Fish Oil May Benefit Alcohol Abusers, Reduce Risk of Neurodegeneration and Ensuing Dementia

(Loyola University Health System) Omega-3 fish oil might help protect against alcohol-related neurodamage and the risk of eventual dementia, according to a study published in the journal PLOS ONE.

Many human studies have shown that long-term alcohol abuse causes brain damage and increases the risk of dementia. The new study found that in brain cells exposed to high levels of alcohol, a fish oil compound protected against inflammation and neuronal cell death.

The study was conducted by Michael A. Collins, PhD, Edward J. Neafsey, PhD, and colleagues at Loyola University Chicago Stritch School of Medicine, and collaborators at the University of Kentucky and the National Institute of Alcohol Abuse and Alcoholism (NIAAA).

Collins and colleagues exposed cultures of adult rat brain cells over several days to concentrations of alcohol equivalent to about four times the legal limit for driving – a concentration seen in chronic alcoholics. These brain cultures were compared with cultures exposed to the same high levels of alcohol, plus a compound found in fish oil called omega-3 docosahexaenoic acid (DHA).

Researchers found there was up to 90 percent less neuroinflammation and neuronal death in the brain cells exposed to alcohol plus DHA than in the cells exposed to alcohol alone.

An earlier meta-analysis by Collins and Neafsey, which pooled the results of about 75 studies, found that moderate social drinking may have the opposite effect of reducing the risk of dementia and/or cognitive impairment during aging. (Moderate drinking is defined as a maximum of two drinks per day for men and 1 drink per day for women.)

It appears that limited amounts of alcohol might, in effect, tend to make brain cells more fit. Alcohol in moderate amounts stresses cells and thus toughens them up to cope with major stresses and insults down the road that could cause dementia. But too much alcohol overwhelms the cells, leading to neuroinflammation and cell death.

Further studies are needed to confirm whether fish oil protects against alcohol-related cognitive injury and dementia in adult rodent models.

“Fish oil has the potential of helping preserve brain integrity in chronic alcohol abusers,” Collins said. “At the very least, it is unlikely that it would hurt them.”

But Collins added that the best way for an alcohol abuser to protect the brain is to cut back to low or moderate amounts or quit entirely.

“We don’t want people to think it is okay to take a few fish oil capsules and then continue to go on abusing alcohol,” he said.

PLOS ONE is an international, peer-reviewed, open-access online journal. Collins earlier reported findings at the 14th Congress of the European Society for Biomedical Research on Alcoholism in Warsaw.

Collins, principal investigator of the study, is a professor in the Department of Molecular Pharmacology and Therapeutics at Loyola University Chicago Stritch School of Medicine. Co-authors are Neafsey, Nuzhath Tajuddin, MS, and Kwan-Hoon Moon, PhD, of the Stritch School of Medicine; Kimberly Nixon, PhD, of the University of Kentucky; and Hee-Yong Kim, PhD, of the NIAAA. The research was funded by grants from the NIAAA at the National Institutes of Health.

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Bexarotene’s Effect on Alzheimer’s May Depend on Severity of Disease

(University of Illinois at Chicago) A cancer drug that has shown promise against Alzheimer’s disease in mice and has begun early clinical trials has yielded perplexing results in a novel mouse model of AD that mimics the genetics and pathology of the human disease more closely than any other animal model.

The drug, bexarotene, was found to reduce levels of the neurotoxic protein amyloid-beta in experimental mice with late-stage Alzheimer’s but to increase levels during early stages of disease.

The finding, by researchers at the University of Illinois at Chicago College of Medicine, was reported July 16 at the Alzheimer’s Association International Conference in Copenhagen by Mary Jo LaDu, who in 2012 developed a transgenic mouse that is now regarded as the best animal model of the human disease.

That experimental mouse carries a human gene that confers on people a 15-fold elevated risk of developing AD, making it the most important known genetic risk factor for the disease.

DG14_07_05_028-387x258Mary Jo LaDu, professor of anatomy and cell biology, and Leon Tai, research assistant professor.
Photo: Roberta Dupuis-Devlin/UIC Photo Services

Alzheimer’s disease is the most common form of dementia, affecting more than five million Americans. The disease is progressive and eventually fatal. One of the hallmarks of AD is the appearance of dense plaques in the brain composed of clumps of amyloid-beta. But recent research indicates that smaller, soluble forms of amyloid-beta — rather than the solid plaques — are responsible for the death of nerve cells that leads to cognitive decline.

Humans carry a gene for a protein in cells called apolipoprotein E, which helps clear amyloid-beta from the brain by binding to it and breaking it down. LaDu’s mice carry the most unfortunate variant in humans, called APOE4, or APOE3, which is neutral for AD risk.

“APOE4 is the greatest genetic risk factor for Alzheimer’s disease,” said LaDu, who is professor of anatomy and cell biology at UIC.

“Our previous work showed that compared to APOE3, the apolipoprotein produced by the APOE4 gene does not bind well to amyloid-beta and so does not clear the neurotoxin from the brain.”

Results of previous studies in mice of bexarotene’s effect on AD have been mixed, and none of those studies were done in mice that carry a human APOE gene and also develop progressive, AD-like pathology. The UIC research presented in Copenhagen is the first to do so.

LaDu, working with Leon Tai, research assistant professor in anatomy and cell biology, and their coworkers gave bexarotene to mice carrying APOE4 or APOE3 for seven days during the early, intermediate, or late stages of AD. The researchers then measured the levels of soluble amyloid-beta in the brains of the mice.

In mice carrying human APOE4 with later-stage AD, the researchers saw a 40 percent reduction in soluble amyloid-beta and an increase in the binding of apolipoprotein to amyloid-beta. But in APOE4 or APOE3 mice with earlier-stage AD, the amount of soluble amyloid-beta actually increased. When the researchers gave APOE4 mice bexarotene for one month starting when they had early-stage AD to see if the drug could prevent disease progression, there was no beneficial effect.

Tai thinks that for people who carry the APOE4 gene, short-term treatment with bexarotene in the later stages of disease may be beneficial. But further research is needed, he said, to determine length and timing of treatment — and, importantly, whether the drug will benefit APOE3 carriers.

“Bexarotene also is extremely toxic to the liver,” Tai said. “For prevention, where a drug is given before the symptoms of Alzheimer’s disease appear, and likely over longer periods of time, bexarotene is not likely a viable therapeutic because of this known toxicity unless dosing is carefully controlled and patients are closely monitored.”

Other contributors to the research are Kevin Koster and Nicole Collins, both research associates in the UIC College of Medicine; and from the UIC College of Pharmacy, Greg Thatcher, professor of medicinal chemistry and pharmacognosy; Jia Luo, research assistant professor; and graduate student Sue Lee.

The research was supported by an Alzheimer’s Drug Discovery Foundation grant P01AG030128 from the National Institute on Aging, and UIC Center for Clinical and Translational Science Grant UL1RR029879.

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Music Can Penetrate the Fog of Alzheimer’s Disease

(UCLA Health) Can listening to music soothe an agitated patient with Alzheimer’s disease, or even unlock happy memories from better days? Although much of the evidence is anecdotal, there is plenty to suggest that songs can, at minimum, bring a smile to the face of a dementia patient.

And that is good enough for Joshua Grill, PhD, assistant professor of neurology and director of the Katherine and Benjamin Kagan Alzheimer’s Disease Treatment Development Program at UCLA’s Mary S. Easton Center for Alzheimer’s Disease Research. Dr. Grill is on a campaign to collect pre-owned iPods and MP3 players, iTunes gift cards, headphones and related items for Alzheimer’s patients in nursing homes. The program is a partnership between the Easton Center and the national nonprofit organization Music & Memory, which provides music therapy to nursing homes in the Los Angeles area. Dr. Grill discusses the evidence for music’s benefits for dementia patients.

VitalSignsHow much is known about music’s therapeutic potential for patients with Alzheimer’s disease?

Studies have found that music has the ability to uniquely activate the brain. One need look no further than a child learning the alphabet to see the power of musical melody in learning. Music clearly affects the brain differently from spoken word or a series of tones that don’t form a melody, and studies have even shown that it can activate pleasure and reward centers in the brain. Specifically thinking about music and dementia, there are many anecdotal reports of Alzheimer’s patients who are so amnestic they can’t remember their own family members, yet they retain the ability to recall, perform and, perhaps most important, enjoy music. In fact, one case report described a musician who was well into the course of dementia and could still learn new songs.

Given music’s power to evoke memories in all of us, is it possible it could have memory-related benefits for dementia patients?

There are a few studies to support music as a strategy to improve memory in patients with amnestic disorders like Alzheimer’s disease. One study suggested mild cognitive benefits in patients in a nursing home after group music therapy, including improved memory function. Another small study suggested that mild patients who listened to Vivaldi’s “Spring” movement from Four Seasons had improved autobiographical memories — memories from their own childhood, adult life and recent past. Unfortunately, however, most large, well-controlled studies looking specifically at memory have not found a benefit of music therapy. Still, there are many anecdotal reports of music unlocking happy memories in patients.

Many dementia patients show behavioral symptoms that are difficult to control. Can music help there?

I think the evidence is more compelling for music’s effect on the behavioral symptoms. The longer someone has Alzheimer’s disease, the more likely he or she is to experience behavioral problems, including depression, apathy, agitation and frustration. These are some of the more challenging symptoms that patients and their caregivers and families face. If music can reduce those symptoms, that would be incredibly helpful. We know that the regions of the brain affected by Alzheimer’s disease are diffuse and increase in number and severity over time. But even late in the disease, music may be able to activate the circuits that remain intact and provide pleasure and improved mood. Studies have found that music therapy can reduce agitation and anxiety, decrease depression and improve quality of life. At the facility where we donated the first batch of iPods, staff reported that some patients were eating a whole meal or sleeping through the night for the first time in months after individualized music therapy.

What inspired you to establish this program?

I was struck when I heard about what Music & Memory was doing. At our center we spend most of our time conducting research and running clinical trials for Alzheimer’s disease, and we are very excited about where the field is going. We think we are on the cusp of having drugs that, for the first time, can actually slow the course of the disease. Unfortunately, though, right now we are not able to revert severely demented patients back to mild states. So while we are very excited about the future, we can’t and won’t leave behind the millions of people who have dementia now. They still need us, and their families still need us, and if there are ways we can help them, we will.

To make a tax-deductible donation of iPods and MP3 players, as well as related items, to the Mary S. Easton Center for Alzheimer’s Disease Research at UCLA’s Tunes for Alzheimer’s Patients program, go to: eastonad.ucla.edu

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Minority Populations at Risk for Alzheimer’s

(Alzheimer’s Prevention Registry) Alzheimer’s disease impacts millions of Americans, and it does not discriminate by gender or race. In fact, researchers are doubling their efforts to educate minority communities about the disease.

apistoryAccording to Stephanie Monroe, from the organization Us Against Alzheimer’s, more than 20 percent of Alzheimer’s patients are African American.

“And we are 13 percent of the population,” Monroe said. “We think these reported numbers could be low because there are also patients who do not go to the doctor.”

Dr. Reisa Sperling, Professor of Neurology, Harvard Medical School and Director, Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital and Massachusetts General Hospital, believes it is important to discover why Alzheimer’s is impacting minority populations.

“For reasons that are not completely understood, multiple studies have indicated a higher risk of Alzheimer’s disease and dementia in general in both African American and Latino/Hispanic older individuals,” Dr. Sperling said. “We desperately need to understand the factors that contribute to this increased risk – likely a combination of genetics and co-morbidities (hypertension, diabetes), possibly early life influences, such as education.”

Monroe notes that the Alzheimer’s research community has increased its efforts in the past few years to reach out to minority communities to not only educate them about the disease, but to encourage them to participate in clinical trials. She added that researchers are now partnering with organizations like hers with ties to minority communities.

“The research community is getting smart about this and realizing there are groups like us that can partner with them,” Monroe said. “There is a real issue of trust, so organizations like us can go in and talk to pastors and community members. They (researchers) are now learning what they need to do to become more engaged in the community. It’s a learning process.”

Jennifer J. Manly, PhD, Associate Professor of Neuropsychology at Columbia University’s Taub Institute for Research on Alzheimer’s disease and the Aging Brain, said that there is not enough minority participation in clinical trials and this does impact research.

“There is the possibility that any results of these trials are not generalizable to minority populations. Because of the higher burden of cognitive impairment in these communities, this is a problem,” Manly said. “In addition, because of the higher burden of risk factors for cognitive impairment, we are missing out on an opportunity to test whether our interventions are effective in a group of people who are at highest risk.”

Dr. Sperling agrees that minority participation in clinical trials is not what it needs to be.

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Diagnostic Tests for Alzheimer’s Disease

(BrightFocus Foundation)  With the adoption of the Diagnostic and Statistical Manual of Mental Disorders 5 (DSM 5), the definition of the condition formerly called dementia has been significantly transformed and updated. That makes this an excellent time to review the approach to diagnostic assessment of dementia and identification of Alzheimer’s disease (AD). Previously, a diagnosis of probable AD required the presence of a decline in memory and at least one of several other cognitive domains, not attributable to another medical or psychiatric disorder, resulting in an impairment of social and/or occupational functioning.

mri-300-X-200DSM 5 updates this approach in light of our greater understanding of neurocognitive disorders. Now, the presence of decline in one or more cognitive functions warrants the diagnosis of Major Neurocognitive Disorder (MND) if this impairment interferes with independence and is not better explained by another medical or psychiatric disorder. AD is the most common MND, but clinicians can use information from the history, current mental status examination, and neuropsychological or medical testing to refine the diagnosis further and specify whether AD or another type of MND is suspected.

Careful assessment of a person’s history, current complaints, and mental status examination remains the cornerstone of diagnostic assessment, but clinical assessment runs a risk of missing early and subtle indicators of MND, misclassifying AD as a different cognitive disorder, or mistaking another cognitive disorder for AD. Fortunately, a variety of additional tests are available to increase the accuracy of diagnosis, which are discussed below. Some less reliable or less widespread tests will not be covered in this discussion.

Medical History and Mental Status Examination

Clinical assessment of a patient’s history and performing a mental status examination are necessary steps in the evaluation of cognitive disorders. In identifying the presence of AD, the presence of a typical slow and insidious progression of symptoms is sought. Other factors capable of producing cognitive impairment are identified, including medical disorders, substances or medications that can cause cognitive impairment, or psychiatric conditions associated with cognitive changes. The characteristic clinical syndrome of AD includes a prominent disturbance of what is known as episodic memory (long-term memory that involves the recollection of situations, specific events, and experiences).

Memory of recent events is particularly impaired, and evidence that reminders are of limited benefit is consistent with the memory storage problem typically found in AD. Language and visuospatial problems may also be reported or identified. In less common variants of AD, the disturbance of language or visual functions may be more prominent than memory difficulties in the disease’s early stage.

Neuropsychological Screening Tests

Brief Neuropsychological Assessment Tools such as the Mini Mental State Exam (MMSE) and the Montreal Cognitive Assessment (MoCA) are available to screen for cognitive difficulties, although large scale routine screening of asymptomatic people is not recommended. In a busy primary care practice setting or in other appropriate contexts, these examination aids can justify further diagnostic testing in an individual who reports or shows cognitive changes. Longer and more comprehensive neuropsychological test batteries can estimate the severity of decline and characterize specific cognitive strengths and weaknesses. Administration of these test batteries requires training and certification. Evidence from neuropsychological testing, whether brief or more extensive, is interpreted in the context of a person’s overall medical and psychosocial circumstances.

Blood Tests

Currently available blood tests do not definitively identify the presence or absence of AD, but they are nonetheless useful. Blood tests can examine for other causes of cognitive impairment that can mimic AD’s clinical presentation. Infections such as HIV, metabolic disturbances such as hypothyroidism or hyponatremia (low blood sodium), autoimmune disorders such as giant cell arteritis, nutritional deficiencies such as pernicious anemia, and toxic conditions such as heavy metal poisoning are among the many conditions that can impair cognition and might be revealed by appropriately chosen blood tests.

Cerebrospinal Fluid (CSF) Tests

A lumbar puncture is required for withdrawal of cerebrospinal fluid. When clinicians are searching for infectious causes of cognitive impairment such as herpes encephalitis, examination of cerebrospinal fluid may be necessary in order to reach a definitive diagnosis. It is possible to quantify the relationship between cerebrospinal fluid beta amyloid and tau, proteins associated with Alzheimer’s disease. An abnormal result for this test, in the context of clinically measured cognitive impairment, is considered a “biomarker” associated with AD. CSF tests, however, are used infrequently in many settings due to the potential discomfort, possible complications, and limited availability of trained clinicians available to perform this procedure.

Brain Imaging

Brain imaging (neuroimaging) studies are recognized as an important component of the evaluation of any individual with a prominent change in cognitive functioning. Neuroimaging techniques fall into two major categories:

Computed Tomography and Magnetic Resonance Imaging

Structural imaging such as Computed Tomography (CT) or Magnetic Resonance Imaging (MRI) yields a picture of the brain that allows identification of such features as volume loss or abnormal structural features such as white matter disease, masses, or vascular abnormalities, which are considered indications of neuronal degeneration. Newer techniques such as diffusion tensor imaging reveal subtle structural changes that may precede more easily identifiable volume loss in the brain. Functional imaging such as fMRI can be used to identify abnormal patterns of brain activation or metabolic activity.

Positron Emission Tomography

Positron Emission Tomography (PET) scanning uses radioactively labeled tracers to investigate the brain’s inner workings. Pictures of the brain distribution of radioactively labeled glucose is injected intravenously. Glucose is used for energy by the brain, and can help to identify areas of abnormal metabolic activity. Most insurances will cover the cost of using this FDG-PET to differentiate between suspected AD and frontotemporal dementias.

A newer class of PET tracers identifies the presence of accumulated beta amyloid. Abnormal results for this scan are associated with a high probability of clinical AD, but the expense of this test (which is not routinely covered by insurance) has impeded its widespread use. Amyloid PET scans provide a biomarker of amyloid accumulation.

EEG

Electroencephalography (EEG) is occasionally ordered during the course of the evaluation of an individual with new cognitive changes. EEG changes associated with a very specific cause of dementia, such as the typical pattern seen in Creutzfeldt-Jakob disease, are uncommon. EEG can identify the presence of a treatable seizure disorder or suggest the presence of a delirium that may be at least partly reversible.

Summary

In many cases, the diagnosis of AD is made with considerable accuracy on the basis of history and mental status examination. AD, however, is only one of many disorders capable of interfering with cognitive function. We still await the availability of a clinical test for AD that is very accurate, widely available, and covered by insurance, but the diagnostic tests described here are very useful for supporting a clinical diagnosis and seeking treatable alternate explanations for cognitive changes.

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Two-Year Clinical Trial of Multifaceted Lifestyle-Based Intervention Provides Cognitive Benefits for Older Adults at Risk of Dementia

(AAIC) Positive results presented at the Alzheimer’s Association International Conference® 2014 (AAIC® 2014) in Copenhagen include data from a two-year clinical trial in Finland of a multi-component lifestyle intervention, known as the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER Study).

The study with 1,260 older adults at risk for cognitive impairment and Alzheimer’s showed that physical activity, nutritional guidance, cognitive training, social activities and management of heart health risk factors improved cognitive performance, both overall and in separate measures of executive function, such as planning abilities, and the relationship between cognitive functions and physical movement.

“AAIC is the premiere Alzheimer’s and dementia research conference, and this year’s topics are exciting both in their scope and findings,” said Keith Fargo, Ph.D., Alzheimer’s Association director of Scientific Programs & Outreach. “Regarding the FINGER Study, researchers have previously observed a number of modifiable factors associated with increased risk of late-life cognitive impairment and Alzheimer’s, but short-term studies focusing on single, isolated risk factors have had modest results, at best. Longer, larger, better controlled trials looking at modifying multiple risk factors – like the FINGER Study – have been needed. This new data is very encouraging, and we look forward to further studies to confirm and extend these findings.”

With the support of the Alzheimer’s Association and the Alzheimer’s community, the United States created its first National Plan to Address Alzheimer’s Disease in 2012. The plan includes the critical goal, which was adopted by the G8 at the Dementia Summit in 2013, of preventing and effectively treating Alzheimer’s by 2025. It is only through strong implementation and adequate funding of the Plan, including an additional $200 million in fiscal year 2015 for Alzheimer’s research, that we’ll meet that goal. For more information and to get involved, visit www.alz.org

Lifestyle Changes Improve Memory and Thinking in At-Risk Older Adults in Two-Year Clinical Trial

At AAIC 2014, Miia Kivipelto, M.D., Ph.D., Professor at the Karolinska Institutet, Sweden and the National Institute for Health and Welfare, Helsinki, Finland, and colleagues reported on the results of the FINGER Study, a two-year randomized controlled trial of 1,260 participants age 60 to 77 with modifiable risk factors for cognitive impairment and Alzheimer’s. Randomized controlled clinical trials are considered the “gold standard” for demonstrating treatment efficacy and safety.

Participants were divided into two groups; one received an intervention that included nutritional guidance, physical exercise, cognitive training, social activities, and management of heart health risk factors, while the control group received regular health advice. After two years, the intervention group performed significantly better on a comprehensive cognitive examination. In addition to performing better overall, the intervention group did significantly better on specific tests of memory, executive function (complex aspects of thought such as planning, judgment, and problem-solving), and speed of cognitive processing.

“This is the first randomized control trial showing that it is possible to prevent cognitive decline using a multi-domain intervention among older at-risk individuals. These results highlight the value of addressing multiple risk factors in improving performance in several cognitive domains,” said Kivipelto. “Participants told us their experience was very positive, and dropout rate only 11 percent after two years.”

The researchers say an extended, 7-year follow up study is planned, and will include measures of dementia/Alzheimer’s incidence and biomarkers including brain imaging with MRI and PET

About AAIC

The Alzheimer’s Association International Conference (AAIC) is the world’s largest gathering of leading researchers from around the world focused on Alzheimer’s and other dementias. As a part of the Alzheimer’s Association’s research program, AAIC serves as a catalyst for generating new knowledge about dementia and fostering a vital, collegial research community. Scientists leading the advancement of research gather to report and discuss the most current data on the cause, diagnosis, treatment and prevention of Alzheimer’s disease and related disorders.

About the Alzheimer’s Association

The Alzheimer’s Association is the world’s leading voluntary health organization in Alzheimer care, support and research. Our mission is to eliminate Alzheimer’s disease through the advancement of research; to provide and enhance care and support for all affected; and to reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer’s. Visit www.alz.org or call 800.272.3900.

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Genentech Alzheimer’s Drug Crenezumab Misses Goals in Studies

(AP) An experimental drug from the biotech company Genentech failed to slow mental decline in mid-stage studies on more than 500 people with mild to moderate Alzheimer’s disease, but showed some promise in the least-impaired participants who received a higher dose.

Pneumonia and deaths were more common among those receiving the drug, but researchers downplayed that. Study leader Dr. Jeffrey Cummings of the Cleveland Clinic said none of the deaths seemed due to the drug and pneumonia occurred at a rate to be expected in older people.

“We’re very encouraged” by the hint of benefit for patients with milder dementia and will talk with regulators about next steps for the drug, crenezumab (cruh-NEZ-oo-mab), said a Genentech scientist, Dr. Carole Ho. The results fit with other evidence suggesting that treating earlier in the course of the disease is better, she said.

Results were revealed Wednesday at the Alzheimer’s Association International Conference in Copenhagen.

They are the latest mixed bag on treatments aimed at clearing away the sticky amyloid plaques clogging Alzheimer’s patients’ brains. About 35 million people worldwide have Alzheimer’s, the most common form of dementia. There is no cure and current treatments only temporarily ease symptoms.

Last year, an Eli Lilly & Co. medicine, solanezumab, that also sought to clear away amyloid missed main goals in two studies but combined results suggested it might help people with milder disease. It’s in further study now. Before that, bapineuzumab, a similar drug being developed by Pfizer Inc. and Johnson & Johnson, showed promise in mid-stage testing but flopped in larger, more definitive trials.

The Genentech drug has been closely watched because it targets amyloid more broadly than the other drugs do, and the California-based company has a long track record of success with many biological medicines against cancer.

Mid-stage studies aim to give some idea of safety and whether the drug is effective enough to advance to larger, more definitive studies aimed at winning market approval.

In one study, 431 patients ages 50 to 80 with mild to moderate Alzheimer’s were given crenezumab or dummy drug as shots every two weeks, or as a higher dose in infusions every four weeks for 17 months. No significant difference was seen among the groups on two widely used measures of thinking and functioning skills.

However, the 70 most mildly impaired participants who received the higher dose declined 35 percent less on the cognitive measure than the 33 mildly impaired people given dummy infusions. The difference was about 3.5 points on the roughly 70-point scale — “equivalent to six or nine months” of delay in decline, Cummings said.

This result isn’t definitive, though, and can only be considered a signal worth exploring in future research because it didn’t involve the whole group tested. And even in this mildly impaired group, the drug did not improve the second measure, ability to function in daily life.

In the second study, 73 people who showed amyloid plaques on brain imaging also were given crenezumab or dummy shots or infusions. The main outcome — levels of amyloid seen on brain imaging after treatment — will be presented at a medical conference in November. Results on cognitive function seem to mirror those in the larger study, Cummings said.

Five people given crenezumab died — one from sudden death, two from respiratory failure, one from pneumonia and one from worsening Alzheimer’s.

“We believe that the safety profile is acceptable,” because deaths do not seem related to the drug, Genentech’s Ho said. “It is not a show stopper.”

Genentech and its corporate parent, Switzerland-based Roche Holding AG, paid for the study and Cummings is a paid adviser to Genentech.

In a statement Wednesday, the Alzheimer’s Association noted that crenezumab was being tested in another study aimed at preventing the disease, and said the new results give hope it will be more successful in that setting.

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Can An Eye Test Predict Alzheimer’s? Scientists Unveil New Vision Scans

(Forbes) A simple eye test could soon reveal whether you have Alzheimer’s Disease – or even if the disease looms in your future. In fact, according to trial results released this week, the vision test detected signs of Alzheimer’s 15 to 20 years before the appearance of clinical signs.

This potentially game-changing news comes out of the Alzheimer’s Association International Conference, currently ongoing in Copenhagen, Denmark, where two presentations highlighted the potential of new vision screening technologies that use retinal imaging to measure amyloid plaque formation in the back of the eye.

The technology is based on an astoundingly simple idea: The brain-clogging amyloid plaques considered an indicator of Alzheimer’s can also be seen in the back of the eye, which is considered a mirror for brain health.

“If this test works, then one day screening for Alzheimer’s disease may be as simple as getting your eyes checked” said Yogi Kanagasingam, one of the researchers conducting clinical trials.

670px-pet_alzheimerPET scan of a human brain with Alzheimer’s disease (Photo credit: Wikipedia)

The first test, from Neurovision Imaging of Sacramento, California, utilizes retinal image fluorescence photography to scan the supranucleus region of the retina for a fluorescent signature characteristic of beta amyloid plaques. In preparation for the scan, participants take curcumin, the ingredient in turmeric that gives the spice its fluorescent yellow color, to “light up” the amyloid plaques with a specific fluorescent signature.

Preliminary data released on 40 trial subjects showed that levels of amyloid in the retina correlated closely with amyloid levels in the brain as revealed by PET (positron emission tomography) scans, the current detection method of choice.
The retinal imaging was also able to tell subjects with Alzheimer’s from those without the disease with 100 percent sensitivity and 80.6 percent specificity. Neurovision is working with Australia’s Edith Cowan University McCusker Alzheimer’s Research Foundation to test their retinal imaging scan.

NeuroVision isn’t alone in the retinal imaging field; a second data presentation, this time from Massachusetts-based Cognoptix, also showed promising results from another pioneering technology. Cognoptix’s SAPPHIRE II technology utilizes a fluorescent ligand eye scanning (FLES) process in which a topical ointment applied to the lens of the eye binds to beta-amyloid. The plaques are then detected with a laser scanner.

The Cognoptix clinical trial data, published in February in the Journal of Alzheimer’s Disease and Other Dementias, involved 40 participants and predicted Alzheimer’s with 85 percent sensitivity. It differentiated participants with Alzheimer’s from those without the disease with 95% accuracy.

A retinal imaging test for Alzheimer’s, if it proved accurate, could drastically change the way Alzheimer’s is diagnosed. “Presently the tests that are used in clinical trials are PET scan of the brain and CSF via lumbar puncture to measure levels of amyloid and tau,” says CEO NeuroVision CEO Steven Verdooner. ”Our retinal imaging test is expected to be meaningfully less expensive than a PET scan, is noninvasive, and potentially more sensitive.”

Early detection of Alzheimer’s disease is a key goal of current research because the treatments currently available to slow the progression of the disease are much more effective if started early.

What’s more, because a retinal imaging test is relatively simple to take and without major longterm health effects, it could be re-administered regularly to monitor the progress of the disease. “We believe the ability to measure progression is very powerful and are engaging in partnerships for therapeutic trials to prove that out,” says Verdooner.

Right now, because PET scans are radioactive, doctors don’t like to repeat them multiple times and usually wait at least 18 months before administering a second PET scan. According to Verdooner, Neurovision’s test can be repeated after an interval as short as three months.

While a vision test for Alzheimer’s isn’t going to be commercially available anytime soon, the wait isn’t going to be as long as you might think, either. The current trial winds up in the fall, at which point Neurovision will begin working with academic institutions to continue validating the retinal imaging procedure.

NeuroVision’s test could be available as soon as the second half of 2015, Verdooner says. “Once commercialized, we expect it to be available in doctors’ offices and can be administered by request from the patient or a referring doctor.”

The retinal imaging test will be administered as part of a package, along with blood-based biomarkers and cognitive screening, Verdooner says. “The paradigm we’re aiming at is a battery of tests that is cost-effective, fast, and non-invasive.”

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