Jul 152011
 

The use of positron emission tomography (PET) imaging to diagnose Alzheimer’s disease (AD) appears to be closer to becoming a clinical tool, based on results from two articles published online in the Archives of Neurology.

In one study, Adam S. Fleisher, M.D., from Banner Alzheimer’s Institute in Phoenix, and colleagues, evaluated PET imaging using the tracer florbetapir F 18. The study population included 68 individuals with probable Alzheimer’s disease, 60 individuals with mild cognitive impairment, and 82 healthy individuals who served as controls. PET scanning was used to monitor activity of the agent being studied. Dr. Fleisher and colleagues found differences in the brain uptake of florbetapir F 18, between the three groups, and in the detection of amyloid plaque; the differences may be large enough to help distinguish between the conditions, and between impaired versus unimpaired brains.

In another study, David A. Wolk, M.D., from the Penn Memory Center in Philadelphia, and colleagues, evaluated use of a tracer called fluorine 18-labeled flutemetamol for imaging the brain. The study involved conducting PET scans on seven patients who were given the tracer. All had previously undergone a biopsy for normal pressure hydrocephalus, a progressive condition that includes dementia and can be difficult to distinguish from Alzheimer’s disease. Researchers found correspondence between readings of the PET scans and evidence of amyloid lesions the plaque associated with Alzheimer’s disease (provided by microscopic evaluation of the biopsied tissue).

    The greatest use of such scans may ultimately be to help rule out Alzheimer’s disease, instead of rule it in. That is, in the physician’s office, having a negative scan (meaning no detectable amyloid buildup in the brain) may be helpful to clinicians in ruling out Alzheimer’s disease as the cause of the memory and thinking changes a person is experiencing. However, a positive scan (showing that there is amyloid buildup in the brain) has limited utility at this point.

    Having amyloid buildup does not mean for certain that one has Alzheimer’s dementia, especially in a patient who may not have symptoms. About 30 percent of elderly people have plaque, but not Alzheimer’s dementia. It is believed that having a positive amyloid scan may reflect the early stages of Alzheimer’s disease (prior to the dementia phase) and increase one’s risk of developing Alzheimer’s dementia in the future.

    1. D. A. Wolk, I. D. Grachev, C. Buckley, H. Kazi, M. S. Grady, J. Q. Trojanowski, R. H. Hamilton, P. Sherwin, R. McLain, S. E. Arnold. Association Between In Vivo Fluorine 18-Labeled Flutemetamol Amyloid Positron Emission Tomography Imaging and In Vivo Cerebral Cortical Histopathology. Archives of Neurology, 2011

    2. A. S. Fleisher, K. Chen, X. Liu, A. Roontiva, P. Thiyyagura, N. Ayutyanont, A. D. Joshi, C. M. Clark, M. A. Mintun, M. J. Pontecorvo, P. M. Doraiswamy, K. A. Johnson, D. M. Skovronsky, E. M. Reiman. Using Positron Emission Tomography and Florbetapir F 18 to Image Cortical Amyloid in Patients With Mild Cognitive Impairment or Dementia Due to Alzheimer Disease. Archives of Neurology, 2011.

    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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    Jan 252011
     

    Using a new technology that relies on thousands of synthetic molecules to fish for disease-specific antibodies, researchers have developed a potential method for detecting Alzheimer’s disease with a simple blood test. The same methodology might lead to blood tests for many important diseases, according to the report published by Thomas Kodadek’s group at the Scripps Research Institute in the January 7th issue of the journal Cell.

    The new method relies on the notion that many diseases lead to the production of modified proteins. At some point, the adaptive immune system might begin to recognize those proteins as foreign and mount a response. If tests could be developed to recognize those disease-specific proteins or the antibodies that recognize them, it could be the basis for early diagnosis. But in most cases, researchers have had little luck identifying those abnormal proteins.

    Kodadek’s team decided to take a different tack. They used a large library of randomly selected, unnatural molecules known as “peptoids” to screen for antibodies found in the bloodstream of animals or patients with specific diseases and not in healthy controls.

    Their method uncovered three peptoids that appear to discriminate between healthy and Alzheimer’s disease blood samples with high accuracy. Three of them reacted strongly to the blood of six patients with the condition, but not that of 16 healthy individuals used as controls. Although this is encouraging the findings must be corroborated by further studies to demonstrate that antibodies can indicate whether the attack opens a picture for diagnosing the disease.

    * Reddy MM, Wilson R, Wilson J, Connell S, Gocke A, Hynan L, German D, Kodadek T. Identification of candidate IgG biomarkers for Alzheimer’s disease via combinatorial library screening. Cell 2011 January 7;144:132-142.

    Michael S. Rafii, M.D., Ph.D.
    Associate Medical Core Director, Alzheimer’s Disease Cooperative Study
    This post originally appeared in Alzheimer’s Insights, an ADCS Blog.

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