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Monday, April 11, 2016

Why AD Patients Cease Recognizing Loved Ones Faces

Dear Readers,

A recent study has demonstrated that, besides triggering memory lapses, Alzheimer’s disease also impairs visual face perception. Research conducted by the team of Dr. Sven Joubert, PhD, a researcher at the Centre de recherche de l’Institut universitaire de gériatrie de Montréal and a Professor with the Department of Psychology at Université de Montréal, was published today in the Journal of Alzheimer’s Disease.

Scientists know that face perception plays a primary role in human communication, and is why humans have become experts at quickly detecting and identifying faces. This ability is thought to depend on the capacity to perceive the entire face. Also known as “holistic perception,” this ability differs with the local and detailed analysis required to recognize individual facial features, such as the eyes, nose or mouth. Dr. Joubert’s study verified that Alzheimer’s disease impairs the holistic ability to perceive faces.

The Montreal team recruited people with Alzheimer’s along with healthy seniors to examine their capability at perceiving faces and cars in photos that were either upright or upside down. Dr. Joubert explains the team’s findings: “The results for people with Alzheimer’s were similar to those in the control group in terms of answer accuracy and the time to process the upside-down faces and cars. To perform these tasks, the brain must perform a local analysis of the various image components perceived by the eye. However, with the upright faces, people with Alzheimer’s were much slower and made more mistakes than the healthy individuals. This leads us to believe that holistic face recognition in particular becomes impaired. Subjects with Alzheimer’s disease also demonstrated normal recognition of the upright cars, a task that in theory does not require holistic processing. This suggests that Alzheimer’s leads to visual perception problems specifically with faces.” He noted that what was also surprising about this impairment is that it is observed in the early stages of the disease.

The study clarifies the mechanism involved when people with Alzheimer’s have trouble recognizing the faces of family members or celebrities. The fact that impaired facial recognition might stem from a holistic perception problem–and not just a general memory problem–opens the door to different strategies (such as the recognition of particular facial traits or voice recognition) to help patients recognize their loved ones for longer.

Full abstract:

Thanks for reading,

Jeffree Itrich, M.S.W., M.J.
Mgr, ADCS Communications
Author: Jeffree Itrich at 12:11 PM 0 Comments

Monday, April 04, 2016

Apathy: the Silent Wound of Alzheimer’s Bisease

Dear Readers,

While cognitive and functional decline are the hallmark of Alzheimer’s disease (AD), neuropsychiatric symptoms (NPS) also affect almost all patients. NPS can include agitation, hallucinations, depression, sleep disturbances, and various problem behaviors. These symptoms cause a significant strain on both patients and caregivers and often lead to a lower quality of life.

Apathy is one of the most prevalent NPS in AD patients, affecting as many as half. Patients suffering from apathy experience decreased motivation and rely heavily on caregivers to initiate and oversee daily activities. One study found that apathetic patients were 2.8 times more likely to struggle with at least one activity of daily living, such as dressing, bathing, or eating. This is further complicated by caregivers who lack an understanding of apathy and may perceive apathetic patients as insensitive or uncaring. Caregivers of apathetic AD patients report significant levels of distress and fewer positive experiences than those of non-apathetic patients. Greater caregiver distress is linked with increased service utilization and accelerated institutionalization, which, in turn, creates a significant financial burden. Therefore, the management of apathy should be a major priority in caring for patients with AD.

Despite the high prevalence and serious consequences of apathy in AD, there are no proven treatments for this condition. In the past, clinicians have preferred non-pharmacologic treatment strategies and the available data suggests reliable but limited effects. Recently, several pharmacologic options have been explored. Antidepressant medications have been considered, but some evidence suggests they could actually be detrimental in the treatment of apathy. Cholinesterase inhibitors have also been researched. While these studies have demonstrated a modest improvement in apathy, about half of the patients still showed no relief. Furthermore, these studies were not tailored specifically for apathy. In fact, some studies deliberately excluded apathetic patients since they tend to be less likely to participate and are less easily “engaged” while performing neuropsychological assessments.

The evaluation of dopaminergic (dopamine related, e.g. opiods and amphetamines) agents for the treatment of apathy is another potential approach. The rationale for their use is based on the strong tie between the dopaminergic reward system and the expression of motivated behaviors in brain damaged populations. Preliminary data in one study suggests that dopamine agonist methylphenidate is superior to placebo for the treatment of apathy in AD21. This study reported that the two patients who experienced serious adverse events during the study also experienced extreme AD symptoms (delusions, agitation, and more) prior to the treatment. This suggests methylphenidate might not be a viable option for patients with certain existing symptoms.

Unfortunately, there have been few randomized, placebo-controlled trials of dopamine agonists that address their efficacy for treatment of apathy in AD17. The few that do exist are showing promising results but are also identifying adverse events that will need to be considered as these treatments find their way to the clinic. Currently, a large study on methylphenidate is being conducted under the support of the National Institute of Aging. Data from this study is expected to help find the appropriate place for methylphenidate in the treatment of apathy in Alzheimer’s patients. Apathy is a silent wound of Alzheimer’s disease. Our job is to identify and treat it for the benefit of our patients and their caregivers.

Thanks for reading,

Jacobo Mintzer, M.D., Director, Roper St. Francis Clinical Biotechnology Research Institute, Charleston, S.C.

Jennifer Rowell, B.S., Research Administrative Assistant, Roper St. Francis Clinical Biotechnology Research Institute, Charleston, S.C.

Author: Guest at 1:44 PM 0 Comments

Wednesday, March 23, 2016

Viruses Could Be Causing Alzheimer’s

Dear Readers,
An international team of 31 researchers wrote an editorial in the Journal of Alzheimer’s Disease suggesting that viral and bacterial infections caused by viruses such as herpes, generate plaque build-up in the brain, the hallmark of Alzheimer’s. They suggested that treating these infections with antimicrobial drugs might stop dementia. The herpes virus, Chlamydia bacteria and spirochaete bacteria were named as major triggers.

The authors pointed out that viruses and bacteria are common in the brains of older people, and while they are usually dormant, they can come to life from stress or if the immune system is compromised. It is well known that the herpes virus can damage the central nervous system. In addition they brought up that a gene mutation - APOEe4 - also raises vulnerability to infectious disease. Viral infections in the brain are known to cause symptoms similar to Alzheimer’s; the experts say the link has been ignored for too long.

“Alzheimer’s disease causes great emotional and physical harm to sufferers and their carers as well as having enormously damaging economic consequences,” they wrote. “We write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest Alzheimer’s disease progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain.”

The authors propose further research on the role of infectious agents in Alzheimer’s disease development, saying that the inclusion of antimicrobial therapy in clinical trials is now justified.”

They added that new findings could also have significance for future treatment of Parkinson’s Disease, and other progressive neurological conditions.

To read the full editorial, please visit:

Thanks for reading,

Jeffree Itrich, M.S.W., M.J.
Mgr, ADCS Communications
Author: Jeffree Itrich at 10:41 AM 0 Comments

Wednesday, March 16, 2016

Ohio State University Researchers Establish Link Between Chronic Stress and Short Term Memory Loss

Dear Readers,

According to a new mouse study out of Ohio State University, continuous stress wears down memory. Lead researcher Jonathan Godbout, associate professor of neuroscience at Ohio State says the type of stress they looked at is not everyday stress that everyone encounters, but chronic stress. The study appeared in the March 2nd issue of Journal of Neuroscience and built upon earlier work corroborating associations between chronic stress and lasting anxiety.

In the new study, researchers trained mice on the location of an escape hole in a maze. All the mice mastered the escape route. Later, researchers introduced an aggressive intruder mouse into the maze. The mice that were repeatedly exposed to the intruder had difficulty recalling the location of the escape hole, whereas the mice that were not exposed to the intruder and were not stressed, easily found it.

In addition, the researchers discovered quantifiable changes in the mice brains, such as signs of inflammation instigated by the immune system’s response to outside pressure. They associated this finding to the presence of macrophages (immune cells) in the brains of the stressed out mice. The research team was able to isolate the short-term memory loss to the inflammation as well as the immune system, which the team called important new discoveries. In the future the team hopes to interrupt the inflammation, possibly by identifying targets that could be treated pharmacologically or by employing behavior changes.

This new study focused on the hippocampus, the brain’s center of memory and emotional response. The researchers found that the stressed mice had trouble with spatial memory that resolved within 28 days. They also found that the mice exhibited social avoidance, which measures depressive-like behavior that continued after four weeks of monitoring. Moreover, they were also able to calculate deficits in the development of new neurons 10 days and 28 days after the prolonged stress ended. When they gave the mice a compound that hindered inflammation, neither the depressive symptoms nor brain-cell problems resolved. However, the memory loss and inflammatory macrophages did disappear. This led the researchers to deduce that the post-stress memory issue was directly linked to inflammation – and the immune system – rather than to other damage to the brain. They hope that this type of finding can pave the way for immune-based treatments.

Thanks for reading,

Jeffree Itrich, M.S.W., M.J.
Mgr, ADCS Communications

Author: Jeffree Itrich at 11:25 AM 0 Comments

Wednesday, March 02, 2016

Connectivity Disruptions May Cause Cognitive Deficits in Traumatic Brain Injury

Each year approximately 1.7 million Americans suffer a traumatic brain injury (TBI). Cognitive impairment following a TBI is not uncommon. Researchers at the Center for BrainHealth at The University of Texas at Dallas wondered if connectivity disruptions could be the reason behind the development of cognitive deficits in these patients.

To test their theory, the researchers analyzed 40 MRI scans of TBI patients against MRI scans of 17 healthy individuals matched for gender, age and years of education. Participants were aged 19 to 45 years. Although everyone in the TBI group was at least six months post-injury at the time of the study, the average length of time since injury was eight years with no history of any noteworthy, clinically-diagnosed neurological or psychiatric disorders prior to suffering their TBI.

The researchers discovered that people who are at least six months post-TBI display between-network, long-range and inter-hemispheric connectivity interruptions in the default mode and dorsal attention networks, as well as the frontoparietal control networks. This is key because interactions among the networks are essential for achieving daily life goals such as controlling internal trains of thought and accomplishing daily tasks such as planning, learning and problem solving. The research indicates that cognitive deficits could be the end result of brain network communications inefficiency.

Kihwan Han, Ph.D., served as the study’s lead author and is a post doctoral research associate at the Center for BrainHealth. Daniel Krawczyk, Ph.D. served as principal investigator he is associate professor of cognitive neuroscience and cognitive psychology at the Center for BrainHealth and Debbie and Jim Francis Chair at The University of Texas at Dallas. Their study was recently published in the Journal of International Neuropsychological Society.

Previously most research has focused on separating out individual brain networks. The researchers say this is the first study of its kind to show the relationships among different networks and disruptions in individuals with TBI. In the future the group hopes to study how networks can be improved, even after a TBI.

Funding was provided by US Department of Defense and The Meadows Foundation.
Author: Jeffree Itrich at 10:08 AM 0 Comments

Tuesday, February 23, 2016

The Immune System May Play a Larger Role in AD Than Previously Thought

Dear Readers,

According to a new study out of UC Irvine researchers found that immune cells that normally help us fight off various infections may also fight off AD. Study results appeared in the February 16,2016 online issue of the Proceedings of the National Academy of Sciences.

Microglia, immune cells that dwell in the brain, attempt to clear sticky amyloid plaques. However in AD, the effort is an uphill battle. Many studies have looked at the role microglia plays in AD, but very few researchers have explored whether another set of immune cells called T-cells and B-cells that live outside the brain could play a part in autoimmune diseases that might also affect AD.

To test this theory Mathew Blurton-Jones, assistant professor of neurobiology and behavior, and doctoral student Samuel Marsh bred genetically modified mice to develop AD. While this is common in animal research, their mice lacked three key immune cell types, T-cells, B-cells and NK-cells.

During autopsy they compared the immune-deficient mice brains to other mice bred to develop AD, but with intact immune systems. They found a better than twofold increase in beta-amyloid accumulation in the mice lacking the three significant immune cell types. Furthermore they found that AD mice with the intact immune systems that harbored antibodies, which are made by B-cells, accumulated in the brain, showing an association with microglia that resulted in improving beta-amyloid clearance.

To further confirm the value of this relationship between immune cells in the blood and those in the brain, the researchers transplanted healthy bone marrow stem cells into the immune-deficient Alzheimer’s mice. Since T-, B- and NK-cells develop from bone marrow stem cells, this transplantation led to a reconstitution of the missing immune cells. This allowed the B-cells to produce antibodies that once again reached the brain and aided microglia in eliminating the beta-amyloid.

Thanks for reading,

Jeffree Itrich, M.J., M.S.W
Alzheimer's Disease Cooperative Study
UC San Diego
Author: Jeffree Itrich at 3:55 PM 0 Comments

Tuesday, February 09, 2016

Blood Protein Could Be a Biomarker for Alzheimer’s

A discovery by researchers at Tel Aviv University, Technion (Rambam Medical Center), and Harvard University advance the screening and diagnosing Alzheimer’s disease (AD). A new study, published in the Journal of Alzheimer’s Disease, proposes a new biomarker for cognitive aging and AD: activity-dependent neuroprotective protein (ADNP). Levels of ADNP can be easily examined in routine blood tests. The study also found that ADNP levels tested in the blood correlate with higher IQ in healthy older adults.

The research was led by Professor Illana Gozes, the incumbent of the Lily and Avraham Gildor Chair for the Investigation of Growth Factors and former director of the Adams Super Center for Brain Studies at TAU’s Sackler Faculty of Medicine and a member of TAU’s Sagol School of Neuroscience, conducted by TAU PhD student Anna Malishkevich and spearheaded by Dr. Gad Marshall, Dr. Aaron Schultz, and Prof. Reisa Sperling of Harvard University, and Prof. Judith Aharon-Peretz of Rambam Medical Center – The Technion Institute of Technology.

Significant increases in ADNP RNA levels were observed in patients ranging from mild cognitive impairment (MCI) to AD. ADNP levels tested in plasma and serum samples, as well as white blood cell RNA levels, differentiated between cognitively normal elderly, MCI, and AD participants.

The researchers analyzed blood samples taken from 42 healthy adults, MCI patients, and AD patients at Rambam Medical Center in Israel. After comparing the ADNP expression in the blood samples, the researchers prepared plasma samples and once again compared the protein levels. Professor Gozes determined that they could detect the biomarker in a routine blood test. Her plans are to take these groundwork findings into clinical trials, to hopefully create a pre-Alzheimer’s test that will help shape potential preventative treatments and to clarify ADNP’s ability to predict cognitive decline and disease progression.

This latest research builds on Professor Gozes’ earlier exploration of neuronal plasticity and nerve cell protection at the molecular, cellular, and system level, and her discovery of unique protein families, including ADNP, associated with cross-communication among neural nerve cells and their support cells.
Author: Jeffree Itrich at 3:14 PM 0 Comments

Thursday, February 04, 2016

UCLA Nursing Research Finds Possible Answer to Why Some Develop AD and Others Don’t

Dear Readers,

Alzheimer’s disease affects millions, but there is no cure and no real test for the diagnosis until death, when an examination of the brain can reveal the amyloid plaques that are a telltale characteristic of the disease.

Interestingly, the same plaque deposits have also been found in the brains of people who had no cognitive impairment, which has led scientists to wonder: Why do some develop Alzheimer’s and some do not?

Researchers at the UCLA School of Nursing, led by Professor Karen Gylys, may have just uncovered the answer. Their study, published in the January issue of the American Journal of Pathology, is the first to look at disease progression in the synapses — where brain cells transmit impulses.

The researchers analyzed autopsy tissue samples from different locations of the brains of patients who were considered cognitively normal and those who met the criteria for dementia. Using flow cytometry — a laser-based technology that suspends cells in a stream of fluid and passes them through an electronic detection apparatus — they measured the concentration of two of the known biochemical hallmarks of Alzheimer’s: amyloid beta and p-tau, proteins that when found in high levels in brain fluid are indicative of Alzheimer’s. This allowed the scientists to see large populations of individual synapses — more than 5,000 at a time — versus just two under a microscope.

They found that people with Alzheimer’s had elevated concentrations of synaptic soluble amyloid-beta oligomers – smaller clusters of amyloid-beta that are toxic to brain cells. These oligomers are believed to affect the synapses, making it harder for the brain to form new memories and recall old ones.

“Being able to look at human synapses has almost been impossible,” Gylys said. “They are difficult to get a hold of and a challenge to look at under an electron microscope.”

To overcome that challenge, the UCLA researchers cryogenically froze the tissue samples — which prevented the formation of ice crystals that would have otherwise occluded the synapses had the samples been conventionally frozen. Researchers also did a special biochemical assay for oligomers, and found that the concentration of oligomers in patients who had dementia was much higher than in patients who had the amyloid plaque buildup but no dementia.

Researchers also studied the timing of the biochemical changes in the brain. They found that the accumulation of amyloid beta in the synapses occurred in the earliest stages of the amyloid plaques, and much earlier than the appearance of synaptic p-tau, which did not occur until late-stage Alzheimer’s set in. This result supports the currently accepted “amyloid cascade hypothesis” of Alzheimer’s, which says that the accumulation of amyloid-beta in the brain is one of the first steps in the development of the disease.

The researchers now plan to examine exactly how soluble amyloid-beta oligomers lead to tau pathology and whether therapies that slow the accumulation of amyloid-beta oligomers in the synapses might delay or even prevent the onset of Alzheimer’s-related dementia.

“The study indicates there is a threshold between the oligomer buildup and the development of Alzheimer’s,” Gylys said. “If we can develop effective therapies that target these synaptic amyloid beta oligomers, even a little bit, it might be possible to keep the disease from progressing.”

Gylys said people can reduce their risk for Alzheimer’s through lifestyle and diet choices, but added that one solution is not going to be enough. “Alzheimer’s disease, like heart disease or cancer, is a lot of things going wrong,” she said. “But understanding this threshold effect is very encouraging.”

Other investigators involved in the study were Tina Bilousova, Harry Vinters, Eric Hayden, David Teplow, Gregory Cole and Edmond Teng of UCLA; Carol Miller of the University of Southern California; and Wayne Poon, Maria Corrada, Claudia Kawas, Charles Glabe and Ricardo Albay III of UC Irvine.

The research was supported by grants from the National Institutes of Health and National Institute of Aging.

by Laura Perry, UCLA School of Nursing
Author: Guest at 9:30 AM 0 Comments

Thursday, January 28, 2016

Slower Mental Decline Linked to Higher Amounts of Growth Factor in the Brain

Dear Readers,

Older people with higher amounts of a key protein in their brains also had slower decline in their memory and thinking abilities than people with lower amounts of protein from the gene called brain-derived neurotrophic factor, or BDNF, according to a study published in the Jan. 27, 2016, online issue of Neurology.

“This relationship was strongest among the people with the most signs of Alzheimer’s disease pathology in their brains,” said study author Aron S. Buchman, MD, of Rush University Medical Center in Chicago and a member of the American Academy of Neurology. “This suggests that a higher level of protein from BDNF gene expression may provide a buffer, or reserve, for the brain and protect it against the effects of the plaques and tangles that form in the brain as a part of Alzheimer’s disease.”

For the study, 535 people with an average age of 81 were followed until death, for an average of six years. They took yearly tests of their thinking and memory skills, and after death, a neurologist reviewed their records and determined whether they had dementia, some memory and thinking problems called mild cognitive impairment or no thinking and memory problems. Autopsies were conducted on their brains after death, and the amount of protein from BDNF gene expression in the brain was then measured. The participants were part of the Rush Memory and Aging Project and the Religious Orders Study.

The rate of cognitive decline was about 50 percent slower for those in the highest 10 percent of protein from BDNF gene expression compared to the lowest 10 percent. The effect of plaques and tangles in the brain on cognitive decline was reduced for people with high levels of BDNF. In the people with the highest amount of Alzheimer’s disease hallmarks in their brains, cognitive decline was about 40 percent slower for people with the highest amount of protein from BDNF gene expression compared to those with the lowest amount.

On average, thinking and memory skills declined by about 0.10 units per year on the tests. Higher levels of protein from BDNF gene expression reduced the effect of plaques and tangles in the brain on cognitive decline by 0.02 units per year.

The researchers found that the plaques and tangles in the brain accounted for 27 percent of the variation in cognitive decline, demographics accounted for 3 percent and BDNF accounted for 2 percent.

Michal Schnaider Beeri, PhD, of the Icahn School of Medicine at Mount Sinai in New York, noted in an accompanying editorial that exercise has been shown to increase levels of BDNF in the blood, but that the relationship between BDNF protein levels in the blood and in the brain is not clear.

“More research is needed to confirm these findings, determine how this relationship between protein produced by BDNF gene expression and cognitive decline works and see if any strategies can be used to increase BDNF in the brain to protect or slow the rate of cognitive decline,” said Buchman.

Buchman noted that the study does not prove that BDNF is the cause of a slower rate of cognitive decline; further work is needed to determine if activities which increase brain BDNF gene expression levels protect or slow the rate of cognitive decline in old age.

The study was supported by the National Institutes of Health, Illinois Department of Public Health and the Robert C. Borwell Endowment Fund.

“Higher brain BDNF gene expression is associated with slower cognitive decline in older adults” by Aron S. Buchman, Lei Yu, Patricia A. Boyle, Julie A. Schneider, Philip L. De Jager, and David A. Bennett in Neurology. Published online January 27 2016.

Thanks for reading,

Jeffree Itrich, M.J., M.S.W,
UC San Diego
Author: Jeffree Itrich at 11:20 AM 0 Comments

Wednesday, January 20, 2016

Is this the key to fighting Alzheimer’s?

Dear Readers,

Every four seconds, somewhere in the world, there is a new case of dementia. Alzheimer’s disease, which was considered rare 50 years ago, has today reached pandemic proportions, affecting some 45 million people globally. The cost of caring for Alzheimer’s has skyrocketed to more than $600 billion (about 1% of global GDP) and – if a breakthrough doesn’t come soon – those costs are projected to exceed $1 trillion by 2025.

Doctors have made significant progress towards understanding the causes of Alzheimer’s. For the first time, brain scans are revealing changes in the brains of living Alzheimer’s patients, allowing scientists to see how the disease develops. A disease in a dish model of Alzheimer’s is helping researchers efficiently and rapidly screen hundreds of drugs. New cognitive assessment tools and blood tests for early detection are in development. Experimental medicines targeting abnormal brain proteins are in clinical trials, and the first stem-cell trial for Alzheimer’s is about to begin in the United States. Meanwhile, a team of leading researchers recently published a roadmap for accelerating the testing phase of novel regenerative therapies. One of the most interesting areas is optogenetics, which uses light to activate brain cells, and has been shown to restore memories in amnesiac mice.

Despite these advances, there are still a lot of things we don’t know about dementia, and still room for research. We need better tools for detecting Alzheimer’s before it becomes full-blown, as well as new interventions that can delay the onset of disease in those at high risk, plus new treatments that can target tiny regions of the brain and boost memory. At a basic scientific level, we still need to gain clearer insight into what causes Alzheimer’s and the role played by proteins (such as amyloid and tau), as well as the immune system. It’s time for that to change, and a scientific competition with a lucrative prize could be just the thing to bring it about.

If there’s one thing stalling progress on Alzheimer’s, it’s a lack of resources. Our current investment levels remain modest: we spend 400 times less on research than the sum of the economic toll of the disease. More than 100 “promising” experimental medicines for Alzheimer’s have failed in clinical trials and no new treatments have come to market in the past decade. This failure rate also highlights the need to move from conventional thinking to new paradigms when it comes to dementia research.

The good news, however, is that today we are living in an extraordinary time, when technology is allowing small teams of individuals to accomplish what was once the province of only governments and the largest corporations. Empowered by machine learning, artificial intelligence, ubiquitous networks, cloud computing, robotics and digital manufacturing, small teams are building platforms and enterprises that are touching the lives of billions. If these creative and interdisciplinary teams begin to tackle Alzheimer’s, we may have a way forward. The challenge is to motivate them to do so.

Throughout history, our indomitable spirit of competition has brought about breakthroughs and solutions that once seemed unimaginable and impossible. In 1714, the British government’s Longitude rewards inspired a solution to the great scientific challenge of pinpointing a ship’s location at sea. The Apollo Project, to land a man on the moon, was spurred by intense competition between the US and USSR.

More recently, in 2004, a $10 million competition dubbed the Ansari XPRIZE challenged private entrepreneurs to build a spacecraft. The award spurred the advent of the private space industry and ushered in a new era of scientific prizes. Unlike awards given decades after a discovery, and often to an individual or small academic group (such as the Nobel or Lasker award) competition-based XPRIZEs offer a fast payout (two to seven years depending on the challenge) and revolve around narrowly defined, preset goals. Since the Ansari challenge began, XPRIZEs have led to the development of new oil-spill clean-up methods and a portable, real-life Star Trek Tricoder to diagnose disease. Prior XPRIZES have ranged from $2 million to $30 million.

Ken Dychtwald of Age Wave, a leading think tank on ageing, has co-conceived an Alzheimer’s XPRIZE. By offering a large monetary award, he hopes to inspire brilliant innovators who wouldn’t otherwise study Alzheimer’s to delve into the challenge. Whether they come from academia, industry or the general public, the hope is that new teams will look at dementia with fresh eyes and be able to see things that have been missed. A sponsor is now being sought to create the prize.

P. Murali Doraiswamy,MD,MBBS, FRCP, is Professor of Psychiatry and Medicine at Duke University and a leading researcher at the Duke Institute for Brain Sciences. He chairs the World Economic Forum’s Global Agenda Council for Brain Research and is a co-author of The Alzheimer’s Action Plan.

Peter H. Diamandis, MD, is the Chairman and Founder of the Xprize Foundation, which designs and launches large incentive prizes to drive radical breakthroughs for the benefit of humanity. He is Co-founder and Chairman of the Singularity University, which counsels the world’s top enterprises on how to utilize exponential technologies. He is the coauthor of BOLD: How to Go Big, Create Wealth and Impact the World.

Originally published in World Economic Forum.
Author: Guest at 9:41 AM 0 Comments

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About Us

The Alzheimer's Disease Cooperative Study (ADCS) was formed in 1991 as a cooperative agreement between the National Institute on Aging (NIA) and the University of California, San Diego. The ADCS is a major initiative for Alzheimer's disease (AD) clinical studies in the Federal government, addressing treatments for both cognitive and behavioral symptoms. This is part of the NIA Division of Neuroscience's effort to facilitate the discovery, development and testing of new drugs for the treatment of AD and also is part of the Alzheimer's Disease Prevention Initiative.

The ADCS was developed in response to a perceived need to advance research in the development of drugs that might be useful for treating patients with Alzheimer's disease (AD), particularly drugs that might not be developed by industry.