Tuesday, March 28, 2017

Vascular System Changes May Trigger Alzheimer’s disease

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Neuroscience News


Summary: Researchers report a plasma component that is usually involved in blood clotting and inflammation may also play a role in the development of Alzheimer’s disease.
Source: Rockefeller University.
As the average age of Americans increases, so too does the problem of Alzheimer’s, one of the world’s most common neurological diseases. In recent years, scientists have explored many new approaches to clear the plaques and tangles in the brain that characterize the condition, but the new drugs have largely turned out to be disappointing.
A team of Rockefeller scientists is now using a fresh approach to look at biological processes that occur in the development of Alzheimer’s disease (AD). Somewhat unexpectedly, they have found that a plasma component normally involved in blood clotting and inflammation may also be part of the problem in some patients.
This isn’t the first time the condition has been linked to the vascular system. “There’s a lot of evidence that exercise, which helps keep your blood vessels healthy and blood flow consistent, can be protective against AD,” says Sidney Strickland, head of the Patricia and John Rosenwald Laboratory of Neurobiology and Genetics. “In addition, we know that diseases that compromise the vascular system, like diabetes, put people at higher risk.”
Yet it’s still not clear precisely how changes in the blood might spur Alzheimer’s. The latest study from Strickland’s lab, published recently in the journal Blood, offers a clue and a possible path to early diagnosis and new drugs.
Exploring the link
The plasma protein, called Factor XII, is part of a cascade of enzymes that induces blood coagulation and inflammation. Previous studies from Strickland’s lab had shown that this cascade can be activated by beta-amyloid, a molecule that forms sticky plaques in the brains of Alzheimer’s patients. Other research had demonstrated that the process might be overly active in the disease.
Because people with AD don’t show cognitive problems until their disease is quite advanced, it’s been difficult to study what’s transpiring in the brain at the earlier stages. But in recent years, genes linked to an early-onset hereditary form of the disease have been found, and researchers have been able to study what’s happening in the brains of people genetically predetermined to develop Alzheimer’s, even before they show any symptoms.
“It’s a devastating disease to have,” Strickland says about this inherited form of AD, “but it’s given us new research opportunities. The first changes observed in these patients are in beta-amyloid levels. The second changes are brain abnormalities related to the vascular system, which can occur 20 years before overt cognitive symptoms appear.”
“We speculated that activation of Factor XII by beta-amyloid could play a role in initiating Alzheimer’s,” says Zu-Lin Chen, a senior research associate in the Strickland lab. “That’s not something you can study in humans, so we looked at mouse models of disease to see what happens when Factor XII is knocked down.”
Exploring results in mice
To take out Factor XII, the team used a molecule that prevented the gene from making the protein. Normally, AD mice show much greater brain inflammation than healthy mice. However, AD mice whose Factor XII had been knocked down had much less inflammation than untreated AD mice and had brains that were more similar to those of healthy mice.
Image shows brain slices from a mouse with Alzheimer's disease.
The brain of a mouse with Alzheimer’s disease is infiltrated with inflammatory cells, which light up in red when activated (left). These cells become less active when Factor XII is removed (right). NeuroscienceNews.com image is credited to Laboratory of Neurobiology and Genetics at The Rockefeller University/Blood.
In addition, behavioral studies of AD mice with reduced Factor XII showed that their cognitive function improved. In one test, the mice were introduced to a maze with an escape hole. The animals learn the location of the hole by remembering visual cues around the maze, allowing them to escape through the hole on subsequent visits. Unlike normal mice, AD mice are unable to remember where the hole was located.
Knocking down Factor XII helped: AD mice lacking the protein learned to find their way quicker than the untreated AD mice, although their memory wasn’t as good as that of normal mice.
These and other findings in the study point to one potential factor in initiating AD, though the researchers caution they may not lead to new drugs anytime soon. “We need to further define what’s going on, so we can identify patients with vascular problems and develop a targeted therapy to help that aspect,” Chen says. “We had great improvements in our mice but we didn’t fully correct the problem. Alzheimer’s is a complex disease, and there are multiple elements involved.”
“Our work contributes to the increasing evidence that vascular abnormalities are playing an important role in cognitive decline and inflammation in some AD patients,” Strickland concludes. “The hope is that defining the vascular mechanisms involved will allow for better diagnosis and eventually new treatments. Each step forward is a step closer to understanding this terrible disease.”
ABOUT THIS ALZHEIMER’S DISEASE RESEARCH ARTICLE
Source: Katherine Fenz – Rockefeller University 

Saturday, March 25, 2017

Drink Cuts Alzheimer’s Risk Up To 86%

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Dr. Feng Lei, the study’s first author, said:
“While the study was conducted on Chinese elderly, the results could apply to other races as well.
Our findings have important implications for dementia prevention.
Despite high quality drug trials, effective pharmacological therapy for neurocognitive disorders such as dementia remains elusive and current prevention strategies are far from satisfactory.
Tea is one of the most widely consumed beverages in the world.
The data from our study suggests that a simple and inexpensive lifestyle measure such as daily tea drinking can reduce a person’s risk of developing neurocognitive disorders in late life.”
For the research, 957 Chinese people were followed from 2003 to 2005
They were regularly tested for signs of cognitive aging.
Dr. Feng explained why tea is likely to be beneficial:
“Based on current knowledge, this long term benefit of tea consumption is due to the bioactive compounds in tea leaves, such as catechins, theaflavins, thearubigins and L-theanine.
These compounds exhibit anti-inflammatory and antioxidant potential and other bioactive properties that may protect the brain from vascular damage and neurodegeneration.
Our understanding of the detailed biological mechanisms is still very limited so we do need more research to find out definitive answers.”
The study was published in The Journal of Nutrition, Health & Aging(Feng et al., 2016).

Wednesday, March 22, 2017

Can Stabilizing Amyloid Stop Alzheimer's?

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Alzheimer's and Dementia Weekly



BREAKTHROUGH: Never-before-seen images have exposed a missing link in the early-Alzheimer's cascade. Taken by the world's largest synchrotron, they imply new drugs may do better stabilizing amyloid than eliminating it. Learn more about this course-changing discovery. 




Researchers at Lund University in Sweden have used the MAX IV synchrotron in Lund - the strongest of its kind in the world - to produce images that predate the formation of toxic clumps of beta-amyloid, the protein believed to be at the root of Alzheimer's disease. 

The unique images appear to contradict a previously unchallenged consensus. Instead of attempting to eliminate beta-amyloid, or so-called plaques, the researchers now suggest stabilizing the protein. 

It is a long-held belief in the scientific community that the beta-amyloid plaques appear almost instantaneously. Hence the term "popcorn plaques". The infrared spectroscopy images, however, revealed something entirely different. 



The researchers could now see structural, molecular changes in the brain. 

"No one has used this method to look at Alzheimer's development before. The images tell us that the progression is slower than we thought and that there are steps in the development of Alzheimer's disease that we know little about. This, of course, sparked our curiosity," says Gunnar Gouras, professor in experimental neurology at Lund University and senior author of the study. 

What was happening at this previously unknown phase? Through biochemical identification the first author of the study, Oxana Klementieva, was able to look closer at these early brain changes. 

The results revealed another discovery. Namely, that the beta-amyloid did not appear as a single peptide, a widely held belief in the field, but as a unit of four peptides sticking together, a tetramer. 

This breakthrough offers a new hypothesis to the cause of the disease. The abnormal separation of these four peptides could be the start of the beta-amyloid aggregation that later turns into plaques. 

"This is very, very exciting. In another amyloid disease, transthyretin amyloidosis, the breaking up of the tetramer has been identified as key in disease development. For this disease, there is already a drug in the clinic that stabilizes the tetramers, consequently slowing down disease progression. We hope that stabilizing beta-amyloid in a similar fashion may be the way forward in developing future therapies" says Gunnar Gouras. 

The discovery could therefore alter the direction of therapy development for the disease. The aim of most clinical trials today is to eliminate plaques. 

Researchers at Lund University will now try to understand the interaction patterns of beta-amyloid preceding the aggregation process. Finding the antidote to whatever breaks the beta-amyloid protein apart could open doors towards a major shift in­ the development of therapies for Alzheimer's disease. 


Sunday, March 19, 2017

Alzheimer's disease facts and figures 2017

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Alzheimer's Association

2017 ALZHEIMER’S DISEASE FACTS AND FIGURES

Alzheimer’s Disease Facts and Figures. 

Alzheimers Dement 2017;13:325-373. 2017 
Alzheimer’s Disease Facts and Figures 1 
Specific information in this year’s Alzheimer’s Disease Facts and Figures includes: • Proposed guidelines for diagnosing Alzheimer’s disease from the National Institute on Aging and the Alzheimer’s Association (pages 15-16). • 
How the diagnosis of Alzheimer’s disease has evolved from 1984 to today (pages 64-65). • Overall number of Americans with Alzheimer’s dementia nationally (page 18) and for each state (pages 20-22). • 
Proportion of women and men with Alzheimer’s or other dementias (page 19). • Lifetime risk for developing Alzheimer’s dementia (page 23). •
 Number of deaths due to Alzheimer’s disease nationally (page 27) and for each state (pages 28-29), and death rates by age (page 31). •
  Number of family caregivers, hours of care provided, economic value of unpaid care nationally and for each state (pages 38 and 39), and the impact of caregiving on caregivers (pages 37 and 40-43). • Cost of care for individuals with Alzheimer’s or other dementias in the United States in 2017, including costs paid by Medicare and Medicaid and costs paid out of pocket (page 47). • 
Health care and long-term care payments for Medicare beneficiaries with Alzheimer’s or other dementias compared with beneficiaries without dementia (page 48). • 
Medicaid costs for people with Alzheimer’s and other dementias, by state (page 55). The Appendices detail sources and methods used to derive statistics in this report. This report frequently cites statistics that apply to individuals with dementia regardless of the cause. When possible, specific information about Alzheimer’s dementia is provided; in other cases, the reference may be a more general one of “Alzheimer’s or other dementias.” 

The whole report


Wednesday, March 15, 2017

Prevention Study Introduces Alzheimer's Eye Test

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Alzheimer's and dementia weekly


The famous "A4 Alzheimer's Prevention Trial" continues to build momentum. It is adding an Alzheimer's eye test that can detect signs of Alzheimer's long before symptoms appear. Learn about Neurovision's "Retinal Imaging Technology" in the A4 Trial. See how it works. 




NeuroVision announced its participation in the landmark Anti-Amyloid Treatment in Asymptomatic Alzheimer’s (or “A4”) clinical trial. 

They will be working with investigators at the University of California San Diego School of Medicine (UC San Diego) and the University of Southern California (USC). 

The purpose of the A4 study is to test whether a new investigational treatment called "solanezumab" can slow or prevent memory loss caused by Alzheimer’s. 



Beta-amyloid is the main suspect behind Alzheimer's. Solanezumab works by reducing beta-amyloid accumulation in the brain. That may also slow or prevent memory loss caused by Alzheimer’s disease. Amyloid is a protein normally produced in the brain that can build up in older people, forming amyloid plaque deposits. 

The main A4 study is a public-private partnership, funded by the National Institute on Aging at the National Institutes of Health, Eli Lilly and Company, and several philanthropic organizations. USC’s Alzheimer’s Therapeutic Research Institute coordinates the trial, with about 70 study sites in several countries, including the United States, Canada, Australia and Japan. 

Scientists believe this buildup of deposits may play a key role in the eventual development of Alzheimer’s disease-related memory loss. The overall goal of the A4 study is to test whether decreasing amyloid accumulation with an antibody investigational treatment can help slow the memory loss associated with Alzheimer’s disease. 

“Our best chance of altering the disease may be to start treatment before people have symptoms,” said Dr. Robert Rissman, substudy principal investigator and associate professor of neurosciences at UC San Diego. “Evaluating new approaches such as retinal imaging will allow us to understand how Alzheimer’s neuropathology develops in the eye and how this parallels what is occurring in the brain itself. We are very fortunate to have the opportunity to conduct this substudy in A4 with our USC colleagues.” 

Using NeuroVision’s retinal imaging technology, the substudy will characterize retinal amyloid imaging findings in subjects with preclinical AD prior to administration of experimental treatment received as part of the primary A4 study protocol. The substudy will also assess longitudinal changes in retinal amyloid imaging in subjects with preclinical AD and whether it correlates with brain amyloid and cognitive change. One hundred subjects will be recruited into the substudy and imaged annually over three years. 


“If successful, this technique could one day be used in the clinic to identify at-risk patients,” said Dr. Michael Rafii, associate professor of neurology at USC and associate professor of neurosciences at UC San Diego. “Dr. Rissman and I recently identified a strong neuropathological signal using NeuroVision’s retinal imaging system in adults with Down Syndrome, a group of individuals who are at increased risk for developing Alzheimer’s disease.” 

Steve Verdooner, CEO of NeuroVision, remarked that “this is an exciting opportunity to evaluate our technology in a setting in which it could potentially add significant clinical value. Currently, evaluating amyloid plaque burden in the clinical setting is challenging and has limited scope for scaling up to meet the potential demand for effective new drugs. Our technology is designed to be easy-to-use, reliable and, being noninvasive, have minimal impact on patients. If it works in the way we expect, retinal imaging would streamline enrollment into clinical studies and could help identify candidates for new drugs and monitor their efficacy in a practical and accessible setting.” 

Sunday, March 12, 2017

New treatment for Alzheimer's disease

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Science News

w Approach to Treating Alzheimer’s Disease
Researchers at Ulsan National Institute of Science and Technology (UNIST) in South Korea have introduced a new approach to treat Alzheimer's Disease.

Alzheimer's disease (AD) is one of the most common forms of dementia. In the search for new drugs for AD, the research team, led by Professor Mi Hee Lim of Natural Science at UNIST has developed a metal-based substance that works like a pair of genetic scissors to cut out amyloid-β (Aβ), the hallmark protein of AD.

The study has been featured on the cover of the January 2017 issue of the Journal of the American Chemical Society (JACS) and has been also selected as a JACS Spotlight article.

Alzheimer's disease is the sixth leading cause of death among in older adults. The exact causes of Alzheimer's disease are still unknown, but several factors are presumed to be causative agents. Among these, the aggregation of amyloid-β peptide (Aβ) has been implicated as a contributor to the formation of neuritic plaques, which are pathological hallmarks of Alzheimer's disease (AD).

As therapeutics for AD, Professor Lim suggested a strategy that uses metal-based complexes for reducing the toxicity of the amyloid beta (Aβ). Although various metal complexes have been suggested as therapeutics for AD, none of them work effectively in vivo.

The research team has found that they can hydrolyze amyloid-beta proteins using a crystal structure, called tetra-N methylated cyclam (TMC). Hydrolysis is the process that uses water molecules to split other molecules apart. The metal-mediated TMC structure uses the external water and cut off the binding of amyloid-beta protein effectively.

In this study, the following four metals (cobalt, nickel, copper and zinc) were placed at the center of the TMC structure. When the double-layered cobalt was added to the center, the hydrolysis activity was at the highest.

The research team reported that the cobalt-based metal complex (Co(II)(TMC)) had the potential to penetrate the blood brain barrier and the hydrolysis activity for nonamyloid protein was low. Moreover, the effects of this substance on the toxicity of amyloid-beta protein were also observed in living cell experiments.

"This material has a high therapeutic potential in the treatment of Alzheimer's disease as it can penetrate the brain-vascular barrier and directly interact with the amyloid-beta protein in the brain," says Professor Lim.

This study has also attracted attention by the editor of the Journal of the American Chemical Society. "Not only do they develop new materials, but they have been able to propose details of the working principles and experiments that support them," according to the editor.

"As a scientist, this is such a great honor to know that our recent publication in JACS was highlighted in JACS Spotlights," says Professor Lim. "This means that our research has not only been recognized as an important research, but also has caused a stir in academia."

This study has been conducted in collaboration with Professor Jaeheung Cho of Daegu Gyeongbuk Institute of Science and Technology (DGIST), Professor Kiyoung Park of Korea Advanced Institute of Science and Technology (KAIST), and Dr. Sun Hee Kim of Korea Basic Science Institute (KBSI). It has been also supporte by the National Research Foundation of Korea (NRF) and the Ministry of Science, ICT and Future Planning (MSIP).

Thursday, March 9, 2017

MOUSE LEMURS’ ROLE IN NEW ALZHEIMER’S HYPOTHESIS

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Duke Lemur Center

Lemurs aren’t just cute, they’re crucial

Why are lemurs so special? Here’s just ONE reason: Because non-invasive research on grey mouse lemurs has helped shed light on devastating human diseases like Alzheimer’s: https://today.duke.edu/2017/03/jumping-genes-suspected-alzheimers.
Like humans, mouse lemurs develop amyloid brain plaques and other Alzheimer’s-like symptoms as they age. Studying these tiny primates has helped lead to a new hypothesis from the lab of Anne Yoder, a biology professor at Duke University and Director of the Duke Lemur Center, and rethinking how to treat people with diseases like Alzheimer’s. If the lab’s hypothesis holds up, “it could help identify people at risk sooner, before they develop symptoms, or point to new ways to delay onset or slow progression of the disease.”
So the moral of the story is, lemurs aren’t just cute; they’re crucial for research! Because they’re primates, they’re a closer genetic match to humans than mice or rats are — and their unique contributions to science are just one of MANY reasons we should protect these extraordinary animals and learn everything we can about them.

Resources

Read more about the Yoder lab’s new hypothesis in “Jumping Genes Suspected in Alzheimer’s: Mechanism might explain initial states of neurodegenerative disease” published in Duke Today on March 8, 2017. 
Or, read the paper itself in Alzheimer’s and Dementia: The Journal of the Alzheimer’s Association: “The Alu Neurodegeneration Hypothesis: A primate-specific mechanism for neuronal transcription noise, mitochondrial dysfunction, and manifestation of neurodegenerative disease.”
All DLC research is non-invasive, meaning that we do not allow research that will harm our animals. Learn more about the Duke Lemur Center’s research program here.
In 2011, the blog That’s Basic Science! described in easily understandable terms (for non-scientists!) why “the mighty mouse lemur” is an ideal candidate for Alzheimer’s research. Note that this article was written before the Duke Lemur Center began working with mouse lemurs, and that now there IS a lab outside of Europe researching these tiny animals: The Yoder lab right here at Duke!

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