Wednesday, May 31, 2017

Alzheimer's & Incontinence

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Alzheimers&Demantia Weekly

SOURCE:
The Alzheimer's Disease Education and Referral (ADEAR) Center

Here are some good ways you can deal with incontinence in dementia care.

A person with Alzheimer’s disease may have other medical problems over time. These problems can cause more confusion and behavior changes. The person may not be able to tell you what is wrong.

One problem, incontinence, means a person can’t control his or her bladder and/or bowels. This may happen at any stage of Alzheimer’s disease, but it is more often a problem in the later stages. Signs of this problem are leaking urine, problems emptying the bladder, and soiled underwear and bed sheets. Let the doctor know if you see any of these signs. He or she may be able to treat the cause of the problem.

Causes of Incontinence

Incontinence has several possible causes. Some can be treated:
Urinary tract infection
Enlarged prostate gland
Too little fluid in the body (dehydration)
Diabetes that isn’t being treated
Taking too many water pills
Drinking too much caffeine
Taking medicines that make it hard to hold urine

When you talk to the doctor, be ready to answer the following questions:

What medicines is the person with Alzheimer’s taking?
Does the person leak urine when he or she laughs, coughs, or lifts something?
Does the person urinate often?
Can the person get to the bathroom in time?
Is the person urinating in places other than the bathroom?
Is the person soiling his or her clothes or bed sheets each night?
Do these problems happen each day or once in a while?

What To Do About Incontinence

Here are some ways you can deal with incontinence:

Remind the person to go to the bathroom every 2 to 3 hours. Don’t wait for him or her to ask.
Show the person the way to the bathroom, or take him or her.
Watch for signs that the person may have to go to the bathroom, such as restlessness or pulling at clothes. Respond quickly.
Make sure that the person wears loose, comfortable clothing that is easy to remove.
Limit fluids after 6 p.m. if problems happen at night. Do not give the person fluids with caffeine, such as coffee or tea.
Give the person fresh fruit before bedtime instead of fluids if he or she is thirsty.

Here are some other tips:

Mark the bathroom door with a big sign that reads “Toilet” or “Bathroom.”
Use a stable toilet seat that is at a good height. Using a colorful toilet seat may help the person identify the toilet. You can buy raised toilet seats at medical supply stores.
Plan ahead if you are going out with the person. Know where restrooms are located. Take an extra set of clothing in case of an accident.
Help the person when he or she needs to use a public bathroom. This may mean going into the stall with the person or using a family or private bathroom.

Accidents Happen

Be understanding when bathroom accidents occur. Stay calm and reassure the person if he or she is upset.

Incontinence supplies, such as adult disposable briefs or underwear, bed protectors, and waterproof mattress covers, may be helpful. You can buy these items at drugstores and medical supply stores. A drainable pouch may be useful for the person who can’t control his or her bowel movements. Talk to a nurse about how to use this product.

Some people find it helpful to keep a record of how much food and fluid the person with Alzheimer’s takes in and how often he or she goes to the bathroom. You can use this information to make a schedule for going to the bathroom.

Sunday, May 28, 2017

Alzheimer's disease-associated Aβ42 peptide

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EurekAlert

This article by Dr. Natalia Carulla et al is published in Current Chemical Biology, Volume 11, Issue 1, 2017

BENTHAM SCIENCE PUBLISHERS

ggregation of the amyloid-beta peptide (Aβ) in the brain is strongly associated with Alzheimer´s disease (AD). This process is highly heterogeneous and transient in nature, thus hindering identification of the exact molecular form of Aβ responsible for the neurotoxicity observed in this disease. Therefore, characterizing Aβ aggregation is of utmost importance to make headway in the field of AD. Nuclear magnetic resonance spectroscopy (NMR), a technique used to obtain structural information, holds great potential to achieve this goal, as it could contribute to determining the structure of Aβ aggregate forms. However, it requires large amounts of peptide, as well as isotopic labels that are introduced through the Aβ peptide production process.

In this article, we report a new and straightforward production protocol to obtain the Aβ most strongly linked to AD, the so-called Aβ42 form, with the required labels for NMR experiments. Specifically, we describe an inexpensive strategy through which to obtain [U-15N]- and [U-2H,13C,15N]-labeled Aβ42. Notably, this approach does not require reversed phase high performance liquid chromatography (RP-HPLC), a costly and time-consuming purification technique widely used in previously reported Aβ production protocols. Instead, all the purification steps required in our production protocol can be performed with the fast protein liquid chromatography system (FPLC), which is widely available. The peptides that we obtained are of high purity and have the required isotope labeling to support NMR-based structural studies.Therefore, we conclude that this strategy offers a simpler and inexpensive approach to obtain isotopically labeled Aβ42 than previously described methods, thereby paving the way for NMR-based Aβ structural studies.

###

Thursday, May 25, 2017

SILK Blood Test: Solving Alzheimer's & Aging

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REFERENCE: Patterson BW, Elbert DL, Mawuenyega KG, Kasten T, Ovod V, Ma S, Xiong C, Chott R, Yarasheski K, Sigurdson W, Zhang L, Goate A, Benzinger T, Morris JC, Holtzman D, Bateman RJ

The Stable Isotope Labeling Kinetics (SILK™) blood test is a recent technology that sees Alzheimer's years before signs appear. It can open doors to researchers trying to solve problems like the connection between Alzheimer's and aging. See how.

Biomarkers in the blood, indicating Alzheimer's, may appear 15 years before there are signs of trouble. Researchers are using the SILK™ blood test to track those biomarkers and gain a better shot at finding ways to prevent and treat Alzheimer's.

The Stable Isotope Labeling Kinetics (SILK™) platform was pioneered at Washington University School of Medicine (WUSM) in St. Louis and is marketed by C2N. It includes new technologies that enable a novel approach to measure the metabolism of brain-derived proteins implicated in Alzheimer's disease (AD) and mild cognitive impairment (MCI).

Why Does Aging Increase Alzheimer's?

The greatest risk factor for Alzheimer’s disease is advancing age. After 65, the risk doubles every five years. As many as half of the elderly who are over 85 are estimated to be living with some type of dementia, usually Alzheimer's.

A sizable study demonstrated that in our 30s, a healthy brain clears amyloid-beta every four hours. At 80 years old, it takes more than 10 hours. This may explain the link between age and Alzheimer's, as well as what we need to do to fight this disease. Researchers at Washington University School of Medicine in St. Louis have identified some of the key changes in the aging brain that lead to the increased risk. The changes center on amyloid beta 42, a main ingredient of Alzheimer’s brain plaques. The protein, a natural byproduct of brain activity, normally is cleared from the brain before it can clump together into plaques. Scientists long have suspected it is a primary driver of the disease.

A new study reveals that the brain's ability to clear the main ingredient of Alzheimer's plaques slows with age (the plaques are red in this image). The findings could help explain why risk of the disease increases with age.

“We found that people in their 30s typically take about four hours to clear half the amyloid beta 42 from the brain,” said senior author Randall J. Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology. “In this new study, we show that at over 80 years old, it takes more than 10 hours.”

The slowdown in clearance results in rising levels of amyloid beta 42 in the brain. Higher levels of the protein increase the chances that it will clump together to form Alzheimer’s plaques.

The result details appear online in the Annals of Neurology.

Results Sum-Up

For the study, the researchers tested 100 volunteers ages 60 to 87. Half had clinical signs of Alzheimer’s disease, such as memory problems. Plaques had begun to form in the brains of 62 participants.

The subjects were given detailed mental and physical evaluations, including brain scans to check for the presence of plaques. The researchers also studied participants’ cerebrospinal fluids using a technology developed by Bateman and co-author David Holtzman , MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology at Washington University. The technology — known as stable isotope-linked kinetics (SILK)— allowed the researchers to monitor the body’s production and clearance of amyloid beta 42 and other proteins.

In patients with evidence of plaques, the researchers observed that amyloid beta 42 appears to be more likely to drop out of the fluid that bathes the brain and clump together into plaques. Reduced clearance rates of amyloid beta 42, such as those seen in older participants, were associated with clinical symptoms of Alzheimer’s disease, such as memory loss, dementia and personality changes.

Scientists believe the brain disposes of amyloid beta in four ways: by moving it into the spine, pushing it across the blood-brain barrier, breaking it down or absorbing it with other proteins, or depositing it into plaques.

How the SILK™ Blood Test Works

Biomarkers are chemicals in our bodies that are markers for an illness, such as Alzheimer's. Until now, doctors looking for Alzheimer's biomarkers would go through the delicate process of taking cerebrospinal fluid from patients. For the first time, instead of analyzing Alzheimer's proteins in cerebrospinal fluid, the SILK™ Blood Test makes it possible to detect the same metabolic markers in patients’ blood samples.

This capability has implications for the advancement of new treatments, early prevention, and personal wellness. Alzheimer’s is now one of the major global healthcare concerns. Approximately 44 million people currently have clinical Alzheimer's disease (AD). Millions more have MCI that places them at high risk for progression to clinical AD. The number of cases of AD and MCI are expected to increase sharply in the years ahead due to the aging baby boomer population.

Pharmaceutical companies developing new drugs targeting AD increasingly recognize that early intervention provides the greatest chance of halting or reversing disease progression. Biomarkers are needed to detect this early pathology, which can begin at least 15 years before the onset of any clinical symptoms. At the same time, dynamic biomarkers, like those offered by the SILK™ platform, may also track treatment responses during the pre-symptomatic stages of disease.

Since 2008, C2N has applied the SILK-Aβ® test to measure the kinetics of beta-amyloid in cerebrospinal fluid. The test has served as a primary endpoint in clinical drug studies to demonstrate target engagement and guide dose selection. The SILK-Aβ® isoforms test is also highly sensitive to identifying people with brain amyloidosis (one of the earliest indicators of Alzheimer's), even before amyloid deposits are seen with brain imaging. Still, the more invasive nature of cerebrospinal fluid sampling has impeded the full potential of the SILK-Aβ® method.

“With a simplified SILK-Aβ® test available through blood sampling, we now have an opportunity to validate a unique therapeutic and diagnostic marker,” stated Dr. Joel B. Braunstein, CEO of C2N. “We plan to achieve this validation by collaborating with pharmaceutical companies that are testing their compounds in phase 2 and phase 3 clinical studies, as well as by participating in natural history studies tracking the progression of AD. If successful, we expect to be able to offer a reliable and informative screening test that is also convenient for patients.”

Alzheimer’s Disease & Mild Cognitive Impairment

Currently AD is diagnosed based on clinical assessment by skilled neurologists or based on an amyloid imaging brain scan: there are no approved blood based biomarkers for this disease. Early detection of AD is a major research focus since early detection would pave the way for early intervention. Mild cognitive impairment (MCI) is often a precursor of clinical AD. The disorder is associated with cognition changes that are serious enough to be noticed by the individuals experiencing them or to other people, but the changes are not severe enough to interfere with activities of daily living. Individuals with MCI have a significantly increased risk of eventually developing AD, with approximately 50% of such individuals converting to AD within three years.

SILK-Aβ® Technology

Dr. Randall Bateman and Dr. David Holtzman originally developed the SILK™ technology at WUSM. Scientific American recognized the SILK-Aβ® assay as one of the top 50 new innovative technologies of the year. Similar to a pulse chase assay, the SILK-Aβ® assay relies on in vivo labeling of human subjects with a stable isotope labeled amino acid. The stable isotope labeled amino acid is non-radioactive, safe to the environment and to humans, and is incorporated into newly generated proteins. Using a highly sensitive mass spectrometer, we can measure the incorporation of the stable isotope into Aβ and thereby assess the metabolism of Aβ. This ability is particularly useful for early detection of brain amyloidosis or when assessing the pharmacodynamic effect of drugs that are hypothesized to alter the metabolism of Aβ in humans. With these new developments, we have expanded the use of the assay to measuring Aβ metabolism in plasma.

“Through additional studies like this, we’re hoping to identify which of the first three channels for amyloid beta disposal are slowing down as the brain ages,” Bateman said. “That may help us in our efforts to develop new treatments.”

How the SILK™ Blood Test Works

Alzheimer’s Disease & Mild Cognitive Impairment

SILK-Aβ® Technology

Monday, May 22, 2017

Hippocampal-Sparing Alzheimer's Goes Dangerously Misdiagnosed

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Hundreds of thousands of people with Hippocampal-Sparing Alzheimer's go misdiagnosed. With a correct diagnosis, existing medicines can do more. Learn about the diagnosis and treatment for this common type of dementia.

JACKSONVILLE, Fla. — Neuroscientists at Mayo Clinic in Florida have defined a subtype of Alzheimer’s disease (AD) that they say is neither well recognized nor treated appropriately.

The variant, called hippocampal sparing AD (short for hippocampal sparing Alzheimer's disease), made up 11 percent of the 1,821 Alzheimer's-confirmed brains examined by Mayo Clinic researchers — suggesting this subtype is relatively widespread in the general population. The Alzheimer’s Association estimates that 5.2 million Americans are living with Alzheimer’s disease (AD). With nearly half of hippocampal sparing AD patients being misdiagnosed, this could mean that well over 600,000 Americans make up this AD variant, researchers say.

Unique Symptoms

In an oral presentation at the annual meeting of the American Academy of Neurology in Philadelphia, scientists say hippocampal sparing AD often produces symptoms that are substantially different from the most commonly known form of AD, which affects the hippocampus, the center of memory.

The patients, mostly male, are afflicted at a much younger age, and their symptoms can be bizarre — behavioral problems such as frequent and sometimes profane angry outbursts, feelings that their limbs do not belong to them and are controlled by an “alien” unidentifiable force, or visual disturbances in the absence of eye problems, researchers say.

They also decline at a much faster rate than do patients with the most common form of AD.

“Many of these patients, however, have memories that are near normal, so clinicians often misdiagnose them with a variety of conditions that do not match the underlying neuropathology,” says the study’s lead author, Melissa Murray, Ph.D., an assistant professor of neuroscience at Mayo Clinic in Florida.

Misiagnosis & Consequences

Many of these patients are misdiagnosed with frontotemporal dementia, a disorder characterized by changes in personality and social behavior, or corticobasal syndrome, characterized by movement disorders and cognitive dysfunction. Language dysfunction is also more common in hippocampal sparing AD, although patients do not have vocal or hearing deficits.

“What is tragic is that these patients are commonly misdiagnosed and we have new evidence that suggests drugs now on the market for AD could work best in these hippocampal sparing patients — possibly better than they work in the common form of the disease,” Dr. Murray says.

The researchers benefit greatly from one of the largest brain banks in the country — more than 6,500 brain donations — as well as a collaborative environment between neuroscience research and neurology at Mayo Clinic, she says.

Both hallmark proteins of AD — amyloid beta (Aβ), which forms Aβ plaques, and tau, which produces tangles — are found across all subtypes of AD, including hippocampal sparing AD. The researchers developed a mathematical algorithm to classify AD subtypes using tangle counts. “What is fascinating is that all the AD patient subtypes had the same amount of amyloid, but for some reason tau tangles were found in strategic cortical regions disproportionate to the hippocampus.”

In these patients, tau preferentially damages and eventually destroys neurons in parts of the brain involved in behavior, motor awareness and recognition, as well as use of speech and vision, Dr. Murray says.

She says she hopes this research, the second high-profile Mayo study to highlight hippocampal sparing AD, will “open the minds” of clinicians who are trying to diagnose dementia, helping them understand that loss of memory is not present in every AD patient.

“Our studies support the notion that dementia related to AD does not necessarily equate to a loss of memory, and points to the need for more research in amyloid and tau imaging biomarkers to help clinicians accurately diagnose AD — regardless of subtype,” Dr. Murray says.

Friday, May 19, 2017

Are Silent Seizures a Symptom of Alzheimer's Disease?

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Alzheimer's Reading Room

I clearly remember our doctor telling me - if you get worried call 911 immediately. He then said to me, you call me after you get her settled down in the hospital.

I also worried about silent seizures because they can present as a form of confusion. Alzheimer's patients often present signs of confusion.

Dealing with Confusion in Dementia Care

Researchers are beginning to suspect that treating these seizures could help manage Alzheimer's or possibly slow it down.

Silent seizures recorded in the hippocampus of two patients with Alzheimer's disease

Seizure-like activity in key memory structure may contribute to cognitive symptoms, offering new therapeutic target

Massachusetts General Hospital (MGH) investigators have identified silent, seizure-like activity in the hippocampus – a brain structure significantly affected in Alzheimer’s disease.

These alterations in the brain’s electrical activity could not be detected by standard EEG readings taken on the scalp and primarily occurred during sleep, a time when the preceding day’s memories are consolidated.

How the Loss of Memory Works in Alzheimer’s Disease, and How Understanding This Could Help You

“While it is not surprising to find dysfunction in brain networks in Alzheimer’s disease, our novel finding that networks involved in memory function can become silently epileptic could lead to opportunities to target that dysfunction with new or existing drugs to reduce symptoms or potentially alter the course of the disease.”

“We now have to study more individuals to validate this finding and understand how prevalent it is in Alzheimer’s patients, whether it occurs in other neurodegenerative disorders and how it responds to treatment.” ~ Andrew Cole, MD, director of the MGH Epilepsy Service and senior author of the Nature Medicine paper.

The investigators describe two patients – both women in their 60s – who had developed symptoms suggestive of Alzheimer’s disease, such as confusion and repeatedly asking the same questions.
Brain imaging studies and cerebrospinal fluid analysis for both patients were consistent with Alzheimer’s disease.
It is common for patients with Alzheimer’s to experience fluctuations in their symptoms, but in both of these patients, those fluctuations were more exaggerated than typically seen.

Alzheimer's Affects the Way a Person Thinks, Feels, and Acts

While scalp EEG recordings did not reveal seizure-like activity, the investigators suspected that there may be undetected seizures within the hippocampus – a key structure affected by Alzheimer’s disease that is critical for memory consolidation and is a common source of seizures in people with epilepsy.

They decided to try a more direct way of monitoring electrical activity in the hippocampus and related structures.

Electrodes were placed adjacent to those structures on both sides of the brain through the foramen ovale (FO), naturally occurring openings at the base of the skull. Each patients’ brain activity was monitored simultaneously with both implanted electrodes and with scalp EEG for 24 to 72 hours.

7 Ways To Deal With Difficult Behavior Caused by Alzheimer's and Dementia

In one patient, the FO electrodes revealed frequent bursts of electrical activity called spikes, often associated with seizures, most which were not detectable by scalp EEG.

During a 12-hour period she experienced three seizures, all taking place during sleep but not producing any visible symptoms.

Treatment with an anti-seizure medication eliminated the seizure-like activity, and in the following year, she experienced only one episode of confusion, which occurred after she missed several doses of her anti-seizure medication.

Solutions to challenges facing caregivers

FO electrode recording in the other patient also revealed frequent spiking during sleep, but anti-seizure treatment had to be discontinued because of adverse effects on her mood.

“Our findings confirmed the presence of serious dysfunction of the neuronal networks affected by Alzheimer’s disease and confirmed our hypothesis that epileptic phenomena are an important component of that disturbance,” says Cole, who is a professor of Neurology at Harvard Medical School. “

Additional recordings with FO electrodes in patients with Alzheimer’s disease will help us develop better tools based on computerized analysis of EEG signals and possibly functional neuroimaging studies to ascertain how common silent seizures are in Alzheimer’s disease without the need for the minimally invasive electrodes we used in these patients.”

The Connection Between UTI and Worsening Dementia

The report appeared in the online publication in Nature Medicine.

A recent study led by Alice Lam, MD, PhD, also of the MGH Epilepsy Service and lead author of the current study demonstrated a novel tool for detecting hippocampal seizures not detectable by scalp EEGs in patients with epilepsy.

The Best Way to Find Solutions to the Problems that Caregivers Face Each Day

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The Alzheimer's Reading Room contains more than 5,000 articles and has been published daily since July, 2009.

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Cole adds, and his team is working to refine this tool and apply it to Alzheimer’s disease. Since there also is evidence that higher levels of neuronal activity can increase the production and deposition of Alzheimer’s associated proteins such as tau and amyloid-beta, understanding whether seizure-like activity accelerates the progression of Alzheimer’s disease will be a high priority for their team.

Atypical (a-TIP-i-kul) seizure means unusual or not typical. The person will stare (as they would in any absence seizure) but often is somewhat responsive. Eye blinking or slight jerking movements of the lips may occur. ~ Epilepsy Foundation

What Are the Symptoms of an Absence Seizure?

Because absence seizures are usually quite brief, tend to strike during times of inactivity, and closely resemble daydreaming or "being off in one's own world," they may pass unnoticed by others and go undiagnosed for some time.

Absence seizures fall into two categories: typical and atypical.

~ WebMD

Undetected or "silent" seizures may contribute to some symptoms associated with Alzheimer's disease, such as confusion.

The seizures occur in the hippocampus -- a part of the brain involved in the consolidation of memories. Researchers suspect that treating these seizures could help manage Alzheimer's or possibly slow it down.

~WebMD

Additional co-authors of the Nature Medicine paper are Gina Deck, MD, MGH Epilepsy Service; Emad Eskandar, MD, MGH Department of Neurosurgery; and Alicia Goldman, MD, PhD, and Jeffrey Noebels, MD, PhD, Baylor College of Medicine. Support for the study includes National Institute of Neurological Disorders and Stroke grants R25-NS065743, U01-NS090362, and R01-NS029709; and grants from Citizens United for Research in Epilepsy and the Blue Bird Circle Foundation.

Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School.

Seizures are a sign of brain injury and are caused by sudden disorganized electrical activity in the brain. Seizures can be characterized by spasms or convulsions.

Alzheimer disease (AD) and epilepsy are disorders commonly seen in the elderly. Many studies have shown that patients with AD are at increased risk for developing seizures and epilepsy.

Transient symptoms in Alzheimer disease (AD) are frequent and include seizures, syncope, and episodes of inattention or confusion.

Undetected or "silent" seizures may contribute to some symptoms associated with Alzheimer's disease, such as confusion.

The main underlying cause of memory loss and confusion is the progressive damage to brain cells caused by Alzheimer's disease.

Tuesday, May 16, 2017

Low Body Mass NOT a Cause for Alzheimer's

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Neuroscience news

Summary: Low body mass index does not appear to be a causal risk factor for developing Alzheimer’s disease, a new study reports.

Source: Endocrine Society.

Research clarifies past studies on weight, common cause of dementia.

A new large-scale genetic study found that low body mass index (BMI) is likely not a causal risk factor for Alzheimer’s disease, as earlier research had suggested, according to a study published in the Endocrine Society’s Journal of Clinical Endocrinology & Metabolism.

“Although prior studies found an association between Alzheimer’s disease and low BMI, the new findings suggest this is not a causal relationship,” said the study’s senior author, Ruth Frikke-Schmidt, M.D., D.M.Sc., Ph.D., Chief Physician at Rigshospitalet in Copenhagen, Denmark, and Associate Research Professor at the University of Copenhagen. “The association can likely be explained by the fact that individuals with Alzheimer’s disease are more likely to have low BMIs due to loss of appetite and weight loss in the early stages of the disease.”

More than 5 million Americans have Alzheimer’s disease, according to the Alzheimer’s Association’s 2017 Alzheimer’s Disease Facts and Figures Report. The disease affects the brain and is a common form of dementia. It is the sixth leading cause of death in the United States.

To examine the association between Alzheimer’s disease and low BMI, the researchers analyzed blood and DNA samples from 95,578 participants in the Copenhagen General Population Study (CGPS). Of the participants, 645 individuals developed Alzheimer’s disease.

The researchers analyzed the study participants’ DNA for the presence of five genetic variants that have strong associations with BMI. Based on how many variants were found, participants were divided into four groups to reflect the likelihood of low BMI. The researchers also analyzed data from up to 249,796 individuals participating in the Genetic Investigation of ANthropometric Traits (GIANT) consortium for the genetic variants closely linked to low BMI.

The analysis found the presence of the genetic variants tied to low BMI was not associated with increased risk of Alzheimer’s disease. NeuroscienceNews.com image is for illustrative purposes only.

The analysis found the presence of the genetic variants tied to low BMI was not associated with increased risk of Alzheimer’s disease. For comparison, the researchers examined if individuals with genetic variants connected to high BMI were more likely to have type 2 diabetes and did find the expected causal relationship.

“We found individuals with lifelong low BMI due to genetic variation were not at increased risk of Alzheimer’s disease,” Frikke-Schmidt said. “Since genetic variants are not affected by other risk factors or diseases, this is a clean measure that can help to determine causality. The findings highlight that testing causality of a risk factor is pivotal before considering changing public health recommendations based on observational data alone.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Other authors of the study include: Liv Tybjærg Nordestgaard and Anne Tybjærg-Hansen, of Rigshospitalet; and Børge G. Nordestgaard, of Herlev and Gentofte Hospital. All three also are affiliated with the University of Copenhagen.

Funding: The research was supported by the Danish Medical Research Council, the Lundbeck Foundation, the Alzheimer Research Foundation, and the Research Fund at the Capital Region of Denmark.

Source: Jenni Glenn Gingery – Endocrine Society
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Body Mass Index and Risk of Alzheimer Disease: a Mendelian Randomization Study of 399,536 Individuals” by Liv Tybjærg Nordestgaard, Anne Tybjærg-Hansen, Børge G. Nordestgaard, and Ruth Frikke-Schmidt in Journal of Clinical Endocrinology and Metabolism. Published online May 9 2017 doi:10.1210/jc.2017-00195

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Endocrine Society “Study Finds Alzheimer’s Disease Likely Not Caused by Low Body Mass Index.” NeuroscienceNews. NeuroscienceNews, 9 May 2017.
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Abstract

Body Mass Index and Risk of Alzheimer Disease: a Mendelian Randomization Study of 399,536 Individuals

Context:
Recently, data on two million people established that low body mass index (BMI) is associated with increased risk of dementia. Whether this observational association reflects a causal effect remains to be clarified.

Objective:
We tested the hypothesis that there is a causal association between low BMI and high risk of Alzheimer disease.

Design, Setting and Participants:
Using a Mendelian randomization approach, we studied 95,578 individuals from the Copenhagen General Population Study (CGPS) with up to 36 years of follow-up, and consortia data on 303,958 individuals from the Genetic Investigation of Anthropometric Traits (GIANT) and the International Genomics of Alzheimer’s Project (IGAP).

Main Outcome Measure:
Risk of Alzheimer disease.

Results:
The causal odds ratio for a 1 kg/m2 genetically determined lower BMI was 0.98 (95 % confidence interval: 0.77-1.23) for a weighted allele score in the CGPS. Using 32 BMI decreasing variants from GIANT and IGAP the causal odds ratio for Alzheimer disease for a one standard deviation lower genetically determined BMI was 1.02 (0.86-1.22). Corresponding observational hazard ratios from the CGPS were 1.07 (1.05-1.09) and 1.32 (1.20-1.46) for a 1 kg/m2 and a 1 standard deviation lower BMI, respectively.

Conclusions:
Genetic and hence lifelong low BMI is not associated with increased risk of Alzheimer disease in the general population. These data suggest that low BMI is not a causal risk factor for Alzheimer disease, and that the corresponding observational association likely is explained by reverse causation or confounding.

“Body Mass Index and Risk of Alzheimer Disease: a Mendelian Randomization Study of 399,536 Individuals” by Liv Tybjærg Nordestgaard, Anne Tybjærg-Hansen, Børge G. Nordestgaard, and Ruth Frikke-Schmidt in Journal of Clinical Endocrinology and Metabolism. Published online May 9 2017 doi:10.1210/jc.2017-00195