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Friday, August 12, 2016

AAIC 2016: Useful Data for AD and Related Public Health Policy


Dear Readers:

We thought it would be useful to summarize some of the data reported out of the Alzheimer’s Association International Conference (AAIC) held in Toronto in late July. AAIC is the most expansive and inclusive gathering of the AD-related research community and this year more than 5,000 people were in attendance in Toronto. Overall, researchers reported significant momentum in identifying specific actions, interactions, and activities that may compensate or offset AD pathology and costs of care.

And for those folks keeping track of investigational drugs in late stage clinical trials in AD, Tau RX reported that the Phase III trial of the anti-tau intervention (LMTM) did not meet its primary endpoints. However, most of the research news from AAIC 2016 didn’t really involve drug therapies.

A vast amount of new research on pathways, biomarkers (especially tau), and novel genetic data was presented. There were invaluable economic and other metrics reported out at AAIC that will fill data gaps and provide much needed context for an increasingly dynamic global AD public health dialogue.

Below you will find summaries of reports monetizing the public costs of AD in the US, as well as a check up on implementation of the US Annual Medicare Wellness (AMC). The reports will help to focus the AD public health research agenda, programs and public investment.

AD Health Economics: A Crib Sheet of the Stats from AAIC

AD is now the most expensive medical condition in the US based on cost of care.
• $226 billion spent annually in US
• ½ of total is Medicare expenditures

First generation AD drugs help!
•People using first generation treatments require fewer hospitalizations
• People using first generation treatments have a lower mortality rate in first 12 months post-diagnosis

Unfortunately, only 35% of people diagnosed with AD receive treatment.
• Diagnosed, untreated AD results in significant and avoidable healthcare costs
• US spent 2.5 billion in avoidable hospitalizations for diagnosed but untreated AD
• A combination of diagnosis, treatment and care planning result in savings
• Stressful for the system and the patient – reduce quality of life and increases caregiver burden
From the Frontlines: The Medicare Annual Wellness Visit (AWV)

The Medicare Annual Wellness Visit (AWV) was instituted in 2011 and offers physicians and Medicare patients an opportunity to assess cognition and to track cognitive changes. The Allina Health care system in Minnesota was an early “early adopter” of the AWV

• Allina used the Mini-Cog (three word recall and clock drawing)
• In the Minnesota system, 44% of eligible people underwent one or more AWV from 2011-2015
• The Allina system increased participation in the AMV from 20% to 30% from 2011-2015.
• Nationally, the AMV participation rate is 11%.
• Participation increased over the years, from about 20% in 2011 to about 30% in 2015.
• Nationally, 11% of Medicare patients used the AWV
• Women are more likely to use the AMV benefit
• Approximately 6% of the population studied were diagnosed with a cognitive impairment

World Health Organization Research Priorities

Hiral Shah, MD, from Columbia University Medical Center, presented the results if the World Health Organization’s dementia research priorities exercise. Truly a global initiative, with more than 160 researchers participating, the results will provide guidance to policymakers and researchers regarding future potential funding decisions related to AD research.

• The exercise was based on a similar process called the Child Health and Nutrition Research Initiative (CHNRI)
• The proposed priorities were scored by 162 researchers/stakeholders
• 39 countries were represented in the process
• The exercise used five criteria including the potential for success, burden reduction, conceptual breakthrough, translation and equity

The following research priorities were identified:
• Basic research into disease mechanisms (identified as the biggest potential for conceptual breakthrough).
• Prevention and reduction of risk and burden on quality of care for people and caregivers

Overarching research goals identified by the exercise were:
• Prevention and risk reduction
• Diagnosis, biomarker development and disease monitoring
• Drug and non-drug treatment research
• Quality and delivery of care for people with dementia and their caregivers
• Physiology and progression of normal aging and disease
• Increasing public awareness and understanding

Thanks for reading,
ADCS Staff Compilation
 
Author: Guest at 3:53 PM 0 Comments

Sunday, July 24, 2016

The Alzheimer's Insights Blog will be Back from Hiatus in August


Alzheimer's Insights will be posting fresh content again in August 2016 and following the ADCS office move the Altman Clinical Translational Research Institute at UCSD.
 
Author: Guest at 2:44 PM 0 Comments

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: http://content.iospress.com/articles/journal-of-alzheimers-disease/jad151027

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: http://content.iospress.com/articles/journal-of-alzheimers-disease/jad160152

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
 
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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.