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.

Amyloid beta plaque.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

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.



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.

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.


“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.

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.

In one patient, the FO electrodes revealed frequent bursts of electrical activity called spikesoften 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.

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 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.

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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.
Image shows an old lady.
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
CITE THIS NEUROSCIENCENEWS.COM ARTICLE
Endocrine Society “Study Finds Alzheimer’s Disease Likely Not Caused by Low Body Mass Index.” NeuroscienceNews. NeuroscienceNews, 9 May 2017.
.

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


Saturday, May 13, 2017

Heal Dementia's Delirium

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Alzheimer's and Dementia Weekly


DENVER - Researchers have discovered that hospital stays for people with Alzheimer's can be hazardous. So much so that an alarming percentage of those patients die within one year of their hospital visits. 

The problem is a condition called "delirium"- a state of extra confusion and agitation brought on by the intensity of hospital stays, most especially the busy environment in hospital E.R.'s. In fact, the problem of delirium is so severe for patients who already have a damaged brain, that both researchers and independent Alzheimer's experts agree that caregivers need to know the risk so they can help a loved one with dementia avoid the hospital altogether if possible. 


Doctors at Lutheran Medical Center, who serve the biggest senior population in the metro area, have made changes to help their older patients avoid the delirium diagnosis if they have no choice but to go the hospital. 

They've essentially taken their traditional 42,000-square-foot emergency room and cut it in half, leaving one side equipped as a traditional ER, and turning the other half into a "Senior ER." 

]
The "Senior ER" is filled with special features to comfort and care for an aging population.
"What we've done is created basically a two tiered concept," says Dr. Scott Miner, Lutheran's Director of Emergency Services. We have a very unique environment for patients of those ages to receive medical care, as well as having developed some new clinical tools to screen for the high risk and under-diagnosed medical conditions that seniors often have."
Special features in the Senior ER include hospital bed mattresses that are extra thick memory foam. They are soft and deep to accommodate any unknown medical conditions that older patients may arrive with.

The rooms in the Senior ER are extra quiet, even though they are bristling with technology, such as screening and listening devices that operate at lower frequencies of noise to reduce the often confusing signals and warnings they emit that very often cause high anxiety.
"We're lucky enough to have an isolated physical space which is much quieter and a lot less chaotic than a typical, busy emergency department," says Dr. Miner
Even the low tech details got big upgrades. The floors in the Senior ER are non-skid to provide sure footing and prevent falls, the #1 reason for all senior visits.
Bathrooms are all senior safe, and the lighting here is warm and in-direct.

There are large digital clocks telling the exact time, day and date. And paint schemes that are proven to be calming, called the "Eden Scheme," are in evidence throughout the facility.
It's a theme that even carries over into the privacy drapes in each room, each providing recreations of soothing and restful destinations.
Dr. Miner says, those little touches have paid huge dividends.
"So we really have created an environment that is much more appropriate and amenable to patients who are aged to receive care. It's also nicer for their families too.

The staff has had special training to deal with the frailties of their aging patients.
And large white message boards in every room give every detail of a patients stay, again, helping to eliminate anxiety and much of the confusion many older patients feel when in the hospital environment.
"We tell patients what are we going to be doing while they are here such as CAT scans, X-ray, ultrasounds, EKG's and blood work. We tell them whether they are going to be receiving medications, what are we going to be doing to get them more comfortable, and then more importantly, how long that may take," Dr.Miner told 9NEWS.

No detail is left unexplained, and everything that happens here happens with great speed. A test that typically can results in long hours or even days of waiting for results, such as cardiac monitoring or labs, happens virtually in the blink of an eye. Getting the patient out of the ER and back home is a top priority.
"It's a lot of the things that might take weeks to even months," says Dr. Miner. "We can get it done in two to four hours."
All of these features are aimed at shortening a hospital stay and eliminating the condition known as "delirium," a red flag for underlying issues that can result in death. And if it is detected, the new set of screening procedures begins.
"We don't want to send patients with acute confusional states, otherwise known as delirium,home from the hospital," says Dr. Miner. And when they have it in the hospital, we want to make sure we identify it and drill down for the reason. Because as I mentioned, it is reversible, and if we identify the cause we can often reverse it. But it is a red flag that there is significant deterioration in a persons health state."

They now have such a big reputation for speed and accuracy and comfort, that many of their patients- no matter their age- now request the senior ER upon arrival at the hospital.
Many hospitals across the country are now looking to deploy any tools they have to help those with dementia and Alzheimer’s. The disease is costing Medicare and Medicaid about 150-billion dollars a year, an unsustainable rate for our public health care system. Solving the issues with "delirium" will be just another step in controlling more of those costs.

source

  • KUSA TV - 9NEWS Senior Source Correspondent Mark Koebrich



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