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Potentially Yes for Clinical Trials but Not Yet for Clinical Practice

Ronald C. Petersen, PhD, MD; John Q. Trojanowski, MD, PhD

JAMA. 2009;302(4):436-437.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Research in Alzheimer disease (AD) is rapidly moving toward the point of the earliest possible identification of the underlying disease processes. These include the accumulation of Aβ plaques, tau tangles, and neuron as well as synaptic loss, and it is likely that these do not all occur contemporaneously. Many investigators contend that, by the time the clinical symptoms appear, sufficient AD pathology and neurodegeneration have occurred, which if irreversible, may reduce the efficacy of disease-modifying therapy for clinically manifest AD.¹ As such, efforts are under way to try to identify the onset of these pathological processes that culminate in clinically manifest AD dementia. However, to accomplish this, the underlying pathology must be detected, possibly through the use of neuroimaging and chemical biomarker measures. In this issue of JAMA, Mattsson and colleagues² report their evaluation of the utility of cerebrospinal . . . [Full Text of this Article]

Author Affiliations: Alzheimer's Disease Research, Mayo Alzheimer's Disease Research Center, Mayo Clinic Study of Aging, Rochester, Minnesota (Dr Petersen); and Institute on Aging, Alzheimer's Disease Core Center, Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia (Dr Trojanowski).

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