Jul 242012
 
researcher_testube

This post originally appeared on the ChicagoNow blog, “Ask Dr. Chill: Practical Answers to the Toughest Caregiving Questions.” It is being reposted here with the author’s permission.

Alas, I was not able to attend the Alzheimer’s Association International Conference in Vancouver this month, but I did follow it closely on the organization’s website. The event attracted over 4,300 scientists, physicians and other professionals in the Alzheimer’s community who gathered to discuss findings from their most recent batches of research.

If your eyes tend to glaze over when you read news blurbs about complicated research, I don’t blame you. The sheer amount of news these days certainly can induce medical information overload.

As an antidote, I offer my Cliff Notes version of the Alzheimer’s Association International Conference:

  • A couple of risk factors emerged, including  late-life binge drinking, changes in gait (walking patterns) and sleep changes(Note: A risk factor implies a correlation between the factor and eventual onset of the disease — it does not imply causality. Just because something is associated with something else does not mean that one causes the other.)
  • Several treatments showed promise, including experimental drug EVP-6124, intravenous immunoglobulin, medical food Souvenaid, dietary supplement citicoline, and home-based care coordination. (Note: Treatment studies focus on treating the symptoms of Alzheimer’s after the disease process is already underway. There is no evidence that any of these treatments are useful for prevention.)
  • But on the upside, four different studies indicated that targeted exercise training could reduce the risk of developing dementia among older adults who were either cognitively healthy or only had mild cognitive impairment. (Get moving, folks!)
  • Diagnostic advances now allow researchers to better identify people with Alzheimer’s when they are still presymptomatic. That’s right  early brain changes and subtle cognitive problems can now be detected so that a diagnosis of “preclinical” or “presymptomatic” Alzheimer’s disease can be made. Granted, this type of diagnostic accuracy is seen mostly in research settings and has yet to become evident in general medical practice. But what this means is that researchers can now test new drugs among presymptomatic individuals to see if the progression to symptomatic Alzheimer’s can actually be prevented.

As I scoured the event’s press releases, I felt a combination of hope, pride and sadness wash over me. My hope emerges from the incredible strides taken by the Alzheimer’s community that have revealed more about the disease in the past 20 to 30 years than we learned during most of the 20thcentury (Alzheimer’s was first identified in 1906). My pride is rooted in the many years I worked for the organization and my first-hand knowledge of its dedication to ultimately finding an end to this wretched disease.

I didn’t want to feel sadness, but it’s best not to suppress such honest parts of the human experience. My sadness stemmed from my long journey with this disease  both professionally and personally  which has taught me that any measure of hope must be balanced with a healthy dose of realism.

Note that the conference highlighted causes, treatments and prevention  but not cures. We’re simply not there yet. We’re closer to a cure than ever before, but using that emotionally-laden word more than sparingly is still premature. I applaud the organization for always putting out balanced, accurate reports with no spin or pretense.

So be hopeful, but be realistic, too. And remember that the greatest barrier to the development of better treatments is the shortage of participants in Alzheimer’s clinical trials. If you want to add a dose of activism to your mixture of hope and realism, check out the Alzheimer’s Association’s TrialMatch program and find out whether there’s a clinical trial near you.

About Guest Blog Author Carrie Steckl, Ph.D.

Carrie Steckl, Ph.D. is a freelance writer specializing in caregiving, psychology, and aging. Her blog, “Ask Dr. Chill,” provides practical answers to the toughest caregiving questions.

 

Nov 152011
 
AB Plaque

Gantenerumab, an antibody that binds to beta-amyloid, clears plaques in a matter of months, report scientists at F. Hoffmann-La Roche Ltd., Basel, Switzerland, in a study published online in Archives of Neurology.

The Phase I study of 16 Alzheimer’s patients tested gantenerumab at two doses against a placebo over six months of treatment. Senior author Luca Santarelli and colleagues used positron emission tomography (PET) scans to visualize and compare levels of amyloid plaques in the brain before and after intravenous antibody treatments, and found the decreases. The current study did not evaluate cognition. Many researchers suspect the build-up of such plaques may be a cause of this memory robbing disease.

There are, in fact, almost a dozen anti-beta-amyloid antibodies in clinical testing, including solanezumab, developed by Eli Lilly and Company, Indianapolis, Indiana, which, along with bapineuzumab, is furthest along in clinical development.

An earlier small study of the Elan Pharmaceuticals/Wyeth antibody bapineuzumab (now developed by Janssen Alzheimer Immunotherapy, Dublin, Ireland) also used PET scans to compare plaque levels in the brain before and after intravenous antibody treatment. This antibody lowered brain amyloid levels in Alzheimer’s patients by an average of 8.5 percent over 18 months, compared with a 16.9 percent increase in untreated patients.

In the current study, 18 patients, aged 50-90, who had mild to moderate Alzheimer’s disease, received either placebo or gantenerumab (60 mg or 200 mg) in up to seven monthly intravenous infusions. At the end of the study, PET scans indicated that the six patients in the low-dose group lost 15.9 percent of their plaques, while the six in the high-dose group dispatched 35.7 percent. If this holds up, it would indicate faster amyloid removal than reported for bapineuzumab.

It is unclear whether beta-amyloid clearance by gantenerumab prevents or slows cognitive decline. We await results of Phase 3 trials of solanezumab and bapineuzumab next year, which will reveal whether clearance of beta-amyloid provides any cognitive benefit in mild to moderate Alzheimer’s. Of course, studies are being planned for prodromal Alzheimer’s disease. Prodromal Alzheimer’s is a condition in which a person’s memory loss is worse than can be expected by the normal aging process, while their ability to engage in daily activities is not affected to the extent that dementia would be diagnosed. Research sites around the world are preparing to enroll patients for the SCarlet RoAD study, to evaluate efficacy and safety of gantenerumab in patients with prodromal AD.

Ostrowitzki S, Deptula D, Thurfjell L, Barkhof F, Bohrmann B, Brooks DJ, Klunk WE, Ashford E, Yoo K, Xu Z, Loetscher H, Santarelli L. Mechanism of Amyloid Removal in Patients With Alzheimer Disease Treated With Gantenerumab. Arch Neurol. 2011 Oct 10

Michael S. Rafii, M.D., Ph.D.

Director, Memory Disorders Clinic
Associate Medical Core Director, Alzheimer’s Disease Cooperative Study
University of California San Diego

This post originally appeared in Alzheimer’s Insights, an ADCS Blog.

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