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07/20/2013 01:05 AM

ongoing ALZHEIMER'S articles(page 20)

Bettyg
 
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Novel Agent May Boost Aricept Efficacy

Published: Jul 18, 2013 | Updated: Jul 18, 2013

By John Gever, Deputy Managing Editor, MedPage Today

Reviewed by Zalman S. Agus, MD; Emeritus Professor, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner

Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.

Addition of a selective 5HT-6 receptor antagonist in patients with moderate Alzheimer's disease on stable donepezil treatment resulted in improved cognitive performance in a phase II randomized, double-blind, placebo-controlled trial.

BOSTON -- Adding an investigational agent targeting the 5HT-6 serotonin receptor to donepezil (Aricept) boosted cognition scores relative to donepezil alone in a mid-stage trial, a researcher said here.

In a placebo-c0ntrolled trial involving 278 patients with moderate Alzheimer's disease stably maintained on donepezil, addition of Lu AE58054 for 24 weeks led to an increase in mean Alzheimer's Disease Assessment Scale cognitive (ADAS-Cog) scores of nearly 1 full point, whereas those assigned to placebo plus donepezil showed a mean decrease of about 1.5 points (P=0.004), reported David Wilkinson, MD, of Moorgreen Hospital in Southampton, England.

The comparison of ADAS-Cog scores was the phase II trial's primary endpoint, Wilkinson told attendees at the Alzheimer's Association International Conference.

The novel drug also showed nonsignificant advantages over placebo on secondary efficacy endpoints, including two major subscales of the Alzheimer's Disease Cooperative Study rating system (activities of daily living and clinician's global impression of change) and on the Neuropsychiatric Inventory.

He added that the drug generally appeared safe and well-tolerated. The major adverse effect that was probably drug-related was transient elevation in liver enzymes, which resolved in all patients irrespective of whether they stopped treatment.

The 5HT-6 receptor has recently become a popular target for Alzheimer's disease therapies that, like donepezil and other acetylcholinesterase inhibitors and N-methyl-D-aspartate receptor antagonists such as memantine (Namenda), provide a boost to cognitive function without affecting the underlying disease process.

Expressed primarily within the central nervous system, the 5HT-6 receptor is especially common in brain regions associated with learning and memory. When activated, it appears to act as a brake on a variety of neurotransmitter systems, including those involving GABA and acetylcholine as well as serotonin.

Consequently, Wilkinson explained, selective 5HT-6 antagonists should stimulate those systems, leading to improved cognitive function.

Best of all, since this mechanism would be independent of existing cognition-boosting drugs such as donepezil, these treatments could be used as add-on therapies.

In the current study, Wilkinson and colleagues recruited patients with Mini-Mental State Examination (MMSE) scores of 12-19, reflecting moderately severe Alzheimer's disease, who were already taking donepezil. Lu AE58054 was given for 24 weeks, with an additional 4-week safety assessment period afterward.

The mean MMSE score at baseline was 17 and the mean ADAS-Cog score was 28. Patients had been taking donepezil for mean of 1.5 years.

When evaluated 4 weeks after starting on placebo or the study drug, both groups showed increases in ADAS-Cog scores, of about 1 point with placebo and 1.5 points with Lu AE58054. Wilkinson explained that this effect is commonly seen in Alzheimer's disease drug trials.

However, patients in the placebo group then showed sharp declines through the remainder of the study period, until the mean was about 1.5 points less than the baseline level.

The active-drug group showed a much smaller mean decline from the 4-week peak, such that the difference from baseline was about 1 point higher than at baseline.

Similar patterns were seen with the two ADCS subscores, but with P values of about 0.12 for the differences at 24 weeks. Neuropsychiatric Inventory scores favored the study drug by 1.45 points on average, also with a nonsignificant P value of 0.222.

Two patients -- one in each study arm -- died during the trial, not unexpected in a 24-week trial given the mean patient age of 75. A total of 27 patients had serious adverse events, also divided equally between groups. However, more than twice as many in the Lu AE58054 arm -- 23 versus 10 -- withdrew from the study because of adverse events.

Liver enzyme abnormalities were responsible for 11 of the withdrawals in the active-drug group, specifically elevations in alanine aminotransferase and gamma glutamyltransferase. Values returned to normal in those who remained on treatment as well as in those who withdrew, Wilkinson said.

He said the investigators were alert for cholinergic side effects because they could be exacerbated with the addition of a 5HT-6 antagonist to an acetylcholinesterase inhibitor. But these remained uncommon, with a total of 17 patients in the active-drug arm reporting diarrhea, nausea, or vomiting, compared with 14 in the placebo group.

Wilkinson said that the drug's developer, Lundbeck, had found the results favorable enough to authorize a large, international phase III trial (partnering with Otsuka) expected to begin later this year.

It would involve about 3,000 patients with mild to moderate Alzheimer's disease, he said, and would include U.S. sites.

Norman Relkin, MD, PhD, of Weill Cornell Medical College in New York City, who was not involved with the trial, told MedPage Today that Lu AE58054 appeared to deserve a larger trial.

He said that adding yet another medication to the already complicated regimens that older, cognitively impaired patients are already on was a concern. But in most cases it would be trumped by the need to maintain as much cognitive and functional ability as possible.

"Most patients are on closer to 10 drugs, when you take into account all the other drugs [for various conditions]," he said.

"Ideally, one would like to avoid that kind of polypharmacy, but ... what we need right now is a new treatment. I'd be less worried about how many pills a patient has to take than what happens if they don't take them."

The study was funded by Lundbeck, and several investigators were employees of the company.

Wilkinson reported relationships with Lundbeck, Pfizer, Eisai, Merz, Shire, Novartis, Debiopharm, Nutricia, GlaxoSmithKline, Medivation, Wyeth, Elan, Lilly, AstraZeneca, and Myriad.

Relkin had relationships with Eisai, Baxter, and Kyowa Hakko Kirin.

Primary source: Alzheimer's Association International Conference

Source reference:

Wilkinson D, et al "A clinical phase II study of Lu AE58054 added to stable donepezil treatment in patients with moderate Alzheimer's disease" AAIC 2013; Abstract O3-06-01.

http://www.medpagetoday.com/MeetingCoverage/AAIC/40548? xid=nl_mpt_DHE_2013-07-19&utm_content=&utm_medium=email& utm_campaign=DailyHeadlines&utm_source=

© 2013 MedPage Today, LLC. All rights reserved.

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07/20/2013 01:10 AM
Bettyg
 
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Size No Problem for AD Med Skin Patch

Published: Jul 18, 2013 | Updated: Jul 18, 2013

By Ed Susman, Contributing Writer, MedPage Today

Reviewed by Zalman S. Agus, MD; Emeritus Professor, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner

Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.

In two studies in patients with Alzheimer's disease, infrequent skin reactions were observed at the application site of the rivastigmine patch. There was no effect of dose on the frequency of reactions.

BOSTON -- Using a larger patch of rivastigmine (Exelon) does not appear to increase dermatologic reactions to the medication, researchers reported here.

In an analysis of two large studies, application site reactions did not differ significantly between patch sizes, said Gus Alva, MD, medical director of the ATP Clinical Research in Costa Mesa, Calif. In the so-called ACTION trial, application site reactions were observed in 24.2% of patients using the 4.6 mg/day patch and in 24.5% of those using the new 13.3 mg/patch.

And in the OPTIMA trial, 12% of patients using the 9.5 mg/day patch experienced site reactions, compared with 11.4% of the patients using the larger 13.3 mg/day patch, Alva said at the annual Alzheimer's Association International Conference.

"Overall, 75.6% of the 714 patients using the patches in the ACTION trial and 88.3% of the 563 patients using the patches in the OPTIMA trial did not have any reactions to the patch," he told MedPage Today at his poster presentation.

"Even though the amount of medicine is greater with the 13.3 mg/day patch, we did not see evidence of greater adverse skin reactions," Alva said. "I think this will give us as clinicians more flexibility in treating patients because we will have three different patches we can offer -- 4.6 mg/day, 9.5 mg/day and 13.3 mg/day."

"These skin reactions are a minor problem for a lot of people. They put some steroid cream on or they start washing the skin to reduce the irritation," said Brian Ott, MD, professor of neurology at Brown University in Providence, R.I.

"Sometimes people do the wrong thing and put the patch on in the same place. I haven't used the larger-size patch that much in my practice, but my experience has been similar to what these studies have shown," Ott told MedPage Today. He did not participate in the studies.

Alva suggested that the skin reactions can be overcome with simple skin hygiene practices. "Localized types of application site reactions are tolerable," he said. "They are manageable with proper rotation and treatment and care of skin." He said the reactions do not have to be a barrier to treatment with the patches, which have proven long-term efficacy versus placebo.

"This analysis suggests that most patients do not experience significant discomfort from application site reactions associated with the rivastigmine patch despite the increased likelihood of thin, fragile skin in this typically elderly population," Alva said.

In both trials, researchers recruited men and women at least 50 years of age who were diagnosed with probable Alzheimer's disease, according to criteria of the Alzheimer's Association and the National Institute of Neurological Disorders and Stroke.

The ACTION (Activities of Daily Living and Cognition) trial was a 24-week study of patients diagnosed with severe pathology -- scores of 3-12 on the Mini Mental State Examination.

OPTIMA (Optimising Transdermal Exelon in Mild-to-Moderate Alzheimer's Disease) was a 72-96 week study. Patients were included in the trial if they had scores between 10 and 24 on the Mini Mental State Examination.

Alva performed a retrospective analysis using the data gleaned from both studies to examine the skin reactions.

In both trials, the most common skin site reaction was erythema and those reactions were similar for both patch sizes tested.

Similarly, the need for treatment for those reactions were similar in both trials and for both patches.

The study was funded by Novartis.

Ott disclosed commercial interests with Lilly, Pfizer, Roche and other pharmaceutical companies.

Alva disclosed commercial interests with Novartis, Lilly, Pfizer, Janssen and Forest.

Primary source: Alzheimer's Association International Conference

Source reference:

Alva G, et al "Infrequent skin reactions at the application site of the rivastigmine patch (4.6, 9.5 or 13.3 mg/24 h): Analysis of two clinical studies revealed most were tolerable and manageable across all doses" AAIC 2013; Abstract P3-299.

http://www.medpagetoday.com/MeetingCoverage/AAIC/40526? xid=nl_mpt_DHE_2013-07-19&utm_content=&utm_medium=email& utm_campaign=DailyHeadlines&utm_source=

© 2013 MedPage Today, LLC. All rights reserved.


07/20/2013 11:11 PM
Bettyg
 
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Rare Mutation May Yield Clues in Alzheimer's

Published: Jul 19, 2013 | Updated: Jul 19, 2013

By Ed Susman, Contributing Writer, MedPage Today

Reviewed by F. Perry Wilson, MD, MSCE; Instructor of Medicine, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner

Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.

Note that this genomic study demonstrated a relationship between a mutation that stabilizes amyloid precursor protein and protection against Alzheimer's disease.

Be aware that drugs that mimic the effect of this mutation (by reducing cleavage of APP) have begun to enter clinical trials.

BOSTON -- A rare genetic variant may give clues for development of new therapeutic targets against Alzheimer's disease, researchers said here.

In a study of 2,600 elderly Icelanders who underwent complete genomic sequencing, Thorlakar Jonsson, PhD, a research scientist at DeCode Genetics, an Amgen subsidiary based in Reykjavik, determined that about 0.45% of the island nation's population harbors the mutation in the Amyloid Precursor Protein gene known as A673T.

The genetic variation is found mainly in peoples of Scandinavia -- 0.51% of the population in Finland, 0.42% in Sweden and 0.21% in Norway, Jonsson said in his oral presentation at the annual Alzheimer's Association International Conference. An estimated 0.01% of the U.S. population also harbors the gene, he said.

There are 10 known cases in which individuals with A673T developed Alzheimer's disease, Jonsson said. Nine were from Jonsson's Icelandic database of the nation's nursing homes.

The average age at death among those individuals was 88 years -- including four individuals who died at ages 95, 98, 100, and 101.

Another report of one case involved a person with the mutation who developed Alzheimer's disease at age 89, he noted.

Jonsson also cited a case in which a Finnish patient died at age 104.8 years with little beta-amyloid pathology.

"These cases suggest that the variant delays the onset of Alzheimer's disease," he said, but may not prevent the disease.

"A673T may, through its effect on the Amyloid Precursor Protein as a BACE1 substrate, shift the curve of normal cognitive decline, thus delaying Alzheimer's disease onset."

"Therapeutic effects that mimic the effect of A673T may be fruitful," Jonsson said.

Heather Snyder, PhD, director of medical and scientific operations for the Chicago-based Alzheimer's Association, said the research by the Icelandic team "underscores how basic science can help in the development of better drugs for the treatment of Alzheimer's disease."

She told MedPage Today, "As the researcher noted, there have been cases of Alzheimer's disease in patients who have been identified as having the A673T variant, so we can't be sure if a person with the variant will be able to delay the onset of Alzheimer's disease until late in life, or if the variant is actually protective against the disease."

Jonsson and his team of researchers scoured the nursing home database in Iceland. "We identified several coding variants in the Amyloid Precursor Protein. We imputed these variants into the genomes of patients with Alzheimer's disease and control participants and then tested [them] for an association with Alzheimer's disease," he reported.

"To our knowledge, A673T represents the first example of a sequence variant conferring strong protection against Alzheimer's disease," Jonsson said. The researchers estimated that the mutation results in an approximately 40% reduction in the formation of amyloidogenic peptides in vitro.

However, Jonsson cautioned that the protective effect of mutations in the Amyloid Precursor Protein is very specific. For, example, the A673V mutation confers virtually no protection at all against the disease.

"The strong protective effect of the A673T substitution against Alzheimer's disease provides proof of principle for the hypothesis that reducing the beta-cleavage of Amyloid Precursor Protein may protect against the disease," Jonsson said. Several pharmaceutical companies are pursuing medication based on BACE-1 inhibitors.

Jonsson is an employee of DeCode Genetics.

Snyder had no disclosures.

Primary source: Alzheimer's Association International Conference

Source reference:

Jonsson T "A coding mutation in APP protects against Alzheimer's disease and age-related cognitive decline" AAIC 2013; Abstract F5-04-02.

http://www.medpagetoday.com/MeetingCoverage/AAIC/40564? xid=nl_mpt_DHE_2013-07-20&utm_content=&utm_medium=email& utm_campaign=DailyHeadlines&utm_source=

© 2013 MedPage Today, LLC. All rights reserved


07/20/2013 11:19 PM
Bettyg
 
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Amyloid Brain Scan Guidelines Updated

Published: Jul 19, 2013 | Updated: Jul 19, 2013

By John Gever, Deputy Managing Editor, MedPage Today

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner

A guideline published in January on brain scans for beta-amyloid plaques has been updated to address concerns raised by a key government advisory committee.

Note that the guidelines recommend that amyloid brain scans should be used only in patients with progressive or unexplained mild cognitive impairment, those with tentative diagnoses of "possible" Alzheimer's disease with features unusual for the illness, and patients younger than 65 with progressive dementia.

A guideline published in January on brain scans for beta-amyloid plaques has been updated to address concerns raised by a key government advisory committee.

In an statement appearing online in Alzheimer's & Dementia, representatives of the Alzheimer's Association and the Society for Nuclear Medicine and Molecular Imaging (SNMMI) sought to clarify several aspects of the groups' January guideline on the proper use of PET scans for beta-amyloid plaques:

The role of so-called dementia experts in interpreting scan results

Documentation to accompany scan reports

Patient groups for whom amyloid scans would be appropriate

Educational materials on amyloid scans

The two groups had quickly developed the initial guideline after last year's FDA approval of florbetapir (AmyVid) as a PET tracer specific for amyloid plaques in the brain.

Among other recommendations, it said that amyloid brain scans should be used only in patients with progressive or unexplained mild cognitive impairment, those with tentative diagnoses of "possible" Alzheimer's disease with features unusual for the illness, and patients younger than 65 with progressive dementia.

These would reflect the cases in which such scans would most likely be informative for patient management, the authors indicated.

The guideline also recommended that a "dementia expert" -- a physician with training and/or experience in managing patients with Alzheimer's disease and other dementias -- be consulted before ordering scans and in interpreting the results.

Dean Hartley, PhD, director of science initiatives at the Alzheimer's Association and an author of both the original guideline and the new update, told MedPage Today that the guideline committee wanted, in part, to address concerns raised by the Medicare Evidence Development and Coverage Advisory Committee (MEDCAC) at a meeting shortly after the guideline came out.

The panel voted against recommending Medicare coverage of the scans. Members' reservations included uncertainty about what exactly defines a "dementia expert," which is not a recognized medical subspecialty.

The panel also questioned whether clinicians would order the scans more broadly than recommended either in the guideline or in florbetapir's label, and whether most radiologists were qualified to interpret the scans.

The update explained that, in the committee's thinking, a dementia expert "should be self-identified as a physician trained and board-certified in neurology, psychiatry, or geriatric medicine who devotes a substantial proportion (≥25%) of patient contact time to the evaluation and care of adults with acquired cognitive impairment or dementia, including probable or suspected Alzheimer disease, as confirmed by peer recognition."

It added that such a physician would "likely" have board certification or fellowship training in geriatric psychiatry or neurology or behavioral neurology or psychiatry.

In response to MEDCAC members' concerns that such experts are rare, the committee opined that their numbers would grow commensurately with "demand for amyloid PET referral." Eventually, Hartley and colleagues wrote, the need for such experts may diminish as more clinicians and radiologists gain experience with the scans.

The guideline update also expanded on the original document's discussion of etiologic uncertainty in cases of mild cognitive impairment.

In particular, the authors cited the situation of patients who may show dementia symptoms along with vascular pathology as well as other "potentially confounding circumstances" such as depression, drug side effects, substance abuse, and other medical conditions with psychiatric complications.

"In these relatively unusual but important cases, substantial uncertainty then remains as to the cause of the syndrome, and further patient care is severely constrained or compromised," Hartley and colleagues wrote, suggesting that amyloid scans can help resolve the uncertainty.

"Once the cause of deficits is properly assessed, a more confident diagnosis frequently helps anticipate future needs, including closer monitoring for progression and safety, periodic functional assessments for retirement planning, and allocation of financial and family resources," the update said.

Finally, both the Alzheimer's Association and the SNMMI committed to developing educational materials to promote use of amyloid scans only within the label indications. The latter group in particular is putting together a maintenance-of-certification module for this purpose.

Hartley told MedPage Today that the guideline would be treated as a "living document" with frequent updates as warranted by advances in knowledge about amyloid pathology and scanning technology.

The work had no commercial funding.

Authors declared they had no relevant financial interests.

Primary source: Alzheimer's & Dementia

Source reference:

Johnson K, et al "Update on appropriate use criteria for amyloid PET imaging: Dementia experts, mild cognitive impairment, and education" Alzheimer's & Dementia 2013; DOI: 10.1016/j.jalz.2013.06.001.

http://www.medpagetoday.com/Neurology/AlzheimersDisease/ 40571?xid=nl_mpt_DHE_2013-07-20&utm_content=& utm_medium=email&utm_campaign=DailyHeadlines&utm_source=

© 2013 MedPage Today, LLC. All rights reserved.


07/22/2013 11:42 PM
Bettyg
 
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Cancer Tied to Lower AD Risk in Vets

Published: Jul 21, 2013 | Updated: Jul 22, 2013

By Charlene Laino, Senior Writer, Gupta Guide

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner

This study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.

New research in war veterans adds to a growing body of evidence that cancer is associated with a reduced risk of Alzheimer's disease, and treatment with chemotherapy appears to further lower that risk.

Note that among veterans with a cancer history, treatment with chemotherapy, but not radiation, reduced Alzheimer's risk by 20% to 45%, depending on cancer type, with the exception of prostate cancer.

BOSTON -- New research in war veterans adds to a growing body of evidence that cancer is associated with a reduced risk of Alzheimer's disease (AD), and treatment with chemotherapy appears to further lower that risk.

In a study of more than 80,000 veterans diagnosed with AD during a median follow-up of 5.65 years, most types of cancer were associated with reduced Alzheimer's risk, ranging from 9% to 51%, reported Laura Frain, MD, from the VA Boston Healthcare System, and colleagues.

Additionally, AD was less frequent in veterans with a history of cancer than in those without: 24% versus 76%, the group stated in a presentation at the Alzheimer's Association International Conference in Boston.

"While more and more studies suggest a possible association of cancer with reduced risk for Alzheimer's disease, little is known about whether the association differs between cancer types or is modified by cancer treatment," Frain said.

So the researchers analyzed the health records of 3.5 million veterans, ages 65 and older, who were seen in the VA healthcare system between 1996 and 2011. Participants were free of dementia at baseline.

Over a median follow-up of 5.65 years, 82,028 veterans were diagnosed with Alzheimer's. A total of 771,285 (22%) of the veterans were diagnosed with cancer before or after study baseline.

After adjustment, the following cancers were associated with reduced risk of AD:

Liver cancer: 51% lower risk

Pancreatic cancer: 44%

Cancer of the esophagus: 33%

Myeloma: 26%

Lung cancer: 25%

Leukemia: 23%

Cancers that did not confer a reduced Alzheimer's risk, or were associated with an increased risk, included melanoma, prostate, and colorectal cancers.

Frain told MedPage Today she thinks that is most likely due to increased screening of these types of cancer. "Most of these patients would never have known they had the cancer during their lifetime had they not been screened," she explained.

The researchers also found that among veterans with a cancer history, treatment with chemotherapy, but not radiation, reduced Alzheimer's risk by 20% to 45%, depending on cancer type, with the exception of prostate cancer.

"Recent experimental studies support this finding," said Frain, noting that "cancer and AD cells behave so similarly that some people have called Alzheimer's the cancer of the brain.

Cells affected by AD try to divide and in that way act very much like cancer cells and chemotherapy may prevent them from dividing," she said.

"The results of this study are interesting because they could help focus future research onto the specific pathways and treatment agents involved in the individual cancers that are associated with a reduced risk of Alzheimer's," Frain added. "This could potentially open new therapeutic strategies for Alzheimer's prevention and treatment."

David S. Knopman, MD, from the Mayo Clinic, said these are "important observational findings. However, much more study is needed before any therapeutic implications can be drawn," he said.

Frain reported no conflicts of interest.

Primary source: Alzheimer's Association International Conference

Source reference:

Frain L, et al "A reduced risk of Alzheimer's disease is associated with the majority of cancers in a national cohort of veterans'" AAIC 2013; Abstract P3-175.

http://www.medpagetoday.com/MeetingCoverage/AAIC/40604? xid=nl_mpt_DHE_2013-07-22&utm_content=&utm_medium=email& utm_campaign=DailyHeadlines&utm_source=

© 2013 MedPage Today, LLC. All rights reserved.


07/23/2013 01:48 AM
Bettyg
 
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This book is packed with info about methylation/detoxification. It's not only relevant for autism.

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07/23/2013 02:04 AM
Bettyg
 
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Alzheimer's Tied to Insulin Resistance

Published: Jul 20, 2013 | Updated: Jul 22, 2013

By John Gever, Deputy Managing Editor, MedPage Today

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner

Note that these studies were published as abstracts and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.

Insulin resistance may be a worthwhile treatment target to prevent or delay Alzheimer's disease, several studies suggested.

Note that in one study, diabetic members who started metformin were less likely to develop dementia later on (including forms other than Alzheimer's disease) compared with those initiating other types of anti-diabetic drugs.

BOSTON -- Insulin resistance may be a worthwhile treatment target to prevent or delay Alzheimer's disease, several studies reported here suggested.

Patients with Alzheimer's disease or mild cognitive impairment receiving 40 IU/day of intranasal insulin detemir in a randomized trial showed improvements in memory relative to the placebo group, but only if they had high levels of insulin resistance at baseline, reported Suzanne Craft, MD, of Wake Forest University in Winston-Salem, N.C.

Also, analysis of Kaiser Permanente health system records indicated that diabetic members who started metformin were less likely to develop dementia later on (including forms other than Alzheimer's disease) compared with those initiating other types of anti-diabetic drugs, according to Rachel Whitmer, PhD, of Kaiser's research division in Oakland, Calif. Both studies were reported at the Alzheimer's Association International Conference.

The latter finding implicates insulin resistance because metformin, in contrast to other anti-diabetic drugs, is an insulin sensitizer.

Earlier reports at the meeting also tied Alzheimer's disease to diabetes and glucose dysregulation.

One had found high rates of previously undiagnosed diabetes in patients with mild to moderate Alzheimer's disease while another indicated that diabetic women were at significantly increased risk for cognitive impairment.

Another suggestion of a link has been in preliminary findings that the diabetes drug pioglitazone (Actos) may slow or prevent onset of Alzheimer's disease. A large randomized trial called TOMMORROW (sic) is in the final planning stages, to be funded by Takeda and Zinfandel Pharmaceuticals.

SNIFF-Long Study

The insulin detemir trial was prompted by earlier observations that inhaled conventional insulin appeared to improve cognition and certain biomarkers of Alzheimer's disease pathology.

Craft explained that the pharmacokinetics of insulin detemir (sold as Levemir for subcutaneous injection), compared with natural insulin, were more attractive for an Alzheimer's disease treatment.

It remains active in the body for up to 24 hours after a single dose, peaking about 5 hours after dosing -- thus mimicking the natural basal secretion of insulin in the pancreas.

The intranasal route helps insulin get into the central nervous system without having to penetrate the blood-brain barrier, by traveling through nerve channels connecting nasal passages to the brain, she said.

Called SNIFF-Long (Study of Nasal Insulin to Fight Forgetfulness-Long Acting Detemir), the study randomized 60 patients with diagnoses of mild Alzheimer's disease or amnestic mild cognitive impairment to 20 or 40 IU/day of intransal insulin detemir or placebo for 3 weeks.

Patients were tested at baseline and at the end of treatment with two verbal memory tests with results combined into a composite score, as well as the Benton Visual Retention Test recognition task and a dot-counting test of working memory.

At baseline, patients' mean age was about 72, with Mini-Mental State Examination scores averaging 26.

Overall, neither dose of insulin was more effective than placebo on the primary outcome, which was change from baseline in memory composite scores.

But when patients in each treatment arm were stratified into those with low versus high Homeostasis Model of Assessment-Insulin Resistance (HOMA-IR) values for insulin resistance, the two subgroups in the 40-IU arm both differed significantly from the stratified placebo groups -- in opposite directions.

Patients with high insulin resistance taking 40 IU showed an improvement of about 0.75 points in the memory composite, compared with an increase of less than 0.1 point in the placebo patients with high insulin resistance. The 40-IU group patients with low insulin resistance, meanwhile, had a decrease of 1 point in memory score, compared with a decrease of about 0.2 points in the low-resistance placebo subgroup (P=0.015 for both placebo-versus-40 IU comparisons).

A similar pattern was seen when the treatment arms were stratified by APOE genotype, with carriers of the epsilon-4 allele benefiting significantly (P=0.025) from 40 IU of insulin detemir relative to placebo, while noncarriers showed worsened memory compared with placebo.

In all analyses, results with 20 IU of insulin detemir were similar to placebo.

Kaiser Study of Diabetes Drugs and Alzheimer Risk

Whitmer presented results from nearly 15,000 Kaiser Permanente members 55 and older who started diabetes drug treatment for the first time from 1999 to 2001, with their subsequent records from 2002 to 2007 checked for new diagnoses of dementia, including Alzheimer's disease, vascular dementia, and other forms.

Drugs were classed as metformin, sulfonylureas, thiazolidinediones, and insulin.

Across the entire cohort, 9.9% developed incident dementia during the follow-up period, Whitmer reported. The raw data indicated little difference in this rate among patients grouped by drug type. But when adjusted for patient age, race, education level, and diabetes duration, metformin users showed clearly lower rates compared with the other groups.

Hazard ratios (HRs) for incident dementia among these other groups relative to metformin users were as follows:

Sulfonylureas: HR 1.24, 95% CI 1.1-1.4

Thiazolidinediones: HR 1.18, 95% CI 1.1-1.4

Insulin: HR 1.28, 95% CI 1.1-1.6

Whitmer reported that adjusting further for baseline glycated hemoglobin (HbA1c) did not alter the results. She also said that restricting the analysis to Alzheimer's disease cases had no effect. Metformin appeared to be protective against vascular dementia as well, with hazard ratios similar to those seen in the overall analysis.

Kathleen Welsh-Bohmer, PhD, of Duke University, who is helping to lead the upcoming pioglitazone trial, told MedPage Today that mitochondrial activity in brain neurons appears to be the link between metabolic dysfunction and dementia.

Put simply, insulin resistance and diabetes appear to starve mitochondria of their fuel -- glucose -- which in turn causes neurons to cease functioning and eventually die.

But the study results also paint a confused picture. Pioglitazone has appeared promising in some early studies, yet thiazolidinediones (the class that includes pioglitazone) were not protective in the Kaiser study. Metformin does appear to protective -- both in the Kaiser study and earlier analyses, but whether it is due to its insulin sensitizing effect remains uncertain.

A placebo-controlled trial of metformin in 80 patients with mild cognitive impairment has reportedly been conducted by researchers at Columbia University in New York City to determine if the patients' cognitive decline was slowed or stopped with the drug, but no results have been published.

The SNIFF-Long study was supported by the National Institute on Aging, the Department of Veterans Affairs, and Kurve Technology, which provided the intranasal inhalers. The Kaiser study had no external funding.

Craft reported relationships with Takeda, Zinfandel, and Eli Lilly.

Whitmer had no disclosures.

Welsh-Bohmer reported relationships with Takeda and Zinfandel.

0

Add Your Knowledge ™

Primary source: Alzheimer's Association

Source reference:

Craft S, et al "Therapeutic effects of long-acting intranasal insulin detemir for Alzheimer's dementia or mild cognitive impairment" AAIC 2013; Abstract O1-06-06.

Additional source: Alzheimer's Association

Source reference:

Whitmer R, et al "Anti-hyperglycemic therapy and risk of dementia: a new user cohort study" AAIC 2013; Abstract O1-05-05.

http://www.medpagetoday.com/MeetingCoverage/AAIC/40595? xid=nl_mpt_DHE_2013-07-22&utm_content=&utm_medium=email& utm_campaign=DailyHeadlines&utm_source=

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07/27/2013 12:59 AM
Bettyg
 
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No Surprises in Report on Failed Alzheimer's Drug

Published: Jul 25, 2013

By John Gever, Deputy Managing Editor, MedPage Today

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner

Detailed results from an aborted phase III trial of semagacestat, a drug aimed at slowing Alzheimer's disease, were published but the major finding remained as previously announced -- it didn't work.

Note that semagacestat was one of numerous drugs targeting beta-amyloid protein, which forms insoluble plaques in the brains of Alzheimer's disease patients.

Detailed results from an aborted phase III trial of semagacestat, a drug aimed at slowing Alzheimer's disease, were published but the major finding remained as previously announced -- it didn't work.

Among 1,537 patients receiving the drug or placebo in the trial, those assigned to 100 or 140 mg/day of semagacestat showed mean increases of 7.5 and 7.8 points, respectively, on the cognition portion of the Alzheimer's Disease Assessment Scale (ADAS-Cog), reflecting diminished cognitive ability, compared with a mean increase of 6.4 points in the placebo group, reported Rachelle Doody, MD, PhD, of Baylor College of Medicine in Houston, and colleagues in the July 25 issue of the New England Journal of Medicine.

The trial had been stopped in 2010 after 463 patients had completed 18 months of treatment as planned, when an earlier-than-planned interim analysis revealed this disadvantage in the primary endpoint for semagacestat.

Although it did not reach statistical significance, the interim results left essentially no hope that the drug could outperform placebo in the full sample.

Eli Lilly & Co., semagacestat's sponsor, had reported the early stoppage in 2010, at which time the company said it was halting a second phase III trial that tested only the 140-mg dose against placebo, and that it was cancelling development of semagacestat altogether.

Other results detailed in the NEJM report indicated that patients in the high-dose semagacestat group fared significantly worse than the placebo group on secondary endpoints, including the Alzheimer's Disease Cooperative Study's activities of daily living subscale, the Neuropsychiatric Inventory, the Mini-Mental State Examination, and the Clinical Dementia Rating-Sum of Boxes.

Patients in the low-dose drug group also showed greater functional declines in these measures than the placebo group, on average, but they did not reach statistical significance.

Semagacestat was one of numerous drugs targeting beta-amyloid protein, which forms insoluble plaques in the brains of Alzheimer's disease patients.

These plaques are one of the two pathological hallmarks of the disease, the other being neurofibrillary tangles made of abnormal tau proteins.

The drug may not have had the necessary effect in the central nervous system, biomarker results suggested.

Plasma levels of the AB40 form of beta-amyloid protein were reduced markedly, Doody and colleagues found. Means declined from baseline by 38% and 48% in the low- and high-dose groups, respectively. Mean levels of the AB42 form of the protein fell by 5% and 18%, respectively.

But in 47 patients with serial lumbar punctures, cerebrospinal fluid levels of these beta-amyloid proteins did not change with treatment.

Moreover, MRI scans in 208 patients to monitor brain atrophy showed no clear differences among treatment groups.

Likewise, PET scans to measure neuronal activity and the total burden of beta-amyloid plaques indicated no differences between treatment groups.

The drug also had a range of adverse effects that were more common than in the placebo group. These included skin cancers (basal and squamous cell) and other dermal conditions as well as gastrointestinal disorders, loss of hair coloring, and alopecia. In the low- and high-dose semagacestat groups, 26% and 30%, respectively, stopped the drug because of adverse events, compared with 11% of the placebo group (P<0.001 for both comparisons).

These safety issues, along with reports of clinical worsening in trial participants, had prompted the trial's investigators to call for the interim analysis earlier than originally planned, Doody and colleagues explained. Some adverse events had not resolved in all patients even 32 weeks after treatment was stopped.

When the topline efficacy results were reported in 2010, it was interpreted as a body blow to the so-called amyloid theory of Alzheimer's disease, which holds that beta-amyloid plaques are the chief neurotoxic agent. Its standing has also suffered because two other drugs intended to break up plaques directly, bapineuzumab and solanezumab, also failed to demonstrate clinical benefit in large trials.

But commercial and academic interest in amyloid as a drug target remains strong nonetheless. Lilly recently announced a new trial of solanezumab in patients with early-stage Alzheimer's disease, and the same drug was chosen for a separate trial sponsored by a nonprofit research consortium to be conducted in asymptomatic individuals with heavy amyloid plaque burdens.

Another amyloid-processing enzyme, beta-secretase -- also called beta-amyloid converting enzyme or BACE -- is still attracting attention from drugmakers. This enzyme acts earlier than gamma-secretase in the production of beta-amyloid protein.

Doody and colleagues suggested that lack of selectivity for gamma-secretase may have been semagacestat's downfall.

"The inhibition of gamma-secretase can interfere with Notch receptor-related nuclear signaling and with the function of cell-surface receptors and the proteins involved in embryonic development, hematopoiesis, cell adhesion, and other cell-cell contacts," they wrote.

Moreover, they added, other research has indicated that "most, if not all, such inhibitors also inhibit Notch, and that semagacestat may be more selective for Notch than for amyloid precursor protein processing by gamma-secretase."

But, even though the drug did not appear to affect beta-amyloid protein levels in the brain, Doody and colleagues said they could not rule out the possibility that clinical worsening seen with semagacestat "represents an on-target effect of central gamma-secretase inhibition."

The trial was funded by Eli Lilly.

Several investigators were Eli Lilly employees.

In addition to the relationships with Lilly, investigators reported financial ties to Abbott, Amgen, Astellas, AstraZeneca, Biomarin, Bristol-Myers Squibb, Daiichi, Dainippon, Eisai, Elan, GlaxoSmithKline, Janssen, Medivation, Merck, Neurophage, Novartis, Otsuka, Solvay, Wyeth, Martek, TransTech, Pfizer, Neuro-Hitch, Braincells, Baxter, Chiesi, Allon, Biotie, Cardeus, Avanir, Genentech, Roche, Nutricia, Prana, Shire, Takeda, Zinfandel, Genzyme, Debiopharm, Elan, Sunovion, Sanofi, Schering-Plough, GE, Bayer, and many others.

Primary source: New England Journal of Medicine

Source reference: Doody R, et al "A phase 3 trial of semagacestat for treatment of Alzheimer's disease" New Engl J Med 2013; 369: 341-50.


07/28/2013 01:33 AM
Bettyg
 
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ACE Inhibitors May Slow Loss of Brain Power

Published: Jul 26, 2013

By Chris Kaiser, Cardiology Editor, MedPage Today

Reviewed by F. Perry Wilson, MD, MSCE; Instructor of Medicine, Perelman School of Medicine at the University of Pennsylvania

Note that this observational study demonstrated a slower rate of cognitive decline among elderly patients taking ACE-inhibitors versus those who were not.

Be aware that the effect of ACE-inhibition, while statistically significant, was very small and unlikely to affect the majority of patients at risk of dementia.

There may be an early cognitive benefit for dementia patients starting on angiotensin-converting enzyme (ACE) inhibitors for blood pressure control, researchers suggested.

Patients taking centrally active ACE inhibitors experienced marginally slower rates of cognitive decline compared with those not on the drugs (drop of 1.8 points versus 2.12 points on the Quick Mild Cognitive Impairment scores [P=0.049]), according to William Molloy, MB, BCh, of the Centre for Gerontology and Rehabilitation at the University College Cork, St. Finbarrs' Hospital, in Cork City, Ireland, and colleagues.

And the brain power of those patients newly prescribed ACE inhibitors actually improved over the 6-month period, by a median 1.2 points on the Standardized Mini-Mental State Examination (SMMSE), compared with those already taking them (median decline of 0.8 points), and those not taking them at all (median decline of 1 point), the researchers wrote in the study published in the online journal BMJ Open.

The difference between the newly prescribed patients and those already on or not on the drugs was significant, they noted.

This is the first time that there has been any evidence to suggest that blood-pressure-lowering drugs may not only halt cognitive decline, but may actually improve brain power, researchers said.

The improvement might be because these patients stuck to their medication regimen better, or it might be a by-product of better blood pressure control, or improved blood flow to the brain, they suggested.

There is also evidence suggesting that another class of antihypertensive drugs –- angiotensin receptor blockers (ARBs) may have protective benefits against Alzheimer's disease.

For the study, Molloy and colleagues compared the rates of cognitive decline in 361 patients who had been diagnosed with Alzheimer's disease, vascular dementia, or a mix of both.

Between 1999 and 2010, the cognitive decline of each patient was assessed using either the Standardized Mini-Mental State Examination or the Quick Mild Cognitive Impairment screen on two separate occasions, 6 months apart.

The Quick Mild Cognitive Impairment screen is a more sensitive screen than the Standardized Mini-Mental State Examination, researchers noted.

A total of 85 of the patients were already taking ACE inhibitors; the rest were not.

The researchers also assessed the first 6 months' impact of ACE inhibitors on cognitive function of 30 patients newly prescribed ACE inhibitors.

The average age of all the participants was 77 and they were just about equally divided between women and men.

The multivariate regression analysis, which adjusted for baseline cognitive scores (both the Standardized Mini-Mental State Examination and the Quick Mild Cognitive Impairment screen), and patient age, education, and duration of follow-up, found a significant difference in the end-point scores for the Standardized Mini-Mental State Examination between all three groups (P=0.002).

The multivariate analysis found no such significant difference when comparing those already on the drugs with those not taking the drugs at all (P=0.172).

"This [study] supports the growing body of evidence for the use of ACE inhibitors and other antihypertensive agents in the management of dementia," the authors wrote.

"Although the differences were small and of uncertain clinical significance, if sustained over years, the compounding effects may well have significant clinical benefits," they added.

They noted a strength of the study is the inclusion of different dementia types -- Alzheimer's, vascular, and mixed.

However, it is limited by its observational design, lack of compliance data, and no Quick Mild Cognitive Impairment and Standardized Mini-Mental State Examination scores recorded for a considerable number of patients, they said.

They also cautioned that recent evidence indicates that ACE inhibitors may contribute to amyloid burden, "potentially accelerating dementia severity and rates of cognitive decline."

It's possible that some but not all patients would see a cognitive benefit from ACE inhibitors, they noted, but larger randomized studies are needed to "confirm these findings and determine if and for how long these effects are sustained."

The Centre for Gerontology and Rehabilitation is funded by Atlantic Philanthropies, the Health Services Executive Ireland, the Irish Hospice Foundation, and the Canadian Institutes of Health Research.

None of the researchers had conflicts of interest to declare.

From the American Heart Association:

Vascular Cognitive Impairment and Dementia

Primary source: BMJ Open

Source reference: Gao Y, et al "Effects of centrally acting ACE inhibitors on the rate of cognitive decline in dementia" BMJ Open 2013; 3:e002881

http://www.medpagetoday.com/Cardiology/Dementia/40699? xid=nl_mpt_DHE_2013-07-27&utm_content=&utm_medium=email& utm_campaign=DailyHeadlines&utm_source=

© 2013 MedPage Today, LLC. All rights reserved.


07/30/2013 11:09 PM
Bettyg
 
Posts: 33642
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Abnormal Glucose Unrelated to Alzheimer's Pathology

Published: Jul 29, 2013 | Updated: Jul 30, 2013

By John Gever, Deputy Managing Editor, MedPage Today

Reviewed by F. Perry Wilson, MD, MSCE; Instructor of Medicine, Perelman School of Medicine at the University of Pennsylvania and Dorothy Caputo, MA, BSN, RN, Nurse Planner

This prospective cohort study demonstrated no association between several measures of glucose homeostasis and pathological or imaging findings consistent with Alzheimer's disease.

These results suggest that associations observed between diabetes and poor cognition (seen in other studies) may be mediated by vascular changes rather than beta-amyloid deposition.

No relationship could be found between insulin resistance or other abnormalities in glucose metabolism and beta-amyloid plaques in the brains of older individuals, researchers said.

In contrast to previous studies that had suggested a linkage between clinically diagnosed Alzheimer's disease and dysregulation of glucose metabolism, brain autopsy findings in 197 older individuals showed no correlation with results of oral glucose tolerance tests (OGTT) performed before death, according to Richard O'Brien, MD, PhD, of Johns Hopkins University, and colleagues.

Similarly, no correlation was found between OGTT results and findings in PET scans using a tracer for beta-amyloid plaques in 53 living individuals, the researchers reported online in JAMA Neurology.

The negative findings in the study were surprising because earlier research had found that individuals with diabetes were at increased risk for Alzheimer's disease.

Also, two studies reported at the recent Alzheimer's Association International Conference had suggested that use of anti-diabetic medications may prevent or treat Alzheimer's disease.

In one, a randomized trial, insulin detemir (Levemir) treatment led to improvements in certain aspects of cognition in patients with mild impairments.

Separately, a retrospective analysis of Kaiser Permanente member records found that individuals starting on metformin, an insulin sensitizer, were less likely to be diagnosed later with Alzheimer's disease or vascular dementia than those using other anti-diabetic drugs.

Noting the apparent discrepancy between this body of research and the current study, O'Brien and colleagues pointed out that insulin resistance within the brain may not necessarily "correlate with peripheral measures of insulin resistance" such as OGTT results.

Moreover, they argued, insulin may affect cognition in ways unrelated to beta-amyloid protein pathology in Alzheimer's disease.

The researchers also observed that the earlier epidemiologic studies of diabetes and Alzheimer's disease did not yield consistent results, with some failing to find a correlation.

In the current study, O'Brien and colleagues analyzed data from two groups of participants in the Baltimore Longitudinal Study of Aging, an ongoing, prospective study.

One group comprised 197 participants who had died after undergoing at least two OGTTs during life (mean 6.6, including 3.6 with insulin values) and in whom brain autopsies that included measurement of Alzheimer's disease-related pathologies were performed.

At the time of death, their mean age was 88.3 (SD 7.3). Clinical dementia had been diagnosed in 101 of these individuals.

The second group involved 53 living participants, who also had undergone at least two OGTTs (mean 7.1, including 4.0 with insulin values), and who had PET scans using the Pittsburgh Compound B (PiCool tracer for beta-amyloid plaques.

Their mean age was 79.2 (SD 5.8) at last follow-up and six of them had been diagnosed with dementia.

In both groups, the OGTTs had been performed over periods averaging about 25 years. Findings from all tests for each participant were averaged for the current analysis.

Participants were divided into tertiles according to their average fasting and 120-minute values for plasma glucose, insulin, and HOMA insulin resistance -- six groups of tertiles for each of the two participant groups, or 12 in all.

O'Brien and colleagues then compared measures of brain pathology in the high versus low tertiles in each of these groups.

In every case , the comparison failed to yield a significant difference in these measures.

The greatest difference the researchers found was in the average fasting insulin level in the living participants. Those in the low tertile had mean PiB binding levels (standardized uptake ratio) of 1.21, compared with 1.13 in the high tertile (P=0.22).

Alternative statistical methods, including continuous mixed-models analyses, led to similar results, the researchers indicated.

O'Brien and colleagues also found no correlation between clinical diagnoses of dementia and any of the OGTT results in the autopsied group.

Limitations to the study cited by the researchers included their methods of measuring insulin resistance (calculated rather than measured with insulin clamping) and Alzheimer's disease brain pathology at autopsy (semiquantitative without use of specific beta-amyloid and tau protein staining).

The researchers also noted that their sample was not representative of the community and had access to high-quality healthcare, making them "unlikely to have experienced prolonged periods of severe hyperglycemia."

The study was funded by the NIH and the Burroughs Wellcome Fund for Translational Research.

Study authors declared they had no relevant financial interests.

Primary source: JAMA Neurology

Source reference: Thambisetty M, et al "Glucose intolerance, insulin resistance, and pathological features of Alzheimer disease in the Baltimore Longitudinal Study of Aging" JAMA Neurol 2013; DOI: 10.1001/jamaneurol.2013.284.

http://www.medpagetoday.com/Neurology/AlzheimersDisease/ 40727?xid=nl_mpt_DHE_2013-07-30&utm_content=& utm_medium=email&utm_campaign=DailyHeadlines&utm_source=

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