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Editorial |

Brain Atrophy on Magnetic Resonance Imaging as a Biomarker of Neurodegeneration ONLINE FIRST

Clifford R. Jack Jr, MD1
[+] Author Affiliations
1Department of Radiology, Mayo Clinic, Rochester, Minnesota
JAMA Neurol. Published online August 22, 2016. doi:10.1001/jamaneurol.2016.2843
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In this issue of JAMA Neurology, Gordon and colleagues1 from Washington University publish a well-done study on an important and topical subject. The investigators used the 2-class Alzheimer disease (AD) biomarker classification scheme that arises when combining biomarker staging for preclinical AD recommended by the National Institute on Aging–Alzheimer Association2 along with suspected non-Alzheimer pathophysiology (SNAP) described by the Mayo group.3 Every participant is placed into 1 of 4 biomarker categories based on dichotomizing biomarkers for β-amyloidosis (Aβ) and neurodegeneration/neuronal injury (ND): Aβ−/ND− (stage 0 preclinical AD), Aβ+/ND− (stage 1 preclinical AD), Aβ+/ND+ (stage 2/3 preclinical AD), Aβ−/ND+ (SNAP).

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Figure.
Frequency of the 4 β-Amyloidosis (Aβ)/Neurodegeneration (ND) Groups by Age With Different Definitions of ND+

Estimates are from a multinomial model adjusted for sex and, therefore, the curves represent a mean frequency over men and women. AD sig indicates cortical thickness in an Alzheimer disease signature set of regions of interest; FDG, 18fluorodeoxyglucose positron emission tomography; HVa, hippocampal volume adjusted for head size. The age trends within each Aβ/ND biomarker group are similar across the different definitions of ND+. For all definitions of ND+, the frequency of suspected non-Alzheimer pathophysiology was 0% at age 50 years, with a monotonic increase into old age. Revised with permission from Oxford University Press.9

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