Monthly Archives: July 2016

Research Highlights from the Alzheimer’s Association International Conference

This year’s Alzheimer’s Association International Conference took place July 22-28 in Toronto. The meeting brings some of the world’s leading Alzheimer’s researchers together to discuss their latest findings. I’ve compiled brief descriptions for some of the most exciting research presented at the meeting.

Mental Stimulation Greatly Influences Risk of Dementia

An unhealthy “Western” diet is associated with an increased risk of many health problems, including dementia. However, results presented at AAIC suggest mental stimulation in the form of higher education, a cognitively complex job, and/or social engagement can reduce the risk of cognitive decline in elderly adults, even those with a poor diet. Additionally, the highly-publicized ACTIVE study found that elderly subjects who participated in 10 years of regular cognitive training (similar to brain-training games like Luminosity) had a 48% reduced risk of dementia during the course of the study. Read more

Symptoms Checklist May Aid in Earlier Diagnosis of Alzheimer’s

Researchers have defined a new later-life neuropsychiatric condition called Mild Behavioral Impairment (MBI), which may be a precursor for Mild Cognitive Impairment and/or dementia later in life. The symptoms associated with MBI are grouped into five broad categories: mood, impulse control, apathy, social appropriateness, and psychosis. A recent study found that more than 80% of elderly adults at a memory clinic displayed at least one symptom of MBI, and that the symptoms were associated with increased caregiver burden. The researchers plan to refine the MBI checklist to be applicable to younger, non-demented subjects. Read more

Alzheimer’s Patients Receiving Treatment Have Reduced Mortality and Financial Burden

The medications for Alzheimer’s disease currently on the market can decrease the rate of cognitive decline but do not slow the overall progression of the disease. However, new results suggest that receiving treatment can reduce both mortality rates and medical costs for Alzheimer’s patients post-diagnosis. Patients who took dementia medications had a 28% reduced risk of dying during the approximately 2-year course of the study, and also paid more than $1,000 less each month in healthcare costs. Read more

High Cost of Preventable Hospitalizations Among Alzheimer’s Patients

A recent study shows that 1 in 7 hospitalizations among individuals with Alzheimer’s and related dementias is potentially preventable. These include hospital visits as a result of acute conditions like infection or dehydration, as well as chronic diseases including diabetes, cardiovascular disease, or respiratory illness. In total, preventable hospitalizations of dementia patients cost Medicare $2.58 billion dollars during 2013. Read more

Smell and Eye Tests May Predict Cognitive Decline

Two of the first brain regions affected by Alzheimer’s disease are the olfactory (smell) and visual systems. Studies presented at AAIC showed that neurodegeneration of the optic nerve or retina could be an effective predictor for the development of Alzheimer’s. Two other labs found that low scores on the University of Pennsylvania Smell Identification Test were associated with cognitive decline and dementia. Read more

Promising Anti-Tau Drug Fails in Clinical Trials

Alzheimer’s is characterized by the buildup of two toxic proteins in the brain: beta-amyloid and tau. After hundreds of drugs targeting beta-amyloid failed in clinical trials, researchers have recently begun to look into anti-tau drugs instead. Unfortunately, a promising anti-tau drug called LMTM failed in phase 3 of clinical trials. Apart from in a small subgroup of participants, the drug did not improve cognitive or neurological symptoms better than a placebo. Additionally, 80% of subjects experienced at least one adverse side effect. Read more

Men with Dementia are More Likely to Be Misdiagnosed than Women

It’s a commonly-held belief that women are at a greater risk of Alzheimer’s than men. However, it’s possible that innacurate diagnoses may contribute to this discrepancy (see Is It Really Alzheimer’s? 10 common misdiagnoses you should know about). A study of more than 1600 postmorten brains found equal rates of Alzheimer’s among men and women. Men typically have a younger age of onset and are more likely to exhibit atypical symptoms, increasing the risk of misdiagnosis. Another postmortem brain study found that across genders, approximately 10% of Alzheimer’s diagnoses were incorrect, with the true cause of memory loss usually being vascular dementia. Read more

Reducing Dependence on Antipsychotics in Dementia Care

Multiple studies have demonstrated that prescribing antipsychotics to dementia patients can accelerate the rate of cognitive decline and death. Nonetheless, this remains a common practice for treating the symptoms of dementia. In a recent study, nurses in 60 long-term care facilities were trained to manage patients’ dementia symptoms without the need for drugs. The patients’ doses of antipsychotics were incrementally reduced until they were eliminated. Most of the subjects were able to successfully cease antipsychotic use after a one-year follow-up. Read more


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Is It Really Alzheimer’s? 10 common misdiagnoses you should know about

Doctors misdiagnose a patient with Alzheimer’s disease at alarmingly high rates, when the true cause may be a different (and often treatable) disease. In 2011, researchers conducted autopsies on the brains of 211 men who had been diagnosed with Alzheimer’s while they were alive. They found that nearly half of the brains did not possess the necessary pathology to meet an Alzheimer’s diagnosis [1]. A 2012 study reported similar misdiagnosis rates by physicians at the National Institute on Aging’s Alzheimer’s Disease Centers [2].

An incorrect Alzheimer’s diagnosis can cause a person to pay $9,500 to $14,000 annually in unnecessary medical procedures and medications [3]. Even worse, it may result in the true cause of the dementia symptoms going untreated, hastening the rate of cognitive decline. To give you the tools to reduce the risk of a misdiagnosis, I’ve compiled this list of ten common conditions that can mimic the symptoms of Alzheimer’s disease. If you or a loved one has been diagnosed with Alzheimer’s disease, be sure that you request tests to rule out these other possibilities.

1. Medication side effects

More than 100 medications can have side effects resembling symptoms of Alzheimer’s. These include a wide variety of common meds including Benadryl, Ambien, Valium, Xanax, and Lipitor [4]. It is particularly important to inform your doctor if you are on anticholinergic drugs, which include many antihistamines, antipsychotics, antidepressants, and muscle relaxants, among others [5]. These drugs block the function of a neurotransmitter called acetylcholine, which can lead to cognitive impairment [6].

2. Normal pressure hydrocephalus

The central nervous system is surrounded by cerebrospinal fluid, which cushions the brain and regulates cerebral blood flow. For unknown reasons, cerebrospinal fluid can sometimes build up in the brain cavities (ventricles) and cause them to swell, resulting in a condition called normal pressure hydrocephalus (NPH). The symptoms of NPH include progressive dementia, difficulty walking, and urinary incontinence [7]. According to the Hydrocephalus Association, NPH affects an estimated 700,000 Americans, though only 1 in 5 of these people receive the correct diagnosis [8]. As many as 10% of patients diagnosed with Alzheimer’s or other forms of dementia may actually have NPH [9]. This condition is easily detected using brain scans and can often be treated by surgically draining the excess fluid from the ventricles. Additional reading on NPH: [10], [11], [12]

3. Vascular dementia

Vascular dementia is the second most common form of dementia after Alzheimer’s. It is caused by a stroke, multiple “mini strokes,” or other cardiovascular disturbances, and can cause similar symptoms to Alzheimer’s [13]. A 2013 study found that 17% of vascular dementia patients were previously given an incorrect diagnosis for Alzheimer’s disease, which led to significantly increased medical costs [14]. Vascular dementia is very difficult to distinguish from Alzheimer’s, and the possibility of misdiagnosis should be considered if the patient has risk factors such as high blood pressure, diabetes, or smoking. There is currently no cure for vascular dementia, but steps may be taken to improve cardiovascular health and reduce the risk of further cognitive decline [15].

4. Vision or hearing loss

Cognitive evaluations such as the Mini-Mental State Examination (MMSE) may yield an incorrect diagnosis of Alzheimer’s disease if a patient is experiencing undiagnosed vision or hearing loss. Studies have shown that individuals with visual [16] or auditory [17] impairments score lower on the MMSE, despite being cognitively normal. Both of these conditions are common among the elerly population. Studies estimate that among individuals over the age of 70, 18% are visually impaired, 33% are hearing impaired, and 8% are both visually and hearing impaired [18]. Regular vision and hearing exams could not only prevent an incorrect diagnosis but also improve the overall quality of life for these patients [19], [20].

5. Depression

Depression can often mimic the early symptoms of Alzheimer’s disease. These include mood changes, withdrawal from daily activities, sleep disruptions, and difficulty concentrating [21]. Depression affects more than 1 in 20 elderly adults and the risk may be increased by the death of a spouse or chronic illness, as well as certain medical or psychological conditions [22]. The symptoms of depression can often be improved through a combination of medications and psychotherapy.

6. Thyroid problems

The thyroid gland produces hormones that regulate metabolism and other body functions. The American Thyroid Association reports that 12% of Americans will develop thyroid problems in their lifetime, and more than half of them are unaware of their condition. Both hypothyroidism and hyperthyroidism can have symptoms resembling Alzheimer’s, including forgetfulness, mood changes, and sleep disturbances. Thyroid problems are often treatable but can cause serious complications if left undiagnosed [23].

7. Vitamin B12 deficiency

Vitamin B12 plays multiple important roles in the nervous and circulatory systems. It is most commonly found in meat, fish, and dairy products. As many as 9% of Americans are deficient in this essential nutrient [24]. Risk factors include a vegetarian or vegan diet without B12 supplements, heavy alcohol consumption, and long-term use of acid-reflux medications. Vitamin B12 deficiency can lead to dementia and changes in mood or personality, which may be mistaken for Alzheimer’s [25]. Individuals with an Alzheimer’s diagnosis might consider requesting a blood test for B12 levels, or increasing their intake of B12 in the form of supplements, fortified cereals, and B12-rich foods to see if their cognitive symptoms improve.

8. Urinary tract infection

Urinary tract infections (UTI’s) are the most common bacterial infection in the United States. They primarily affect women; nearly half of all women will experience at least one UTI in their lifetime [26]. When diagnosed correctly, UTI’s are easily treated using antibiotics and rarely cause complications. However, the little-known neurological symptoms can result in a misdiagnosis as Alzheimer’s. An elderly person with a UTI is at an increased risk of experiencing delirium, which is characterized by sudden behavioral changes such as confusion, agitation, fatigue, or delusions. Be suspicious of Alzheimer’s-like symptoms if they are accompanied by symptoms of a UTI, which include frequent, painful urination and discolored or foul-smelling urine [27].

9. Sleep disorders

We all know the importance of getting 8 hours of sleep each night, but few of us are aware of just how much sleep depravation can affect our cognitive function. A 1999 study reported that 1 in 5 individuals over the age of 65 experience sleep disturbances, though only a minority seek treatment [28]. Sleep disorders such as sleep apnea, chronic insomnia, and restless leg syndrome can lead to fatigue, difficulty focusing, irritability, and memory loss [29]. These conditions can be easily detected by visiting a sleep clinic.

10. Gluten allergy

This might be the most surprising item on this list: a simple dietary change can completely reverse the symptoms of some people’s dementia. Celiac disease is an allergic reaction to gluten, a protein found in wheat, barley, and rye. Celiac was once believed to be rare, but is now classified as one of the most common autoimmune conditions. The University of Chicago’s Celiac Disease Center estimates that 1 in 133 people have celiac disease, of whom an astounding 97% remain undiagnosed [30]. Though people with celiac can live a healthy life on a gluten-free diet, undiagnosed celiac disease can have serious and even fatal consequences, including progressive dementia and other neurological conditions [31]. For individuals with celiac-induced dementia, switching to a gluten-free diet might completely reverse their symptoms [32].


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A Vaccine for Alzheimer’s Disease Could Be in Our Future


Alzheimer’s disease is generally considered to have two key hallmarks: beta-amyloid and tau. These proteins form toxic clumps in the brains of Alzheimer’s patients and are believed to be the main drivers of the disease (see Alzheimer’s Disease: A general overview). In the past, the majority of attempts to develop a vaccine or cure for Alzheimer’s have focused on reducing levels of beta-amyloid. These trials have been largely unsuccessful; of more than 244 drug candidates tested in the past decade, only one has made it past clinical trials, a failure rate of more than 99% (see Where’s our cure to Alzheimer’s disease?[1].

One reason for these failures may be that beta-amyloid begins accumulating long before the symptoms of Alzheimer’s develop, causing vaccines to be ineffective by the time they’re administered. In contrast, tau is believed to accumulate at a later stage than beta-amyloid [2]. Some have proposed that beta-amyloid immunotherapy may be most effective when implemented in the earliest stages of Alzheimer’s, while drugs targeting tau could have therapeutic benefits during more advanced stages [3].

Another reason for the high failure rate of Alzheimer’s drug candidates is the prevalence of harmful side effects in clinical trials. In particular, a severe and possibly fatal condition called meningoencephalitis, which results in inflammation of the brain and meninges, has forced multiple trials to be ended prematurely. Though the direct cause is unknown, one possibility is that autoreactive T cells may be involved. Normally, vaccines work by triggering the creation of memory B cells. These cells produce protective antibodies against the harmful protein, leading to adaptive immunity. It’s believed that in addition to activating B cells, the failed Alzheimer’s vaccines can trigger another type of immune cell called autoreactive T cells, which can enter the brain and cause meningoencephalitis [4].

New Results

In a study published last week in Nature Scientific Reports, researchers created the first vaccine to target both beta-amyloid and tau [5]. The researchers in this study combined a vaccine that had been previously shown to trigger a strong immune response to beta-amyloid with a newly-designed vaccine for tau. When the dual vaccine was administered to mice, along with an immune system enhancer called Advax, they developed high levels of antibodies against both beta-amyloid and tau. This suggests that the mice could be resistant to Alzheimer’s disease in the future.

The new treatment also addresses the common problem of meningoencephalitis. The two vaccines are designed using a new platform called MultiTEP, which allows them to specifically trigger a B cell immune response but not autoreactive T cells [6]. The researchers hope that this may prevent the vaccine from causing autoimmune reactions.

Future studies are still needed to determine the effectiveness of this vaccine at preventing Alzheimer’s in humans. The authors of the study expect clinical trials to begin within the next 3-5 years [7].


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A New Approach to Predicting Risk of Alzheimer’s Disease


An individual’s risk for Alzheimer’s disease is affected by a variety of genetic and environmental factors. While the causes of early-onset Alzheimer’s are well understood, the genetic factors underlying late-onset Alzheimer’s disease (LOAD), which makes up 95% of total cases, are less clear. The APOE4 allele is considered the major risk factor for this form of Alzheimer’s, as it can increase your risk by 2-3 times if you have one copy of the allele or up to 15 times if you have two copies. APOE4 does not guarantee that an individual will develop LOAD, and researchers have been searching for other genes that may be involved. (For more background see The Genetics of Alzheimer’s Disease).

Genome-wide association studies, which systematically analyze the 0.1% of DNA sequence that varies between individuals, have linked at least 21 other genes to an increased risk of LOAD. Individually, each of these genes has only a small influence in comparison to APOE4, often increasing one’s risk by only a few percentage points. However, when many of these small genetic risk factors are combined, they can greatly affect an individual’s chances of developing LOAD.

Overall, studies suggest that approximately 33% of an individual’s risk for developing LOAD is attributable to genetics, with the rest being due to lifestyle choices and environmental factors. Of this, APOE and the 21 already-identified genes account for less than 25% of the genetic risk, suggesting that the majority of genetic risk factors for Alzheimer’s disease remain unknown.

New Results

In a recent study published in the journal Neurology, a group of researchers from the Alzheimer’s Disease Neuroimaging Initiative searched for other genes, outside of the 21 already identified, that could also act as slight risk factors for Alzheimer’s. They used data collected from the International Genomics of Alzheimer’s Project to compute polygenetic risk scores, or PGRS, for both young and elderly adults who did not have dementia. Each person’s PGRS was calculated using his or her unique combination of small genetic risk factors (including many that were not statistically significant in genome-wide association studies) in order to estimate the genetic risk for LOAD. The researchers then analyzed whether PGRS were associated with biological markers of preclinical Alzheimer’s disease.

In elderly subjects who did not have dementia, high PGRS was associated with poorer memory, smaller volume of the hippocampus (the part of the brain that helps us form new memories), and increased levels of toxic beta-amyloid in the brain. High PGRS in these individuals also correlated with an increased rate of cognitive decline and a greater probability of later being diagnosed with Alzheimer’s disease. The researchers also computed PGRS for younger subjects under the age of 35. They found that a high PGRS was associated with reduced hippocampal volume, similarly to the older subjects.

Together, these results suggest that more genes besides the currently-identified 21 may need to be considered when evaluating an individual’s risk for LOAD. The researchers plan to repeat this study using a larger sample size to verify the results. Future studies also will track younger subjects to see if PGRS can predict their risk for Alzheimer’s as they age, and compare these results to less comprehensive systems of genetic prediction. The hope is that by refining PGRS, we may one day be able to develop better genetic tests for young people that yield more accurate predictions of future Alzheimer’s risk.


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How Oral Hygiene Protects Your Brain From Dementia

Let’s be honest, most of us probably aren’t flossing nearly as often as our dentist tells us to. As long as our teeth look fairly white and our breath smells fine, we assume that our oral care routine is good enough. However, this becomes particularly problematic as we get older. Elderly people often neglect their oral hygiene, leading to a variety of oral infections including gum disease. Not only can gum disease make it painful to chew food and increase the risk of tooth loss, but research suggests it may also contribute to the development of Alzheimer’s disease.

Microbes and Dementia

The idea that microbial infections may act as a trigger or cofactor for Alzheimer’s disease, known formally as the pathogen hypothesis, has been around since the 1980s, though only recently has it moved from the fringes to the forefront of mainstream neuroscience. The hypothesis suggests that microbes can enter the central nervous system by passing through a selective membrane called the blood-brain barrier, which tends to become more leaky as we age, particularly in the hippocampus (the brain area most associated with memory).

Once inside, the microbe triggers an immune response that results in the deposition of amyloid beta plaques, the toxic protein clumps that are the hallmark of Alzheimer’s disease. As more microbes slip past the barrier, the brain is unable to clear away the plaques faster than they’re being created, causing them to accumulate and eventually leading to neurodegeneration.

Support for the pathogen hypothesis comes from studies that show positive associations between infections and the development of Alzheimer’s disease. In particular, meta-analyses have shown that the herpes virus, as well as the bacteria that cause pneumonia, syphilis, and Lyme disease, are found at significantly increased rates in Alzheimer’s patients compared to healthy controls of the same age and genetic risk profile. Other studies show that infecting lab-cultured neurons with these viruses and bacteria causes an Alzheimer’s-like pathology to develop.

Researchers now believe certain bacteria that can cause oral infections may be the next microbes to join the list of Alzheimer’s disease risk factors.

Your Oral Microbiome and You

The microbes living in our mouths and throats, known collectively as the oral microbiome, are different for every person and can include nearly 900 unique species of bacteria. Changes in the microbiome’s composition as a result of poor oral hygiene can lead to periodontitis, a severe form of gum disease that gradually destroys the bone sockets holding your teeth in place, resulting in tooth loss. The CDC reports that nearly half of all adults in America suffer from mild, moderate, or severe periodontitis. For adults over 65, that number increases to more than 70%.

The bacteria implicated in periodontitis can cause further complications when they enter the bloodstream and travel to other organs throughout the body. Studies suggest that periodontal bacteria can initiate harmful inflammatory reactions in multiple organ systems, increasing the risk or severity of various conditions including diabetes, cardiovascular disease, and rheumatoid arthritis.

Oral Bacteria Inside the Brain

Due to their ability to travel through the bloodstream, periodontal pathogens can also enter the brain via a leaky blood-brain barrier. A 2002 study observed that DNA from Treponemaa family of bacteria implicated in periodontitis, was more likely to be present in Alzheimer’s brains compared to healthy brains. A more recent study found virulence factors for the periodontal bacteria P. gingivalis in postmortem brain tissue of Alzheimer’s patients.

Multiple studies have repeatedly correlated periodontitis with reduced cognitive function, as well as higher levels of amyloid beta in the brain. Another study of elderly Chinese adults reported the loss of more than 16 teeth being associated with severe cognitive impairment. In addition, a 2016 study presented evidence that periodontitis might worsen dementia symptoms after observing that Alzheimer’s patients diagnosed with periodontitis had a six-fold increase in the rate of cognitive decline during a six month period.

A recent study, published in January 2019, added more evidence to support a role for oral bacteria in Alzheimer’s. The researchers showed that when mice were infected with P. gingivalis, a common type of periodontal bacteria, they developed many key hallmarks of Alzheimer’s. The group then designed a new drug that inhibited a specific protein from P. gingivalis and administered it to the mice. This treatment halted the progression of Alzheimer’s-like pathology in the mice, suggesting that these kinds of drugs could be useful for treating some cases of Alzheimer’s in humans.

In conclusion, more research is still needed to conclusively support a causal relationship between Alzheimer’s disease and oral infections. However, based on the strong correlational evidence with comorbidity of these two conditions, as well as the more definite links between periodontitis and other health problems, it’s clear that we need to place greater emphasis on the importance of oral hygiene for our overall health. This is particularly true for individuals over the age of 65, who have the greatest risk for both dementia and gum disease. If protecting your brain could be as simple as twice daily brushing, daily flossing, and regular trips to the dentist’s office, there’s no reason we shouldn’t all be taking this initiative.


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Cannabinoids May Combat Inflammation in Alzheimer’s

Until the 1990s, it was generally accepted among scientists that amyloid beta (AB), the protein that forms toxic plaques in the brains of Alzheimer’s patients (see Alzheimer’s Disease: A General Overview), only accumulated outside of neurons. This view changed when researchers discovered that AB could also accumulate inside neurons. Later studies suggested that this intracellular AB could kill the neuron and cause it to burst open, releasing the plaques into the brain to potentially kill more cells in a deadly chain reaction. However, it remained unclear exactly how AB was able to kill these neurons from the inside.

A study published in Aging and Mechanisms of Disease suggests an answer to this question and even offers a prospective solution. The researchers observed that when human nerve cells were induced to produce intracellular amyloid beta, the production of immune defense molecules called cytokines was increased. These cytokines initiated an inflammatory reaction that ultimately caused the cell to burst open and die. These results suggest that intracellular AB can kill neurons by essentially tricking the brain’s immune system into attacking itself.

Interestingly, enhancing a specific cannabinoid receptor prevented AB from accumulating in these cells, saving them from the immune system attack. In particular, THC, a cannabinoid that’s found in marijuana, was able to bind the most effectively to this receptor and completely eliminated AB from the cells. These results may explain why mice with genetically-induced Alzheimer’s disease show improved memory when exposed to cannabinoids, though this effect has not yet been confirmed in humans. Future studies plan to test synthetic cannabinoids to see if administering them to people with mild cognitive impairment may prevent the disease from progressing to Alzheimer’s.

Related article: Marijuana and Alzheimer’s Disease: What Does the Science Say?


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The MEND Program Shows Promise for Reversing Cognitive Decline


In September 2014, researchers from the University of California reported the development of the MEND protocol, short for Metabolic Enhancement for Neurodegeneration. MEND was designed to combine the results of multiple studies to create a comprehensive set of guidelines for enhancing cognitive function in elderly adults. The program was also intended to be personalized to each patient based on his or her lifestyle and medical history. The MEND protocol includes the following guidelines, among many others:

  • Eat a diet rich in high-antioxidant foods, such as blueberries and kidney beans, and anti-inflammatory foods, such as tumeric and salmon.
  • Minimize or eliminate simple carbohydrates, such as white bread and pasta, as well as foods with a high glycemic index, which are quickly digested and cause blood sugar spikes.
  • Fast for 12 hours each night, including at least 3 hours before bedtime. For example, if you typically eat breakfast at 7am, you should not eat anything after 7pm the previous night.
  • Reduce stress through yoga, meditation, or other methods.
  • Get 8 hours of sleep every night. Seek treatment for insomnia or sleep apnea. (See: How Sleep “Cleans” Your Brain and Fends Off Alzheimer’s)
  • Maintain healthy digestion using prebiotics and probiotics. (See: Probiotics May Improve Cognitive Function and Alzheimer’s Disease)
  • Optimize oral hygiene through regular, thorough brushing and flossing. (See: How Oral Hygiene Protect Your Brain from Dementia)

A small clinical trial was created to test the effects of the MEND program on cognitive function. Ten middle-aged or elderly adults with Alzheimer’s disease or other forms of cognitive impairment worked with the researchers to develop personalized plans based on MEND’s guidelines. Most of the subjects and their families began noticing improvement within three to six months of starting the program, and several were able to return to work after previously having to discontinue. Though promising, the evidence of this study was short-term and anecdotal, requiring confirmation by additional data.

New Results

The study published this month reports on follow-up exams of the original ten subjects after following the MEND protocol for between 5 and 24 months. The researchers used MRI scans as well as neuropsychological testing to evaluate the subjects’ cognitive function. For two of the subjects, the results were dramatic. The volume of one patient’s hippocampus (the part of the brain most associated with memory) went from the 17th to the 75th percentile after following the program for only 10 months. Another patient with diagnosed Alzheimer’s disease experienced substantial improvement on cognitive exams after 22 months on the program, even moving from the 3rd to the 84th percentile on one of the tests. Though the changes observed in the other eight subjects were more modest, all ten subjects showed some level of improved cognition during the follow-up exams, and none of them experienced any cognitive decline. Additionally, most of the subjects had at least one copy of the APOE4 allele, a strong genetic risk factor for Alzheimer’s, demonstrating that we may be able to combat the effects of our genes through healthy lifestyle choices (see The Genetics of Alzheimer’s Disease).

Due to the very small sample size, larger trials need to be conducted before broad conclusions can be drawn. It also remains to be seen whether this cognitive improvement is permanent or temporary. However, these results give new hope to the prospect of reversing cognitive decline, which previously was deemed impossible for people already experiencing cognitive impairment. If you or a loved one is noticing memory troubles or has been diagnosed with dementia, consider implementing some of the MEND guidelines to possibly reverse the effects of cognitive decline. For more details on reducing your Alzheimer’s risk, see How to Reduce Your Dementia Risk in 2018.


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