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.

 

Jan 112012
 

As 2012 begins, I would like to review some of the highlights of the Alzheimer’s Disease world this past year, and the new directions that we will likely be heading toward in 2012.

  • This year we saw the publication of new diagnostic guidelines for Alzheimer’ s disease formulated by committees sponsored by the National Institute on Aging and the Alzheimer’s Association. The National Institute on Aging and the Alzheimer’s Association also published guidelines for diagnosis of mild cognitive impairment due to Alzheimer’s disease and for preclinical Alzheimer’s disease. These guidelines will be important tools for clinicians to diagnose Alzheimer’s in its earliest stages, and represent the first revision in 25 years.
  • An FDA advisory committee gave preliminary approval of the PET amyloid imaging ligand AV-45, citing work to be done to ensure consistency in reading PET scans. Full approval is expected sometime in 2012, if a uniform training program is implemented for radiologists interpreting the scans.
  • The European Medicines Agency announced the likely approval of hippocampal atrophy as a marker of early Alzheimer’s disease for the purpose of clinical trials. Much work has gone into linking hippocampal atrophy visualized by MRI  as an early and specific biomarker of neurodegeneration seen in Alzheimer’s disease.
  • IGAP—the International Genomics of Alzheimer’s Project, a transatlantic collaboration to create the most detailed map of genetic variants that link to Alzheimer’s disease was also launched in 2011. Meta analysis of genome-wide association studies (GWAS) revealed four new genetic risk variants for Alzheimer’s disease.
  • In terms of clinical trials, Gantenerumab, an antibody against beta-amyloid, was shown to clear plaques when given intravenously, according to results from a Phase 1 trial. The drug seems to be one of the most potent developed thus far in reducing plaques. A Phase 2 gene therapy trial for Parkinson’s disease was deemed a success. A similar Phase II gene therapy trial for Alzheimer’s disease, called the Nerve Growth Factor Study, is currently ongoing and recruiting. Multiple clinical trials, including the ADCS Phase III Resveratrol and Roche Phase II Gantenerumab trial are launching in 2012.
  • A very important paper by the Holtzman group at Washington University further established the relationship between ApoE4 genotype and decreased clearance of beta-amyloid from brain, both in humans and animal models. The idea that ApoE4 is less effective in removing beta-amyloid from the brain is not necessarily novel, per se, and had been previously shown. However, it had never been proven so convincingly and in such a complete manner in humans and animal models of Alzheimer’s disease. Together, the data suggest that ApoE variants contribute to a person’s risk for Alzheimer’s by affecting the clearance of beta-amyloid from the brain long before amyloid plaque deposition begins. Later in the year, the same group reported that, in mice, lowering the levels of ApoE4 results in fewer amyloid plaques. The results imply that ApoE-lowering treatments have a place among proposed Alzheimer’s therapies, including immunotherapy, gene therapy, and beta- and gamma- secretase inhibitors.
  • Results published in the Journal of the American Medical Association showed that women with sleep-disordered breathing (SDB)— pauses in breathing or reduced ventilation quality during sleep — are more likely to develop cognitive impairment five years later. The biology behind this finding may include hypoxia, or decreased oxygen delivery to certain parts of the brain, including the hippocampus which is critical in memory function. In addition, sleep fragmentation, which can interfere with memory consolidation, which occurs during certain stages of sleep, may also lead to cognitive problems. This study has really brought much needed attention to the evaluation of sleep as part of the work-up in individuals with Mild Cognitive Impairment.

We anticipate further progress in understanding the progression of the earliest stages of Mild Cognitive Impairment and Alzheimer’s disease with the Alzheimer’s Disease Neuroimaging Initiative (ADNI2), The Dominantly Inherited Alzheimers Network (DIAN) study and the Alzheimer’s Prevention Initiative (API) during 2012.

By Michael Rafii, M.D., Ph.D.
Director, Memory Disorders Clinic
Associate Medical Core Director
Alzheimer’s Disease Cooperative Study
University of California, San Diego

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