Jul 282011
 

Plants have a long history as a rich source of new compounds for drug discovery. Cinnamon is widely used by humans, both as a spice and as a traditional medicine. It is, perhaps, one of the oldest herbal medicines, having been mentioned in the Bible and in Chinese texts as long as 4,000 years ago.

Previous studies have already demonstrated the potential for herbal extracts to interact with beta-amyloid, and perhaps slow down or even prevent AD. As we move towards earlier identification of Alzheimer’s disease pathology in minimally symptomatic individuals, such therapies will undoubtedly become areas of intense research. Examples for extensively studied naturally occurring compounds are the (-)-epigallocatechin-3-gallate (EGCG) from green tea and Curcumin, which is derived from the natural turmeric.

Now, a research team headed by Michael Ovadia from Tel Aviv University, has isolated one of the ingredients in cinnamon, CEppt, and used it in a series of tests conducted on two-month-old lab mice that were raised with five aggressive strains of Alzheimer’s-inducing genes. The experiment’s results, recently published in the PLoS ONE scientific journal, were impressive. Laboratory rodents, genetically altered to develop dementia, received either the cinnamon extract or an inert treatment for four months. The extract improved the rats’ performance on learning and memory tasks. It also reduced the amount of plaque formed in the brain. The animals were fed drinking water containing a CEppt solution over four months, and researchers found that the disease’s development was delayed, with additional trials showing that existing amyloids had been dissolved. The results show the ability of CEppt to inhibit the progress of beta-amyloid aggregation. CEppt is actually comprised of several molecules, and it remains to be found which molecule is exerting this effect.

Supplements such as Curcumin, EGCG, DHA and CEppt will likely be evaluated in clinical trials in patients who have minimal symptoms, but are on the path towards developing AD. That is, patients with amyloid building up in the brain, but not yet showing symptoms as assessed by Amyloid scans (for example. From studies such as ADNI, we believe that there is a 15 year window during which amyloid is building up in the brain, while there are minimal symptoms, such as memory loss present. This window may be the best time to initiate anti-amyloid therapy.)

Anat Frydman-Marom, et al, Orally Administrated Cinnamon Extract Reduces ß-Amyloid Oligomerization and Corrects Cognitive Impairment in Alzheimer’s Disease Animal Models; PLoS One Jan. 28, 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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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.

    Learn More

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