Metabolic disorders may trigger Alzheimer’s

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

ZeeNews.com

Washington: Researchers who examined the link between metabolic syndrome and cognitive disorders has stressed the need for new lines of research to identify effective therapeutic targets.

No effective treatments are currently available for the prevention or cure of Alzheimer’s disease (AD), the most frequent form of dementia in the elderly.

The most recognized risk factors, advancing age and having the apolipoprotein E 4 gene, cannot be modified or treated. Increasingly, scientists are looking toward other risk factors to identify preventive and therapeutic strategies. Much attention recently has focused on the metabolic syndrome (MetS), with a strong and growing body of research suggesting that metabolic disorders and obesity may play a role in the development of dementia.

Now, a new supplement to the Journal of Alzheimer’s Disease has provided a state-of-the-art assessment of research into the link between metabolic syndrome and cognitive disorders.

The supplement is guest edited by Vincenza Frisardi, of the Department of Neurological and Psychiatric Sciences, University of Bari, and the Geriatric Unit and Gerontology-Geriatrics Research Laboratory, IRCCS, Foggia, Italy, and Bruno P. Imbimbo, Research and Development Department, Chiesi Farmaceutici, Parma, Italy.

The prevalence of MetS and obesity has increased over the past several decades. MetS is a cluster of vascular and metabolic risk factors including obesity, hypertension, an abnormal cholesterol profile, and impaired blood glucose regulation.

“Although molecular mechanisms underlying the relationship between MetS and neurological disorders are not fully understood, it is becoming increasingly clear that cellular and biochemical alterations observed in MetS may represent a pathological bridge between MetS and various neurological disorders,” explained Dr. Frisardi.

Type 2 diabetes (T2D) has been linked with cognitive impairment in a number of studies. The risk for developing both T2D and AD increases proportionately with age, and evidence shows that individuals with T2D have a nearly twofold higher risk of AD than nondiabetic individuals.

Paula I. Moreira, Faculty of Medicine and Center for Neuroscience and Cell Biology, University of Coimbra, Portugal, outline some of the likely mechanisms.

Both AD and T2D present similar abnormalities in the mitochondria, which play a pivotal role in cellular processes that impair their ability to regulate oxidation in the cell. Human amylin, a peptide that forms deposits in the pancreatic cells of T2D patients, shares several properties with amyloid-beta plaques in the Alzheimer’s brain.

Insulin resistance is another feature shared by both disorders. Impairment of insulin signalling is directly involved in the development of tau tangles and amyloid beta plaques.

“Understanding the key mechanisms underlying this deleterious interaction may provide opportunities for the design of effective therapeutic strategies,” Dr. Moreira noted. 

ANI

Medicare Stops Cognitive Therapy for Patients with Alzheimer's Disease

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

PR Newswire

Non-pharmaceutical interventions for Alzheimer's patients & others w memory loss or cognitive impairment are under attack. Info provided, advocacy needed.

FOREST HILLS, N.Y., June 5, 2012 /PRNewswire-iReach/ -- SHARPBRAINS has published an article that is essential reading for all providers, patients and family members who are concerned with the availability of effective interventions to treat Alzheimer's disease. MEMORY TRAINING CENTERS OF AMERICA agrees with the concerns raised in this article, and warns that more 'bad news' is coming.

In his article, "From Anti-Alzheimer's 'Magic Bullets' to True Brain Health," Dr. Peter Whitehouse writes that if one followed the headlines surrounding the National Alzheimer's Plan (NAPA), "you'd probably conclude that the likely solution to maintain lifelong brain health is simple: simply wait until 2025 for a 'magic bullet' to be discovered, to cure (or end or prevent) Alzheimer's disease and aging associated cognitive decline. These kinds of beliefs, often reinforced by doctors and advertising, may explain the billions spent today by pharma companies on discovering new compounds...." (SharpBrains, May 31, 2012)

Dr. Whitehouse continues that the 'magic bullet' approach does not reflect "existing clinical evidence or emerging neuroscientific thinking, nor does it address the lifelong needs and demands of our citizens." Dr. Whitehouse challenges us, instead, to "imagine the implications of being able to maximize cognitive performance and delay cognitive decline," and in so doing, that we build on what we already know."

Much of what we know today results from the comprehensive 2010 NIH 'State of the Science Review,' which provides evidence for the benefits of nonpharmacological interventions. A most significant finding was that cognitive training appears to be protective against cognitive decline, whereas pharmaceutical/'magic pill' interventions had no such effect.

Dr. Whitehouse continues: "It simply makes no sense to put all our eggs in the biomedical basket…. Sure, more research is better than less, and we hope that the new funded trials will result in useful drugs. But neither policy-makers nor citizens should wait until then to foster and make lifestyle decisions than can maximize cognitive performance across the lifespan."

We could not agree more with the concerns raised by Dr. Whitehouse. The NIH report tells us there is so much that can be helpful to healthy older adults as well as individuals suffering from MCI and early stage AD. And yet, NAPA (latest version 5/15/12) does not once mention cognitive therapy or training as an effective intervention, or even mention funding for further study. Even in the face of the NIH report and countless others (not listed in NAPA bibliography), the protective and restorative effects of cognitive training are not discussed.

Is it possible, as Dr. Whitehouse suggests, that the funding from pharmaceutical companies and the search for the "magic bullet" has resulted in neglect of what is already known and available in our "arsenal" to help patients struggling with the early effects of Alzheimer's disease? We think it is, and that a true disservice is being done to patients and families who are in desperate need of help NOW.

We certainly believe that biomedical research should continue, and it is of course our fervent hope that ongoing research will lead to new and improved treatments for patients with chronic neurologic diseases such as Alzheimer's, including the possibility of a "magic bullet — cure". However, we must also make every effort to keep the public well-informed regarding effective non-pharmaceutical intervention.

We know that in clinical practice, biomedical and psychological or rehabilitative interventions are not mutually exclusive. In fact, in the field of cognitive rehab, a March, 2012 review by Cotelli, et al., makes the case for combining biomedical and cognitive rehab interventions in relation to Alzheimer's patients: "The studies described above have shown that non-pharmacological intervention can enhance the effect of ChEI treatment." (Cotelli, 2012)

So we know from the NIH review and others that cognitive training is an effective treatment for cognitive decline and early stage AD. We also know from the NIH review that the benefits of pharmaceutical approaches showed no such effect. And we now know that adding cognitive training to pharmaceutical intervention "enhances" the effect of medication alone. Still, NAPA does not speak of the practice or funding of cognitive intervention.

And there is more bad news coming. Despite the NIH report, and despite recommendations by organizational advocates for the Alzheimer's patient (AA, AFA, & others) regarding the need for early detection and effective interventions, one of Medicare's largest Carriers — NGS — has removed cognitive rehabilitation as treatment for memory loss, when cognitive impairment results from neurological disease. This ruling most directly impacts upon the early Alzheimer's (pre-clinical) patient.

In 2007, NGS reviewed the available research, and changed their policy to allow Alzheimer's patients to receive cognitive rehabilitation, including memory training. However, in 2009/2010, when NGS was reorganized, that decision was reversed - at the very time that NIH informed us that cognitive training was the factor most highly associated with a decreased risk of cognitive decline. Is it possible that NGS was unaware of the latest research? Is it possible that this pivotal finding was known but ignored?

The Memory Training Centers of America has requested that NGS resume coverage for patients suffering from Alzheimer's disease (as well as other chronic, neurodegenerative diseases) allowing such patients to receive one of the only interventions that at this time is known to be helpful. May 23,21012, NGS rejected this request. NGS will not allow cognitive rehab to be applied to memory loss and other cognitive impairments resulting from neurological diseases such as early Alzheimer's. These patients will only be allowed ineffective medication. We are appealing that decision.

One has to wonder what could possibly be the motivation of Medicare to stop a medically necessary treatment that can relieve or delay the major symptoms of this devastating disease, in the face of the research, and in the absence of a "magic bullet," and with NAPA's stated goal of finding that bullet by the year 2025. What are we to tell our patients TODAY, who we know we can help, but from whom Medicare is now withholding treatment?

Bruce Brotter, PhD, Clinical Director, Memory Training Centers of America

Does the way you walk affect your risk of getting dementia

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

CTV.ca

As the American Academy of Neurology points out, dementia is not a specific disease. It is a descriptive term for a collection of symptoms that can be caused by a number of disorders that affect the brain. People with dementia have significantly impaired intellectual functioning that interferes with normal activities and relationships. They also lose their ability to solve problems and maintain emotional control, and they may experience personality changes and behavioral problems, such as agitation, delusions, and hallucinations.  

While memory loss is a common symptom of dementia, memory loss by itself does not mean that a person has dementia. Doctors diagnose dementia only if two or more brain functions -- such as memory and language skills -- are significantly impaired without loss of consciousness.  Although it is common in very elderly individuals, dementia is not a normal part of the aging process. 

Research in this week’s issue of Neurology, shows that changes in walking speed in late life may signal the early stages of dementia known as mild cognitive impairment (MCI).

The study used a new technique that included installing infrared sensors in the ceilings of homes, a system designed to detect walking movement in hallways to get a better idea of how even subtle changes in walking speed may correlate with the development of MCI. 

The study involved 93 people age 70 or older who lived alone. Of those, 54 participants had no cognitive impairment, 31 had non-memory related MCI and eight had memory-related MCI. Participants were given memory and thinking tests and had their walking speed monitored at their homes unobtrusively over a three-year period. Participants were placed in groups of slow, moderate or fast based on their average weekly walking speed and how much their walking speed fluctuated at home.  

The study found that people with non-memory related MCI were nine times more likely to be slow walkers than moderate or fast walkers and the amount of the fluctuation in walking speed was also associated with MCI.  

As the authors point out, if we can detect dementia at its earliest phases, then we can work to maintain people's independence, provide treatments and ultimately develop ways to prevent the disease from developing.  

Presented today at the International Conference on Social Identity and Health is a study on attitude towards our age. The study looked at the how our attitude has a massive impact on the likelihood of being diagnosed with dementia. Their research shows that when seniors see themselves as 'older' their performance on a standard dementia screening test declines dramatically; making them five times more likely to meet the criteria for dementia. 

The research involved 68 people aged between 60 and 70 years, who were primed to either feel older or younger than others taking part in the study. Those in the 'older' group were told the participants ranged in age from 40 to 70, encouraging them to think of themselves as being at the upper end of the age spectrum, while those in the 'younger' group were told that participants ages ranged from 60 to 90 years, encouraging them to think of themselves at the lower end of the age spectrum. All participants were then given one of two articles to read, which either focused on the effects of age on memory loss or on the impact of ageing on general cognitive ability. 

The participants then completed a series of standard clinical tests; 70 per cent of people, who were encouraged to see themselves as older and to believe that aging was associated with a general decline in ability, met the criterion for dementia. This was compared to an average of 14 per cent in the other groups.  

The research shows that the effect of age perceptions on performance can be dramatic, and that seeing oneself as 'older' significantly increases a person's risk of being diagnosed with dementia on such tests. It highlights the importance of taking a person's attitude towards their age into account when assessing for dementia.

Why women are at a higher risk of developing Alzheimer's disease

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

(HealthDay News) -- A common genetic risk factor for Alzheimer's disease disrupts brain function in healthy older women but has little effect in men, a new study has found.

People with two copies (one from each parent) of the ApoE4 gene variant are at extremely high risk for Alzheimer's. Only 2 percent of people have two copies of the variant, while about 15 percent of people carry a single copy.

In this study of 91 healthy older people, researchers looked at those with a single copy of the ApoE4 variant and found that women, but not men, exhibited two characteristics that have been linked to Alzheimer's disease.

The women had a signature change in their brain activity and elevated levels of a protein called tau in their cerebrospinal fluid.

The study, published June 13 in the Journal of Neuroscience, is the first to identify this gender difference in healthy older adults with one copy of the ApoE4 variants, according to a Stanford University news release.

The findings suggest that men who carry a single copy of the gene variant shouldn't be assumed to be at increased risk for Alzheimer's disease. The findings also may help explain why women are more likely than men to develop Alzheimer's disease, said Dr. Michael Greicius, assistant professor of neurology and neurological sciences and medical director at the Stanford Center for Memory Disorders, and colleagues.

Alzheimer's disease affects nearly 5 million people in the United States and nearly 30 million people worldwide, the news release noted. For every three women with Alzheimer's, about two men have the disease.

Amyvid in diagnosing Alzheimer's

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Lilly

INDIANAPOLIS, /PRNewswire/ -- Eli Lilly and Company (NYSE: LLY) and Avid Radiopharmaceuticals, Inc., a wholly owned subsidiary of Lilly announced that Amyvid is available to imaging centers in markets surrounding 16 manufacturing sites located in Atlanta; Charlotte, N.C.; Chicago; Colton, Calif;Columbus, Ohio; Dallas; Fort Lauderdale, Fla.; Hartford, Conn.; Houston; Jacksonville, Fla.; North Wales, Pa.; Orlando, Fla.; Palo Alto, Calif.; Phoenix; Seattle; and St. Louis.

Because Amyvid loses over half of its radioactivity every two hours, it must be distributed directly to imaging centers from the specialized radiopharmacies where it is produced. Patients should speak to their health care provider to determine if Amyvid is an appropriate option for them and to determine if it is available in their area. 

"In the roughly two months since the approval of Amyvid, we have been working closely with imaging centers to ensure they are prepared to provide Amyvid to their customers," said Daniel Skovronsky, M.D., Ph.D., president and CEO of Avid, and global brand development leader for Amyvid at Lilly. "We are committed to providing Amyvid to physicians, patients and their families in as many areas as possible as quickly as we can."

To coincide with the availability of Amyvid, Lilly is also announcing the launch of their reader training program. An online training program, developed by Lilly and Avid, is now available at AmyvidTraining.com. The companies also collaborated with the American College of Radiology to present a live, in-person training program, which will be launched on June 11, 2012, in Miami. These reader training programs were developed to provide training for radiologists and nuclear medicine physicians who will be responsible for reading Amyvid scans. Amyvid images should be interpreted only by readers who have successfully completed the Amyvid reader training. Errors may occur in the estimation of plaque density during image interpretation.

Amyvid is the first-and-only radioactive diagnostic agent approved by the U.S. Food and Drug Administration for PET imaging of the brain to estimate beta-amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for Alzheimer's Disease and other causes of cognitive decline.(1)

Amyvid works by binding to amyloid plaques, one of the necessary pathological features of Alzheimer's Disease,(2),(3),(4) and is detected using PET scan images of the brain.(1)  A negative Amyvid scan indicates sparse to no amyloid plaques are currently present, which is inconsistent with a neuropathological diagnosis of Alzheimer's Disease and reduces the likelihood that a patient's cognitive impairment is due to Alzheimer's Disease.(2),(5) A positive Amyvid scan indicates moderate to frequent amyloid plaques are present; this amount of amyloid plaque is present in patients with Alzheimer's Disease, but may also be present in patients with other types of neurologic conditions and in older people with normal cognition.(1),(4),(6)

It's important to note that Amyvid is an adjunct to other diagnostic evaluations. A positive Amyvid scan does not establish a diagnosis of Alzheimer's Disease or other cognitive disorder. Additionally, the safety and effectiveness of Amyvid have not been established for predicting development of dementia or other neurologic condition, or monitoring responses to therapies.(1)

About Amyvid

Amyvid is a radioactive diagnostic agent, tagged with a radioisotope called fluorine-18. Once Amyvid is injected into a vein, it travels through the bloodstream and into the brain, binding to amyloid plaques. Amyvid produces a positron signal, which is detected by a PET scanner and used to create a brain image. A radiologist, who should have successfully completed Amyvid reader training, then interprets the image to evaluate for the presence or absence of significant amyloid plaques (i.e., moderate to frequent levels of neuritic plaques) in the brain. This information is reported back to the referring physician, who then determines the next steps in the evaluation and management of the patient.

Indications and Usage

Amyvid is indicated for Positron Emission Tomography (PET) imaging of the brain to estimate beta-amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for Alzheimer's Disease (AD) and other causes of cognitive decline.

A negative Amyvid scan indicates sparse to no neuritic plaques and is inconsistent with a neuropathological diagnosis of AD at the time of image acquisition; a negative scan result reduces the likelihood that a patient's cognitive impairment is due to AD. A positive Amyvid scan indicates moderate to frequent amyloid neuritic plaques; neuropathological examination has shown this amount of amyloid neuritic plaque is present in patients with AD, but may also be present in patients with other types of neurologic conditions as well as older people with normal cognition. Amyvid is an adjunct to other diagnostic evaluations.

Limitations of Use:

A positive Amyvid scan does not establish a diagnosis of AD or other cognitive disorder. Additionally, the safety and effectiveness of Amyvid have not been established for predicting development of dementia or other neurologic condition, or monitoring responses to therapies.(1)

Amyvid for intravenous use is supplied in 10 mL, 30 mL, or 50 mL multidose vials containing 500-1900 MBq/mL Florbetapir F 18.

Important Safety Information

Warnings and Precautions

Risk for Image Misinterpretation and Other Errors

Errors may occur in the Amyvid estimation of brain neuritic plaque density during image interpretation.

Image interpretation should be performed independently of the patient's clinical information. The use of clinical information in the interpretation of Amyvid images has not been evaluated and may lead to errors. Other errors may be due to extensive brain atrophy that limits the ability to distinguish gray and white matter on the Amyvid scan as well as motion artifacts that distort the image.

Amyvid scan results are indicative of the brain neuritic amyloid plaque content only at the time of image acquisition and a negative scan result does not preclude the development of brain amyloid in the future.

Radiation Risk

Amyvid, similar to other radiopharmaceuticals, contributes to a patient's overall long-term cumulative radiation exposure. Long-term cumulative radiation exposure is associated with an increased risk of cancer. Ensure safe handling to protect patients and health care workers from unintentional radiation exposure.

Most Common Adverse Reactions

The most common adverse reactions reported in clinical trials were headache (1.8 percent), musculoskeletal pain (0.8 percent), fatigue (0.6 percent), nausea (0.6 percent), anxiety (0.4 percent), back pain (0.4 percent), blood pressure increased (0.4 percent), claustrophobia (0.4 percent), feeling cold (0.4 percent), insomnia (0.4 percent), neck pain (0.4 percent).

Drug Interactions

Pharmacodynamic drug-drug interaction studies have not been performed in patients to establish the extent, if any, to which concomitant medications may alter Amyvid image results.

For Full Prescribing Information, visit http://pi.lilly.com/us/amyvid-uspi.pdf.  

AM HCP ISI 06APR2012

About Eli Lilly and Company

Lilly, a leading innovation-driven corporation, is developing a growing portfolio of pharmaceutical products by applying the latest research from its own worldwide laboratories and from collaborations with eminent scientific organizations. Headquartered in Indianapolis, Ind., Lilly provides answers — through medicines and information — for some of the world's most urgent medical needs. Additional information about Lilly is available at www.lilly.com.  

This press release contains certain forward-looking statements about Amyvid™, a radioactive diagnostic agent indicated for brain imaging of beta-amyloid plaques in patients with cognitive impairment who are being evaluated for Alzheimer's Disease and other causes of cognitive decline. This release reflects Lilly's current beliefs; however, as with any pharmaceutical product, there are substantial risks and uncertainties in the process of development and commercialization. There is no guarantee that future study results and patient experience will be consistent with study findings to date or that the product will prove to be commercially successful. For further discussion of these and other risks and uncertainties, see Lilly's filings with the United States Securities and Exchange Commission. Lilly undertakes no duty to update forward-looking statements.

P-LLY

(1) Amyvid Prescribing Information. April 6, 2012.

(2) Hyman BT, Phelps CH, Beach TG, et al. National Institute on Aging—Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease. Alzheimers Dement. 2012;8:1—13.

(3) Mirra SS, Heyman A, McKeel D, et al; and participating CERAD neuropathologists. The Consortium to Establish a Registry for Alzheimer's Disease (CERAD): part II. standardization of the neuropathologic assessment of Alzheimer's disease. Neurology. 1991;41(4):479—486.

(4) Thies W, Bleiler L; Alzheimer's Association. Alzheimer's Association report: 2012 Alzheimer's disease facts and figures. Alzheimers Dement. 2012;8:131—168. 

(5) McKhann GM, Knopman DS, Chertkow H, et al. The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's Disease. Alzheimers Dement. 2011;7:263—269.

(6) Sperling RA, Aisen PS, Beckett LA, et al. Toward defining the preclinical stages of Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's Disease. Alzheimers Dement. 2011;7(3):280—292.

©Lilly USA, LLC 2012. All rights reserved. AM77832 5/2012

Amyvid™ is a trademark of Eli Lilly and Company.

(Logo:  http://photos.prnewswire.com/prnh/20031219/LLYLOGO )

SOURCE Eli Lilly and Company

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Dementia care model that reduces hospitalizations successfully translated into practice

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Science Codex

INDIANAPOLIS -- An innovative model of dementia care that significantly reduces emergency department visits and hospitalizations, and encourages use of medications that are not harmful to older brains, has now been used to treat over 1,000 patients. The Aging Brain Care model was developed by researcher-clinicians from the Regenstrief Institute and the Indiana University School of Medicine.

Extending the definition of a patient to include family members who enable cognitively impaired individuals to live in the community, physicians, nurses, social workers and other staff members work closely with both the older adult and family caregivers -- in the exam room and in the home, as well as over the phone and via email -- to deliver care to improve both brain and physical health.

This month, the 1,000th patient was seen at the Wishard Healthy Aging Brain Center, the first facility to use the ABC model. The Healthy Aging Brain Center is both a research lab and a treatment facility focused on the mental status of elder adults. The center has seen reductions of 45 percent in hospital emergency department visits and 54 percent in hospitalization stays in patients compared to similar individuals not seen in the center.

"Patients treated utilizing the ABC model have fewer behavioral and psychological symptoms of dementia after one year than they had at the onset of treatment," said Regenstrief investigator Malaz Boustani, M.D., associate professor of medicine at the IU School of Medicine and the medical director of the Wishard center.

Patients receiving care in the Healthy Aging Brain Center are given an initial cognitive assessment including neuropsychological testing, an MRI, a medication review and a structured neurological and physical evaluation. The staff then helps both patient and caregivers develop a personal treatment plan that typically includes recognizing potentially harmful medications, prescribing new medications, initiating brain and physical exercise regimens, and working on reducing stress to improve daily life.

"Our research over the past decade has shown the importance of families and communities, in addition to medical care, in improving the quality of life for older adults with dementia," said Regenstrief investigator Christopher Callahan, M.D., Cornelius and Yvonne Pettinga Professor in Aging Research at the IU School of Medicine. "The HABC uses a team-based approach to help get everyone on the same page in meeting the goals of care for the patient and their family caregivers."

Dr. Callahan sees patients at the Healthy Aging Brain Center and is also founding director of the IU Center for Aging Research.

The Healthy Aging Brain Center receives referrals from across the country and has quickly become a nationally recognized leader in the care of older adults, according to Dr. Boustani, a geriatrician.

Earlier this month, the new Senior Health Implementation Center at the Regenstrief Institute announced that it will disseminate ABC tools, including a how-to manual for clinicians, a dementia symptoms monitor and a resource handbook for caregivers, as well as provide onsite training.

According to the Alzheimer's Association, an estimated 5.4 million Americans -- one in eight older Americans -- have Alzheimer's disease.

Source: Indiana University School of Medicine

Antibody Reaches Major Milestone in Collaboration with Roche

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Reuters

Gantenerumab Clinical Trial Expanded to Pivotal Phase 2/3 Study

MorphoSys AG (FSE: MOR; Prime Standard Segment, TecDAX) announced today that its partner Roche (SIX: RO, ROG; OTCQX: RHHBY) has expanded the ongoing SCarlet RoAD Phase 2 clinical trial of gantenerumab for prodromal (early) Alzheimer's disease to a potentially pivotal study. The trial size will be increased from 360 to 770 participants, and a favorable outcome to the trial could be used by Roche to support a marketing application for gantenerumab. The expansion of the study triggered a clinical milestone payment to MorphoSys, the details of which were not disclosed. MorphoSys stands to receive further developmental milestones as well as royalties on product sales.

"This is a major step forward for a HuCAL antibody program that has genuine blockbuster potential", commented Dr. Marlies Sproll, Chief Scientific Officer of MorphoSys AG. "Gantenerumab is the first investigational antibody development program for Alzheimer's disease to be clinically tested in a setting for which there is great hope, namely the treatment of early-stage, pre-dementia subjects. A potential path to market for this program has become much clearer with this transition to a pivotal trial".

"We believe the greater opportunity to make a difference in patients' lives is in early diagnosis and intervention," said Luca Santarelli, Head of Neuroscience at Roche. "Our attempt is to utilize a biomarker-driven approach, leveraging both our pharmaceutical and diagnostics divisions to develop a companion diagnostic for gantenerumab to select patients at the prodromal stage, before significant damage to the brain has occurred."

Gantenerumab is an optimized, fully human antibody that was developed on behalf of Roche by MorphoSys scientists using the Company's proprietary HuCAL technology. Gantenerumab is unique amongst antibodies in development in that it binds to both the N-terminus and mid-section of the 42 amino acid amyloid-β peptide. It has been shown to break down amyloid plaque both in vitro and in vivo. In Phase 1 clinical trials conducted by Roche¹⁾, the antibody was found to bring about rapid, dose-dependent clearance of plaque from the brains of mild to moderate Alzheimer's disease patients. The ongoing clinical trial is designed to evaluate its effect on cognition and functioning as well as its safety and pharmacokinetics in patients with prodromal, or early-stage, Alzheimer's disease. In this phase of the disease, which can be characterized by measuring certain biomarkers, patients have only mild cognitive impairment and have not yet been diagnosed with Alzheimer's disease. According to recent research, amyloid plaque may accumulate even at this early stage in the brains of sufferers, and may lead to full-blown disease.

MorphoSys's clinical pipeline now comprises one program in phase 3 development, seven in phase 2 and twelve in phase 1. Of these, four are proprietary, as yet un-partnered programs, namely MOR103, which is in a phase 1b/2a trial for rheumatoid arthritis and a phase 1b trial in multiple sclerosis, MOR208, which is in a phase 1 trial for chronic lymphocytic leukemia and MOR202, which is in a phase 1/2a trial for multiple myeloma.

¹⁾ Reference: Ostrowitzki, S. et al (2011) Mechanism of Amyloid Removal in Patients With Alzheimer Disease Treated With Gantenerumab. Archives of Neurology, 68(10); 

Another successful drug trial for Alzheimer's disease

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

(MARKETWIRE via COMTEX) -- Lundbeck Canada announced that its investigational Alzheimer's drug Lu AE58054 met its primary cognition endpoint in patients with Alzheimer's disease. This compound is a novel, selective 5-HT6 receptor antagonist with a different mechanism of action than currently available Alzheimer's medications.

The large, phase 2, proof-of-concept study was conducted in 278 patients in Canada, Europe, and Australia with either Lu AE58054 (plus 10mg/day donepezil) or placebo (plus 10mg/day donepezil).

Augmentation therapy with Lu AE58054 resulted in statistically significant improvement in cognition, as measured by the ADAS-cog (Alzheimer's Disease Assessment Scale-cognitive sub-scale) over a 24-week treatment period versus donepezil monotherapy (10mg/day). Secondary endpoints, including measures of global status and activities of daily living also showed positive trends with the addition of Lu AE58054, compared with patients who only received donepezil. Treatment with Lu AE58054 in this study was well tolerated.

"As our Canadian population ages, effective and safe treatments that can help reduce Alzheimer's symptoms are becoming increasingly crucial," said Dr. Sharon Cohen, behavioural neurologist and Medical Director of Toronto Memory Program. "It is encouraging to see these positive preliminary results and it will be interesting to follow this compound's development."

Lundbeck is now evaluating the future development strategy of Lu AE58054 with the intention to initiate a major pivotal clinical program, potentially including development and commercial partnerships.

"Lundbeck is very pleased with the results," said Jean Proulx, Senior Director, Scientific Affairs at Lundbeck Canada. "We see Lu AE58054 as having a strong potential in Alzheimer's disease, a disease with a huge unmet medical need."

Full data from this study will be made available through scientific disclosure at upcoming medical congresses and in scientific publications.

About Lu AE58054

Lu AE58054 is a potent and selective 5-HT6-receptor antagonist. The 5-HT6-receptor is primarily found in areas of the brain involved in cognition. A number of early trials have demonstrated that a 5-HT6-receptor antagonist could offer potential benefits in the treatment of disorders such as Alzheimer's disease and in December 2009 Lundbeck initiated the above-described 24-week clinical phase 2 trial with Lu AE58054 as augmentation therapy in Alzheimer's disease.

About Alzheimer's disease

Alzheimer's disease is the most common neurodegenerative disorder and most frequent cause of dementia, accounting for 50-70% of cases.(1) Alzheimer's disease is a progressive brain disorder in which the brain gradually degenerates. It most frequently occurs in people aged above 65-70 years. In Canada, an estimated 500,000 Canadians, or 1 in 11 people over the age of 65, have Alzheimer's or a related dementia. Within a generation, it is estimated that between 1 and 1.3 million Canadians will have the disease.(2)

Alzheimer's disease also has an enormous impact on the patient's caregiver. One in five Canadians over the age of 45 is providing unpaid care of some kind to seniors with long-term health problems.(3) Family caregivers contribute over $5 billion of unpaid care every year.(4)

About Lundbeck Canada Inc.

Montreal-based Lundbeck Canada is a subsidiary of H. Lundbeck A/S, a leading international research-based pharmaceutical company. Lundbeck has built its reputation as a leader in specialty treatments. For decades, we've concentrated our expertise on helping people everywhere fight CNS disorders such as Alzheimer, depression, anxiety and schizophrenia. Now, we're directing that same focus and energy to oncology. Visit us at www.lundbeck.ca .

(1) Alzheimer's Association. Basics of Alzheimer's disease: what it is and what you can do. 2010. http://www.alz.org/national/documents/brochure_basicsofalz_low.pdf . Accessed 30/09/11.

(2) Rising Tide - The Impact of Dementia on Canadian Society. Alzheimer Society of Canada.

(3) Eldercare: What We Know Today. Statistics Canada report, October 20, 2008.

(4) A profile of Canadian chronic care providers. Fast, J., Niehaus, L., Eales, J., & Keating, N. 2002a.

Immune System plays a role in preventing Alzheimer's disease

Caregivers, and healthcare professionals, here is some great information


Here is a great dementia resource for caregivers and healthcare professinals,


Your residents will love the Amazon Kindle Fire




Here is information on being the best caregiver you can be


Here is a way for nurses administrators, social workers and other health care  professionals to get an easyceu or two


Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition

Medical News Today

Researchers from the Peninsula College of Medicine and Dentistry at Exeter's University collaborated with a team from the National Institute on Aging in the USA and in Italy to screen expression levels of thousands of genes in blood samples from nearly 700 people. They discovered that the best marker associated with memory in people was a gene called CCR2, which showed immune system activity against beta-amyloid. Using the Mini mental State Examination, the team measured memory and other cognitive functions.

Earlier animal studies demonstrated that memory and function in mice susceptible to Alzheimer's improved when researchers augmented the CCR2-activated part of the immune system in the animals' blood.

Study leader, Professor David Melzer, declared:

"This is a very exciting result. It may be that CCR2-associated immunity could be strengthened in humans to slow Alzheimer's disease, but much more work will be needed to ensure that this approach is safe and effective".

Dr Lorna Harries, who co-authored the study, concluded:

"Identification of a key player in the interface between immune function and cognitive ability may help us to gain a better understanding of the disease processes involved in Alzheimer's disease and related disorders."

Written By Petra Rattue 

Dementia and cancer: Hard diseases to cure

Click image to enlarge


Via: MedicareSupplementalInsurance.com

Healthcare professionals, care givers and others, here is some information that you will find of interest.


Dementia and cancer have many things in common if you think about it. Dementia as with cancer is a hard disease to find a cure for.As with cancer, there are many different types.


As with cancer dementia survival rate is longer and better than it was in the past.
Great strides have been made in curing both sets of diseases, but cures are not absolute. In both cases earl  detection is key. Research will bring about even better survival to those who are unfortunate enough to get them.