgetting how to get to work, etc.

For another family the early signs were a bit different:

The first sign that something wasn't right with Mary was her rapid weight loss—she lost almost 150 pounds without appearing to try. Then Kamaria and others in her close-knit extended family began noticing small personality changes, such as forgetfulness and irritability. But it was a visit from Kamaria's grandmother that spurred her to act.

When her father's mother flew up from Florida, she, Kamaria, and Mary spent the day together. They had lunch at Kamaria's husband's restaurant and visited her father's grave. But when Kamaria mentioned it to Mary a few weeks later, she knew nothing about it and was angry that Kamaria even brought it up. That's when Kamaria realized there was a problem. She quickly started making doctor's appointments.

Mary lost so much weight because she forgot to eat. Unfortunately when they started working with doctors it took two years to figure out that it was Alzheimer’s disease.

Alzheimer’s disease is the 7th leading cause of death in the U.S. It affects countless families. Learning to recognize the early signs of Alzheimer’s disease can help make a difference in someone’s life.

It is important for those afflicted with Alzheimer’s disease or other forms of dementia to have meaningful interactions with others, and to feel loved. It can also be beneficial to family members who are able to have productive relationships with their loved ones who have dementia.

Here are a few tips to successfully communicate:

1. Minimize background noise and distractions. If there is a lot of noise or movement in the background the patient can become overstimulated, overwhelmed and confused. It’s best to clean up clutter, turn off the television (if they let you) and find a quiet space to converse.

2. One-one-one is best. Talking to multiple people at the same time can be confusing and overwhelming for the dementia sufferer. Try to keep interactions one-on-one to the extent possible.

3. Keep it simple—don’t split hairs. It’s best if you just stick to easy-to-understand, straight-forward concepts. If the patient is not getting something it probably won’t work to stay on that point and to keep trying to elaborate.

4. Don’t argue.

5. Just keep talking even if it seems no one is listening or responding.

Alzheimer’s disease can really take a toll on families and care givers. Following these few simple steps to communicating productively with Alzheimer’s patients should help.

If you suspect that you or a loved one may be showing early signs of Alzheimer’s disease, you should see a neurologist right away.

Acknowledgement: This is adapted from something I saw from AgingCare.com.

It’s not completely clear what causes Alzheimer’s disease but from what we can tell, no one is completely safe from the disease. Even very famous people succumb to it despite having access to the best resources and care.

Early diagnosis of Alzheimer's disease is important for several reasons. First, it allows for earlier intervention and treatment, which can help slow the progression of the disease and improve quality of life for the individual. Early diagnosis also allows for better planning for the future, including financial and legal planning, and can facilitate discussions about end-of-life care. Additionally, early diagnosis can help with the identification and management of other potential contributing factors, such as depression or other medical conditions. Furthermore, early diagnosis can help people with Alzheimer's disease and their families access resources and support, such as support groups and care facilities.

Early symptoms of Alzheimer’s disease

The early symptoms of Alzheimer's disease can vary from person to person, but some common early signs include:

• Memory loss, particularly difficulty remembering recent events or conversations.

• Difficulty completing familiar tasks, such as cooking a meal or driving to a familiar location.

• Trouble with language, such as difficulty finding the right word or following a conversation.

• Disorientation in time and place, such as getting lost in familiar surroundings.

• Poor judgment and decision making, such as giving away large sums of money or neglecting personal hygiene.

• Mood changes, such as depression or anxiety.

• Changes in personality, such as becoming more withdrawn or suspicious.

It's important to note that these symptoms can also be caused by other conditions, so it's important to see a doctor for an accurate diagnosis.

What to do if you think you or a loved one may have Alzheimer’s disease

If you are experiencing a combination of these symptoms, you should schedule a visit with a neurologist. Neurologists can diagnose Alzheimer’s disease in its early stages and they can work with the patient and their family to develop a comprehensive treatment plan.

This may include medications to slow the progression of the disease, such as cholinesterase inhibitors or memantine. These medications can help improve memory and thinking, and delay the development of the symptoms. In addition to pharmacological treatments, neurologists may also recommend non-pharmacological interventions, such as cognitive-behavioral therapy, occupational therapy, and supportive therapies to help patients cope with the disease.

Neurologists also provide ongoing care and management of the disease, including monitoring the patient's condition, adjusting medications as needed, and providing education and support to the patient and their family. They can also coordinate care with other healthcare providers, such as primary care physicians, geriatricians, and home health agencies, to provide the best possible care for Alzheimer's patients.

A recent correlational study looked at the occurrence of viral diseases in patients, and how this could predict Alzheimer’s later in life. If they are right about this, it would mean that viral infections may be at least partly to blame for the disease.

The struggle to fight Alzheimer’s disease

Scientists have really struggled to identify the causes of Alzheimer’s or to truly understand the disease process. Not understanding the disease has made it very difficult to develop useful treatments. Two recently FDA-approved Biogen drugs for treating Alzheimer’s by reducing the quantity of amyloid plaques in the brain have been a bust, as has the theory that amyloid plaques cause the disease. Instead, the plaques are probably a mere byproduct of the disease and the medications solve the wrong problem.

Do viral infections lead to Alzheimer’s disease?

Let’s dive in to the study in question (Levine et al. 2023). By the way, the study is a pre-print that has not yet been through peer-review, which is fine but important to declare.

But the answer to the question is “maybe.” Why?

The study is correlational. Two different things could be going on and it’s not very easy to tell which one it is:

1. Viral infection —> Alzheimer’s disease later in life

2. Generally poor health (seen or unseen) —> viral infection and Alzheimer’s disease later in life

So it could be that these viral infections are causing Alzheimer’s disease down the road but it could also be the case that people who have underlying health issues are susceptible to both viral infections and Alzheimer’s disease. We don’t really know for sure which it is (or if it’s a little of both) because it’s correlational.

The connection appears to be greater between viruses that affect the brain and Alzheimer’s disease. This seems intuitive enough. But again, it could be that there is a vulnerability in the brain that allows for both the viral infection and Alzheimer’s disease to occur. Even in the most extreme case the differences are not that great:

24 of 406 viral encephalitis cases went on to develop AD (5.9%); this is higher than the general prevalence of AD in the same population at less than 3%.

Also note that small sample size of 24 Alzheimer’s patients. Sometimes when you have small samples you see crazy numbers that would actually revert to the mean if we saw more data roll in. The total study had way, way more than 24 people but when you look at all of the sub-groups, the sample sizes for some of them are quite small making it difficult to know if viral encephalitis in this case really is a strong predictor of Alzheimer’s.

Conclusions

People who fall ill with severe viral infections at mid-life are more likely to acquire Alzheimer’s disease later but we need more information to know if it’s causal. It could be that an underlying weakness allows both the viral infection and the Alzheimer’s disease to occur. The other thing to note is that we’re not talking big differences here. I should point out that there are a few research-supported ways to reduce the risk of cognitive decline later in life but avoiding viruses (if possible) may or may not be one of them. More research is needed.

References

Virus exposure and neurodegenerative disease risk across national biobanks

Kristin Levine, Hampton L. Leonard, Cornelis Blauwendraat, Hirotaka Iwaki, Nicholas Johnson, Sara Bandres-Ciga, Walter Koroshetz, Luigi Ferrucci, Faraz Faghri, Andrew B. Singleton, Mike A. Nalls

medRxiv 2022.07.08.22277373; doi: https://doi.org/10.1101/2022.07.08.22277373

Sorry it looks like I’ve made a mistake in blindly trusting a research study. I have two biases: first I am very skeptical about scientific research. You can read about my takedown of my own field of marketing research. Most people fall into one of two camps: “science deniers” or “science believers.” I’m one of the rare people that is something in between. I verify. I have the training to do that and I have been very, very successful at finding the problems in my own field.

Unfortunately my skepticism was outweighed by my other bias that healthy living is the solution to most problems of health, so when I saw a claim that obesity causes Alzheimer’s I bought into it without fully checking it. It turns out they were probably wrong and so was I (for believing them).

In that post, I wrote that obesity is a massive predictor of Alzheimer’s disease. According to Whitmer et al. (2007) obesity at mid-life caused a “3.10 fold increase in risk” of Alzheimer’s disease.

There are two issues with this—one minor and one major:

Unclear language around the amount of change

This is a minor issue but it’s not 3.1 times higher; it’s 3.1 times as much. The “3.10 fold” language is misleading and unclear. Using the language in their way, a 1-fold increase would be no change. Perhaps that’s proper usage of the phrase but to me I read it and it says 3.1 times more (4.1 times as much). More clear language would be great.

Not much difference in the raw values

It is kind of a problem that they had to use a whole bunch of control variables in their model to find the obesity issue. If you look at the raw values there’s actually not much difference in the different weight groups:

• Normal weight at mid-life: 4.43% chance of Alzheimer’s disease

• Overweight at mid-life: 5.10% of Alzheimer’s disease

• Obese at mid-life: 4.71% chance of Alzheimer’s disease

If you look at it that way, all the numbers are too close to draw any real conclusions. The differences look like rounding errors. It’s not linear either. Why would it be worse to be overweight than obese? It’s not worse. The problem is a lack of precision due to the sample size of 477 total people with Alzheimer’s disease in the dataset. That number is not large enough to detect minute differences between these three groups.

So how did they find that massive difference then?

They used what’s called “control variables.” In a statistical model, you can include all the variables you are interested in into a model and basically let the model decide which factors are the most important. In some ways this is good but in some ways it’s bad. Here are the control variables used (footnotes of Table 3):

1. Fully adjusted for age (as the time scale),

2. age in midlife,

3. education,

4. race,

5. sex

6. marital status,

7. smoking,

8. hyperlipidemia,

9. hypertension,

10. diabetes,

11. ischemic heart disease and

12. stroke

But here’s the problem. Many of these issues are caused by obesity, or are caused by the same attitudes, lifestyle and behaviors that cause obesity. So if you control for all of these issues then your statistical model is nonsense. You should really only control for the variables *not* caused by your variable of interest (obesity).

Conclusions

While obesity could play a role in Alzheimer’s disease it’s sure not clear from the data used in this research. This indicates that there is no reason to panic about an up-surge in Alzheimer’s disease in the future—at least not based on this research.

Source

Whitmer, R., Gunderson, E., Quesenberry, C., Zhou, J., & Yaffe, K. (2007). Body Mass Index in Midlife and Risk of Alzheimer Disease and Vascular Dementia. Current Alzheimer Research, 4(2), 103–109. doi:10.2174/156720507780362047

Update: this post is probably mostly wrong (sorry!). I made an updated post that I stand behind. Obesity doesn’t seem to be a strong predictor of Alzheimer’s disease at all. The research I based the other article on is misleading.

One of the strongest predictors of Alzheimer’s disease is obesity. A 2007 study of 10,136 people found that mid-life body mass index (BMI) has a huge correlation with occurrence of Alzheimer’s disease later in life. Specifically, those obese at mid-life (BMI ≥ 30) had a 3.1 fold increased likelihood of developing Alzheimer’s disease later in life. People are simply overweight (not obese) have about a two-fold increase in Alzheimer’s disease diagnosis later in life [1].

Currently 39% of U.S. adults are obese and 69% are overweight.

Because the obesity rate was only 12% in 1990, we can expect a massive increase in the occurrence of Alzheimer’s disease in the foreseeable future. So the obesity rate is about 3x as high. Does this mean that Alzheimer’s disease should affect 3x as many people in the future? Yes! One of the biggest obesity-related problems we are faced with is Alzheimer’s disease which is going to be a future plague of biblical proportions.

Obesity can be dealt with through proper nutrition and exercise in many cases. If you need help getting getting your life on track, you should consider working with a health and wellness coach who can help you live your best life, possibly avoiding Alzheimer’s disease down the road. If you think you may be experiencing early stages of Alzheimer’s disease (such as memory loss), you should see a neurologist right away for diagnosis.

Sources

1. Whitmer, R., Gunderson, E., Quesenberry, C., Zhou, J., & Yaffe, K. (2007). Body Mass Index in Midlife and Risk of Alzheimer Disease and Vascular Dementia. Current Alzheimer Research, 4(2), 103–109. doi:10.2174/156720507780362047

2. https://www.hsph.harvard.edu/obesity-prevention-source/obesity-trends-original/obesity-rates-worldwide/#:~:text=Roughly%20two%20out%20of%20three,in%20non%2DHispanic%20White%20adults.

Alzheimer’s disease is a brain disease that mainly affects people later in life. It causes steep declines in memory and other cognitive functions. At advanced stages, the brain shuts down and the person dies. There is no cure or effective treatment for Alzheimer’s disease. Alzheimer’s disease changes the structure of the brain and can be observed in autopsy by (a) neurofibrillary tangles (NFTs), and (b) amyloid plaques. The disease seems to come on slowly, causing structural changes long before it can be detected. Neurologists are able to diagnose Alzheimer’s disease and work with patients and family members to develop tools and systems to deal with the disease.

A recent review of Alzheimer’s disease risk factors (Bendlin et al. 2010) proved very insightful:

Risk factor #1: Genetic risk & family history

Some people may be genetically predisposed to Alzheimer’s disease (or other diseases). For example, it was recently in the news that actor Chris Hemsworth has some sort of genetic marker that makes him far more likely to acquire the disease as he ages. Nothing can currently be done about genetic risk factors but scientists are working on a tool called CRISPR that they have successfully used in some cases to edit peoples’ gene sequences, curing them of genetic diseases. Offspring of parents with Alzheimer’s disease have six time greater risk for developing the disease compared to those without a family history of the disease.

Risk factor #2: Sex

The incidence of Alzheimer’s disease in women is 1.5–3 times higher than the incidence in men. Women’s increased risk for AD coincides with menopause, implicating estrogen deficiency as the primary sex-related risk factor for Alzheimer’s disease.

Risk factor #3: Midlife health factors

Obesity at mid-life is associated with over a 3x increase in likelihood of developing Alzheimer’s disease later in life. Hypertension at mid-life is also associated with a higher likelihood of developing the disease.

Using data from the population-based Cardiovascular Risk Factors, Aging, and Dementia (CAIDE) study (n = 1409), Kivipelto and colleagues confirmed that increased vascular risk at midlife predicted dementia 20 years later [87]. Kivipelto et al. constructed a baseline risk score composed of body mass index, systolic blood pressure, diastolic blood pressure, total cholesterol, current smoking status, and level of physical activity. The risk of dementia for those with the highest baseline risk score was 16.4%, compared to only 1% for those with the lowest risk score. Of the factors comprising the overall risk score, hypertension, hypercholesterolemia, and obesity were the most predictive of dementia.

Midlife health factors appears to be the strongest signal of all the risk factors.

Risk factor #4: Environmental and lifestyle factors

Several more studies show a connection between eating healthy, exercising, having healthy social relationships, etc. and a decrease in the occurrence of Alzheimer’s disease.

Conclusions

The occurrence of Alzheimer’s disease can be reduced by taking care of yourself. Eat healthy, try to keep your weight down, exercise, stop smoking, and make an effort to maintain positive relationships for the best benefits.

Source

Bendlin, B. B., Carlsson, C. M., Gleason, C. E., Johnson, S. C., Sodhi, A., Gallagher, C. L., … Asthana, S. (2010). Midlife predictors of Alzheimer’s disease. Maturitas, 65(2), 131–137. doi:10.1016/j.maturitas.2009.12.014

The FDA recently rush-approved two Biogen drugs aimed at reducing the presence of amyloid proteins in the brain. Amyloid proteins were previously thought to be the cause of Alzheimer’s disease but that concept has basically fallen apart in recent years. Not only have ~16 drugs that reduce the presence of the protein failed to reduce the effects of Alzhiemer’s but it turns out that some of the research the amyloid hypothesis was built on was actually fraudulent.

Despite all of this, the FDA rush-approved two Biogen Alzheimer’s drugs (Aducanumab and Lecanumab). These drugs are excellent at reducing the presence of amyloid proteins but unfortunately they (a) have severe side effects, (b) may not be effective at reducing Alzheimer’s disease, and (c) cost thousands of dollars every month.

Despite pulling off this “heist” as Dr. Robert Howard, an old age psychiatrist at UC London, calls it in getting the drugs approved, it appears that Biogen may not have any success selling their drugs. There has simply been too much push back from providers and researchers. Many people are up in arms about the whole thing.

For example, Doctors for America put out an open letter calling on the FDA to bring in a formal advisory committee to investigate the effectiveness of the drug. We spoke with Dr. Andrea An of Neurology Associates Neuroscience Center and she indicated that her practice would likely not be able to use the drug because (a) the side effects are severe and (b) it’s very expensive. Medicare has already declined to cover aducanumab and they’re still just considering covering lecanumab. Add to this doubts about whether either drug even reduces the effects of Alzheimer’s disease. It seems clear that Aducanumab doesn’t do anything at all about Alzheimer’s and the jury’s still out for lecanumab. Dr. An also indicated that her peers are saying the same things. There is generally a lot of hesitation to prescribe these new Biogen drugs.

A big concern to come out of what is now looking a lot like a fiasco is the question of whether high-trust groups like the FDA and the Alzheimer’s Association will lose credibility for cheer-leading these drugs. Dr. Alberto Espay, a neurology professor at University of Cincinnati compared the FDA’s failure to the failure of the SEC to stop Bernie Madoff.

As for Biogen, they will likely be the biggest losers in all this because they’ve invested so many resources into developing Alzheimer’s drugs that appear to be useless. And physicians and researchers aren’t buying it and the drugs aren’t being prescribed.

According to Costello, Roiser and Howard (2023) there is a lack of scientific evidence showing any benefits of antidepressants for people with dementia (including Alzheimer’s disease). They arrived at this conclusion by reviewing all of the preceding research on the topic and evaluating the totality of the evidence. They found the evidence wanting. According to the research team, if currently available depression drugs do work on Alzheimer’s patients there is certainly no proof, and the effects can’t be large.

Here are their specific conclusions:

1. Anti-depressants developed for depression don’t work on dementia patients because their depression is structurally different/unrelated to regular depression.

2. There is currently no effective drug for reducing the symptoms of depression in dementia patients.

3. They also provide recommendations for how to develop a drug for depression in dementia patients. They emphasize developing it solely for that purpose and disregarding what works for non-dementia depression.

This very somber news comes on the heels of recent revelations that (a) what was thought to be the cause of Alzheimer’s disease (build up of amyloid proteins) is actually not the cause; cause still unknown, and (b) two amyloid reducing drugs recently approved by the FDA appear to be ineffective and harmful (Aducanumab and Lecanemab).

A neurologist is a medical doctor who specializes in the diagnosis and treatment of conditions that affect the brain and nervous system. In the case of Alzheimer's disease, a neurologist may be involved in the initial evaluation and diagnosis of the condition, as well as in the management of symptoms and complications that may arise as the disease progresses. This may include prescribing medications to manage symptoms such as memory loss, confusion, and changes in behavior. A neurologist may also work closely with other healthcare providers, such as geriatricians and primary care physicians, to coordinate the overall care of patients with Alzheimer's disease.

Unfortunately there no cure for Alzheimer’s disease

Currently, there is no known cure for Alzheimer's disease. While there are several medications available that can help to temporarily improve symptoms and *possibly* slow the progression of the disease, there is no treatment that can stop or reverse the underlying degeneration of brain cells that occurs in Alzheimer's.

Research is ongoing to find new treatments and therapies that may be able to better manage the symptoms of Alzheimer's and delay its progression, as well as to identify new ways of preventing or curing the disease. Some possible treatments being researched include the use of drugs to target the specific proteins that are thought to contribute to the development of Alzheimer's, as well as therapies that aim to promote the growth of new brain cells. Unfortunately, most of these drug trials have failed to improve Alzheimer’s patients’ conditions. A few are not fully tested. There are currently none that are fully tested and proven to be effective unfortunately.

The role of the neurologist in working with Alzheimer’s patients

Neurologists are not able to cure or even slow down the progression of the disease. The neurologist’s first role is in diagnosing the disease. Once diagnosed, the neurologist focus on addressing some of the symptoms that arise, and helping the patient, care providers and family have better tools to deal with it.

Margaret Thatcher (left), Ronald Reagan (middle) and Charlton Heston (right) three conservative-minded political allies and friends were all stricken with Alzheimer’s disease some time after this photo was taken. Margaret Thatcher, the former prime minister of the United Kingdom was diagnosed with dementia (likely Alzheimer’s disease), in 2002 and passed away in 2013. Ronald Reagan was a famous western actor and former president of the United States was diagnosed with Alzheimer's disease in 1994 and lived with the condition for more than a decade before his death in 2004. The actor, Charlton Heston, known for his roles in films like "Ben-Hur" and "The Ten Commandments," was diagnosed with Alzheimer's disease in 2002 and passed away in 2008.

Ronald Reagan’s daughter, Patti Davis, cared for him for 10 years in his cognitively diminished state before he passed away. She had this to say about the experience:

None of this is easy. None of us know how to do this when [Alzheimer’s] enters our lives. There was a period where I almost felt like I was losing my faith. But ultimately, [my faith] is what grounded me. He opened his eyes the moment before he died and he was present. He showed up before he died. I thought everything I had believed and thought was validated. - Patti Davis

Alzheimer's disease is a progressive brain disorder that affects memory, thinking, and behavior. Symptoms of Alzheimer's disease usually develop slowly and worsen over time, and may include memory loss, difficulty completing familiar tasks, disorientation, mood and behavior changes, and problems with language. There is no cure for Alzheimer's disease, but neurologists and other healthcare providers have a variety of tools to help manage symptoms and improve quality of life.

Lecanemab was just recently approved for clinical use through a rush approval process. But what are the side effects? First of all, there were a lot of study participants over an 18-month period and they are alzheimer’s patients which basically means they’re sick with a terminal disease so you expect some adverse events. The way side effects are identified is by looking at how many more adverse effects you see in the treatment group vs. the placebo group. If there were zero side effects, you’d see a treatment group that had roughly the same fatality and disease rate as the placebo group. That is certainly not the case with Lecanemab—this drug can hurt you!

Biggest side effects

In what follows I review the reported results from the clinical trial. You can access the paywalled report here and if you’re lucky you can get the full paper for free here.

Brain swelling (ARIA-E)

Excess fluid build up causes excess pressure on the brain. Symptoms of this problem include headaches, nausea, vomiting, seizures, drowsiness, visual disturbances and dizziness (if it doesn’t kill you or put you in a coma). In the trial, brain swelling occurred in 113 (12.6%) people who received the treatment but only 15 (1.7%) people in the placebo group. That’s a bad side effect and a high rate of occurence.

Bleeding in the brain (ARIA-H)

Another really bad side effect. These very tiny releases of blood but they can add up if you have a lot of them. This issue affected 155 (17.3%) of the treatment group but only 81 (9.0%) of the placebo group.

Superficial siderosis

A toxic, debilitating build up of iron in the tissues between brain and skull. The build up is caused by bleeding in the brain over time. It often manifests by abnormal uncoordinated movements and hearing loss. In the treatment group, this affected 50 (5.6%) patients but only 22 (2.5%) in the placebo condition.

Conclusions

These side effects are severe, unfortunate, and common. Patients and their family members should know the risks and weigh them carefully before leaping in. In many cases the drug caused much more harm than good. We all want to see alzheimer’s disease cured but the cost in terms of side effects is very high in this case. It’s definitely good to be cautious.

It is normal for adults to experience some memory loss as they age. However, significant memory loss that disrupts daily life is not a normal part of aging and could be a sign of Alzheimer's disease, or another brain health condition.

Alzheimer's disease is a progressive, degenerative brain disorder that affects memory, cognitive function, and behavior. It can affect people of all ages and walks of life but it is most common in older adults. The exact cause of Alzheimer's disease is not fully understood, but it is thought to be a combination of genetic, environmental, and lifestyle factors.

How is Alzheimer’s disease diagnosed and how does it differ from other cognitive disorders?

Alzheimer's disease is typically diagnosed through a combination of methods, including a neurological examination, laboratory tests, and imaging studies. A diagnosis of Alzheimer's disease is usually made based on the presence of specific symptoms and changes in brain function, as well as the exclusion of other possible causes for these symptoms.

The diagnosis of Alzheimer's disease can be challenging because the symptoms of the condition can be similar to those of other cognitive disorders, such as vascular dementia or Lewy body dementia. It's important for a healthcare provider to carefully evaluate an individual's symptoms and medical history in order to accurately diagnose the condition and determine the most appropriate course of treatment.

Some of the key differences between Alzheimer's disease and other cognitive disorders include:

1. Age of onset: Alzheimer's disease is most commonly diagnosed in people over the age of 65, although it can also occur in younger individuals. Other cognitive disorders, such as vascular dementia, can occur at any age.

2. Symptoms: The symptoms of Alzheimer's disease typically progress gradually over time, starting with mild memory loss and eventually leading to more severe cognitive impairment. Other cognitive disorders may cause more sudden changes in cognitive function, such as after a stroke or brain injury.

3. Causes: The cause of Alzheimer's disease is not 100% clear but other cognitive diseases can be diagnosed based on identifying their respective causes, such as a brain injury, stroke, or blood vessel disease.

Who is affected by Alzheimer’s disease?

Alzheimer’s disease is a common condition that affects millions of people around the world each year. In fact, several famous people have been diagnosed with Alzheimer’s disease before they died including Ronald Reagan, Charlton Heston, Margaret Thatcher, Gene Wilder and Linda Ronstadt. People are much more likely to develop Alzheimer's disease in advanced age. Family history of the disease, certain genetic mutations, and certain medical conditions such as high blood pressure and diabetes are believed to be contributing factors. Lifestyle factors such as diet, exercise, and cognitive activity may also play a role in the development of Alzheimer's disease.

What causes Alzheimer’s disease?

Sorry to disappoint but it’s currently very unclear what causes Alzheimer’s disease. It is clear that it’s a gradual, degenerative disease—not a disease that is caused in an instant by traumatic brain injury, stroke, etc. Up until 2022, it was believed that Alzheimer's disease was somehow caused by the presence of amyloid plaques and tau tangles in the brain. These structures are believed to contribute to the death of brain cells and the loss of brain function that occurs in Alzheimer's disease. Unfortunately, it turns out that this whole line of scientific literature was built on a faulty foundation of fraud.

How is the disease treated?

There is currently no cure for Alzheimer's disease, and treatment is focused on managing symptoms and slowing the progression of the disease. Other cognitive disorders may have more specific treatment options that are tailored to the underlying cause of the condition. For Alzheimer’s disease, like other incurable, progressive diseases, the emphasis is on making the patient, caregivers and family as comfortable as possible and giving the patient the ability to function as normally as possible for as long as possible.

The clock is ticking: As more than 6.5 million Americans live with dementia caused by Alzheimer’s, researchers and scientists are scrambling to develop a drug that slows cognitive decline. One such drug, lecanemab, could receive accelerated approval from the U.S. Food and Drug Administration on Jan. 6.

The news comes after the highly publicized debacle surrounding another experimental drug, Aduhelm (generic name: aducanumab). Incidentally, lecanemab and aducanumab both come from pharmaceutical giants Biogen and Eisai. Read here about what happened with aducanumab; the hope, of course, is that the lecanemab process does not repeat the “rife…irregularities” surrounding the $56,000-per-year Aduhelm. Biogen and Eisai have not revealed the price tag for lecanemab (and cost was only one point of contention regarding the approval of aducanumab).

Lecanemab is Still Experimental

Like Aduhelm, lecanemab qualifies as an experimental dementia drug. It appears to slow the progression of cognitive decline by binding to amyloid beta, an indicator of Alzheimer’s disease. (Note that there is debate as to whether the beta-amyloid protein causes Alzheimer’s.) However, also like aducanumab, lecanemab does come with some safety concerns. Some patients in trials have experienced problems including brain swelling and bleeding. Overall, 14% of the lecanemab group reported serious adverse events, compared to 11.3% in the placebo group.

Even so, the companies behind lecanemab have been pushing for accelerated approvals from the FDA. If that happens, patients could start the drug even as scientists continue to study it in larger, longer trials. 

Alzheimer’s Association Supports Lecanemab Approval

The Alzheimer’s Association supports the efforts. Here’s what the organization’s Maria Carrillo, chief science officer, told CNN:

“We believe, based on the totality of positive data from clinical trials of this treatment, that the FDA should approve. Peer-reviewed, published results show lecanemab will provide patients in the earliest stages of Alzheimer’s more time to participate in daily life and live independently. It could mean many months more of recognizing their spouse, children, and grandchildren.”

As such, the Alzheimer’s Association is asking the Centers for Medicare and Medicaid Services to cover lecanemab. Right now, CMS blocks access to the treatment.

What Might Be Next for Lecanemab?

Again, if the FDA does grant accelerated approval this week, lecanemab will undergo more trials. If those studies confirm clinic benefit, then lecanemab could receive traditional FDA approval. But if those trials show more harm than good, then the FDA would likely take lecanemab off the market.

Clinicians would probably take time to determine how effective lecanemab might be for their patients. Drugs come with risk and doctors have to assess benefit versus drawback for each individual they treat. 

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The content for this site is funded by a neurology practice in Arizona.

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The new drug, Aducanumab, even as of today’s date, 28 December 2022, is heavily touted by the Alzheimer’s Association:

[T]he first therapy to demonstrate that removing beta-amyloid, one of the hallmarks of Alzheimer’s disease, from the brain is reasonably likely to reduce cognitive and functional decline in people living with early Alzheimer’s.

Many other organizations have blindly endorsed the new drug, including the U.S. FDA. Yet the Canadian FDA has declined to approve it (and that won’t change).

But there are several problems:

1. The science supporting the notion that the beta-amyloid protein causes Alzheimer’s disease has not held up to time.

2. The medicine has shown zero ability to slow or prevent the actual symptoms of Alzheimer’s disease.

3. Insurance plans have declined to pay for this $56,000/year drug.

Duke Health provides a voice of sanity

Duke Health has provided a good summary of the issues with Aducanumab and why its pharmacy will not be offering it to its patients. According to Duke Health, although Aducanumab has shown an ability to reduce the presence of the amyloid protein, it is unclear whether the amyloid protein actually causes Alzheimer’s disease. Although the drug maker, Biogen, claims that the drug did work to reduce cognitive decline is some patient subgroups, overall it had no effect.

Explaining the fallacy of Biogen’s subgroup analysis

I am a meta-analyst, which means I specialize in studying research in aggregate, and I have personally exposed multiple cases of scientific fraud in my field of marketing science, so I will attempt to elaborate further. Biogen’s claims of the drug working for certain subgroups is very weak. Consider the following example, suppose you had a hypothesis that women are taller than men at the college you attend. So you measured all the men and women and compared heights and found that on average you were wrong. Instead of accepting that you are wrong, you decide to go around to each classroom to measure height of men and women in each classroom. In most classes the men are taller than the women but in a few classes, you found the opposite to be true. So now you claim that women are taller than men in some subgroups. Specifically, you claim that females are taller than men in industrial economics classes and identity politics classes. Obviously you found this only by random chance. This is the same weak foundation that Biogen’s claims rest on. They claim that—although it may not work generally, it may work for certain subgroups. This claim will not hold up to further testing that is specific to that subgroup just like your “women are taller than men” hypothesis will not hold up if you test it on the same classes for the next semester.

The fallacy of assuming that reduction in the amyloid protein can reverse the causes of Alzheimer’s disease

The biggest problem here is that scientists are not in agreement that the amyloid protein actually does cause Alzheimer’s disease. In fact, a recent scandal revealed that the original research that the whole idea was based on has turned out to be fraudulent. That’s right, the foundation of the field is a fraud. Scientists engage in fraud for many reasons including increased prestige and career benefits. But even if the whole concept were not based on fraud, the goal should not be to reduce a protein but to reduce cognitive decline. Since there is no evidence of the latter, the drug appears to be completely useless. Read more about the fraud case.

Conclusions

Still the best recommendation for staving off Alzheimer’s disease and cognitive decline generally appears to be lifestyle changes: exercise, diet, etc.

Also see:

• Brain Health FAQ: Can I reduce my risk of developing brain disease as I age?

• Why Physicians Should Not Prescribe Aducanumab for Alzheimer Disease