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Utilizing Advanced Imaging and Surrogate Markers Across the Spectrum of Alzheimer's Disease

Published online by Cambridge University Press:  07 November 2014

Mark A. Mintun
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Abstract

Alzheimer's disease is a degenerative neurological condition characterized by the presence of β-amyloid plaques and neurofibrillary tangles in the limbic and neocortical regions of the brain. Pittsburgh Compound-B (PIB), a benzothiazole analog, has recently been found to specifically label amyloid deposits in positron emission tomography (PET) studies of the brain, opening the door for a wide range of applications related to Alzheimer's disease. In this article, data demonstrating the specificity of PIB as a PET tracer for β-amyloid lesions are reviewed, and the potential clinical applications of PIB PET imaging is discussed. Because amyloid plaques are common even in elderly individuals who are not suffering from dementia, the primary diagnostic function of PIB PET imaging presumably would be to rule out, rather than definitively confirm, Alzheimer's diagnoses in elderly patients. Other possible uses include monitoring plaque loads in patients receiving anti-amyloid therapy for Alzheimer's disease, as well as assessing plaque formation in unaffected individuals as a means of evaluating future Alzheimer's disease.

Type
Academic Supplement
Information
CNS Spectrums , Volume 10 , Issue S18: Alzheimer's Disease Pathways to Practice: Assessing Diagnosis and Outcome Measures , November 2005 , pp. 13 - 16
Copyright
Copyright © Cambridge University Press 2005

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References

REFERENCES

1.Braak, H, Braak, E. Neuropathological stageing of Alzheimer-related changes. Acta Neuropathol (Berl). 1991;82:239–259.CrossRefGoogle ScholarPubMed
2.George-Hyslop, PH, Petit, A. Molecular biology and genetics of Alzheimer's disease. C R Biol. 2005;328:119–130.Google Scholar
3.Mathis, CA, Wang, Y, Holt, DP, et al.Synthesis and evaluation of 11C-labeled 6-substituted 2-arylbenzothiazoles as amyloid imaging agents. J Med Chem. 2003;46:2740–2754.Google Scholar
4.Bacskai, BJ, Hickey, GA, Skoch, J, et al.Four-dimensional multiphoton imaging of brain entry, amyloid binding, and clearance of an amyloid-beta ligand in transgenic mice. Proc Nad Acad Sci U S A. 2003;100:12462–12467.Google Scholar
5.Buckner, RI, Snyder, AZ, Shannon, BJ, et al.Molecular, structural, and functional characterization of Alzheimer's disease: evidence for a relationship between default activity, amyloid, and memory. J Neurosci. 2005;25:7709–7717.Google Scholar
6.Passingbam, D, Sakai, K. The prefrontal cortex and working memory: physiology and brain imaging. Curr Opin Neurobiol. 2004;14:163–168.Google Scholar
7.Funahashi, S. Neuronal mechanisms of executive control by the prefrontal cortex. Neurosci Res. 2001;39:147–165.Google Scholar
8.Price, JL, Morris, JC. Tangles and plaques in nondemented aging and “preclinical” Alzheimer's disease. Ann Neurol. 1999;45:358–368.Google Scholar
9.Hulette, CM, Welsh-Bohmer, KA, Murray, MG, et al.Neuropathological and neuropsychological changes in “normal” aging: evidence for preclinical Alzheimer disease in cognitively normal individuals. J Neuropathol Exp Neurol. 1998;57:1168–1174.Google Scholar
10.Tomlinson, BE, Blessed, G, Roth, M. Observations on the brains of non-demented old people. J Neurol Sci. 1968;7:331–356.Google Scholar
11.Katzman, R, Terry, R, De Teresa, R, et al.Clinical, pathological, and neurochemical changes in dementia: a subgroup with preserved mental status and numerous neocortical plaques. Ann Neurol. 1988;23:138–144.Google Scholar
12.Hock, C, Konietzko, U, Streffer, JR, et al.Antibodies against beta-amyloid slow cognitive decline in Alzheimer's disease. Neuron. 2003;38:547–554.Google Scholar
13.Nicoll, JA, Wilkinson, D, Holmes, C, et al.Neuropathology of human Alzheimer disease after immunization with amyloid-beta peptide: a case report. Nat Med. 2003;9:448–452.Google Scholar