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8 October 2002. Enormous strides have been made in the development of whole brain imaging techniques as tools for diagnosing and monitoring neurodegenerative diseases such as Alzheimer's (see related news item from the imaging symposium at the Stockholm meeting). Among these different methodologies, positron emission tomography (PET) is likely to be among the first to deliver a standard diagnostic tool that can be used in the clinic, as it has already proven itself capable of diagnosing AD with a high degree of accuracy (see related news item). One question that remains, however, is whether PET can improve on the battery of diagnostic tests that are already in use.
A report in this month's Molecular Imaging and Biology suggests that it can. Daniel Silverman and colleagues at the University of California, Los Angeles, tested the ability of 2-deoxy-2-[18F]fluoro-D-glucose PET, which monitors neuronal fitness by measuring glucose metabolism, to improve diagnosis in the clinic.
The authors separated patients into two groups. Both received standard tests for Alzheimer's disease as recommended by the American Academy of Neurology, but only one group was given the additional benefit of the PET scan. The imaging analysis was found to decrease the number of false negatives by five percent and the number of false positives by more than 10 percent.
The benefit of PET, according to the authors, is immense for those who have some degree of cognitive impairment but are misdiagnosed. The number of months spent on unnecessary drug therapy for those who appear to have the disease but later turn out to be AD-free could be halved. So too could the time spent on eventual nursing home care for those who are in the beginning stages of the disease but go without precious early intervention.-Tom Fagan
Reference:Silverman DHS, Cummings JL, Small GW, Gambhir SS, Chen W, Czernin J, Phelps ME. Added clinical benefit of incorporating 2-deoxy-2-[18F]fluoro-D-glucose positron emission tomography into the clinical evaluation of patients with cognitive impairment. Mol. Imaging Biol. 2002 October. 4:1-11.
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Related News: Pittsburgh Compound-B Zooms into View
Comment by: georges Otte
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Submitted 31 January 2004
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Posted 2 February 2004
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PIB-PET probing is a very significant step foreward on the road to early Alzheimer diagnosis. The authors deserve sincere congratulations on this significant contribution. However, in order to be generally applicable new techniques should be affordable, which in case of PET scan is not (yet?) the case.
Moreover, we must perhaps focus most of all on the soluble Abeta mayloid fraction to target the main culprit in its early phase, before structural synaptic disturbance, and even before GSK-3 or CDK-5- mediated induction of neurofibrillary tangle accumulation, which then disrupt neurons. More effort is needed in the field of early biomarkers both of Abeta and specific hyperphosphorylated tau. These should be corallated with the authors PIB-PET or (soon to come ?) PIB-II-MRI findings.
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Related News: Pittsburgh Compound-B Zooms into View
Comment by: Scott Small
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Submitted 9 February 2004
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Posted 9 February 2004
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The ability to visualize disease has long motivated and driven the history of Western medicine. The end of the nineteenth century represents a turning point in the ability to do so: At around the same time neuroanatomists perfected staining techniques that made disease visible under the microscope, Wilhelm Roentgen introduced the x-ray, which allowed internal structures to be seen in living patients. In 1906, a few years after Roentgen received the first Noble prize in physics, Alois Alzheimer described amyloid plaques and neurofibrillary tangles—the histological features of his eponymous disease. Now, almost a century later, these two technical developments—in-vivo imaging and in-vitro features of Alzheimer’s disease (AD)—have finally converged. In a landmark study published in this month’s issue of the Annals of Neurology, William Klunk and his colleagues show that amyloid plaques can be visualized in the living brains of AD patients.
In the reported study, they used a radio-labeled hydroxybenzothiazole, termed PIB (Pittsburgh compound B), which...
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Related News: Pittsburgh Compound-B Zooms into View
Comment by: Jorge Barrio, Sung Cheng Huang, Gary Small (Disclosure)
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Submitted 9 February 2004
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Posted 9 February 2004
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Comment by Jorge R. Barrio, Gary W. Small, Henry Huang, and Michael E. Phelps
The pathological aggregation of the β amyloid peptide into fibrillary senile plaques (SPs) and the hyperphosphorylation of the tau protein into neurofibrillary tangles (NFTs) play a central role in the pathogenesis of Alzheimer’s disease (AD). The extent and the pattern of distribution of both lesions are indicators for the progression of AD. The initial neuropathological processes—particularly the formation of NFTs—occur in the medial temporal lobe, expanding later to the rest of the temporal lobe, the parietal lobe, and finally engulfing the whole neocortex in the late stages of disease. It is the prospect of in-vivo visualization of these neuropathological lesions that has driven the Pittsburgh group (e.g., Klunk et al., 1994), the UCLA group (e.g., Shoghi-Jadid et al., 2002), the U. Penn group (e.g.,
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Related News: Pittsburgh Compound-B Zooms into View
Comment by: William Klunk, ARF Advisor (Disclosure), Chester Mathis (Disclosure), Julie Price
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Submitted 11 February 2004
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Posted 11 February 2004
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Response by Bill Klunk, Chet Mathis, and Julie Price
We would like to thank Drs. Otte, Scott Small, and the UCLA group for their thoughtful comments on our recent paper. We acknowledge Dr. Otte’s point that the expense of PET precludes its use as a population screening tool and more work is required in that area. The value of this technology will ultimately be weighed against other economic forces in determining its breadth of applicability. The increasing use of FDG-PET in the diagnosis and follow-up of cancer suggests economic value, but this may only be realized in Alzheimer’s disease if the imaging is tied directly to the use of effective therapies. Soluble Aβ does appear to be a valid target as Dr. Otte suggests, but we must keep in mind that soluble, oligomeric Aβ exists in equilibrium with monomeric and fibrillar Aβ. Insoluble Aβ constitutes over 99 percent of the Aβ present in AD brain; it will likely prove impossible to decrease the level of soluble Aβ over the long term without first decreasing the amount of insoluble Aβ....
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