Evolution of neurodegeneration-imaging biomarkers from clinically normal to dementia in the Alzheimer disease spectrum

David S Knopman; Clifford R Jr. Jack; Emily S. Lundt; Stephen D. Weigand; Prashanthi D Vemuri; Val Lowe; Kejal M Kantarci; Jeffrey L. Gunter; Matthew L. Senjem; Michelle M Mielke; Mary Margaret Machulda; Rosebud O Roberts; Bradley F Boeve; David T Jones; Ronald Carl Petersen

doi:10.1016/j.neurobiolaging.2016.06.003

Evolution of neurodegeneration-imaging biomarkers from clinically normal to dementia in the Alzheimer disease spectrum

David S Knopman, Clifford R Jr. Jack, Emily S. Lundt, Stephen D. Weigand, Prashanthi D Vemuri, Val Lowe, Kejal M Kantarci, Jeffrey L. Gunter, Matthew L. Senjem, Michelle M Mielke, Mary Margaret Machulda, Rosebud O Roberts, Bradley F Boeve, David T Jones, Ronald Carl Petersen

Research output: Contribution to journal › Article

7 Scopus citations

Abstract

The availability of antemortem biomarkers for Alzheimer's disease (AD) enables monitoring the evolution of neurodegenerative processes in real time. Pittsburgh compound B (PIB) positron emission tomography (PET) was used to select participants in the Mayo Clinic Study of Aging and the Mayo Alzheimer's Disease Research Center with elevated β-amyloid, designated as “A+,” and hippocampal volume and ¹⁸fluorodeoxyglucose (FDG) positron emission tomography were used to characterize participants as having evidence of neurodegeneration (“N+”) at the baseline evaluation. There were 145 clinically normal (CN) A+ individuals, 62 persons with mild cognitive impairment (MCI) who were A+ and 20 with A+ AD dementia. Over a period of 1–6 years, MCI A+N+ individuals showed declines in medial temporal, lateral temporal, lateral parietal, and to a lesser extent, medial parietal regions for both FDG standardized uptake value ratio and gray matter volume that exceeded declines seen in the CN A+N+ group. The AD dementia group showed declines in the same regions on FDG standardized uptake value ratio and gray matter volume with rates that exceeded that in MCI A+N+. Expansion of regional involvement and faster rate of neurodegeneration characterizes progression in the AD pathway.

Original language	English (US)
Pages (from-to)	32-42
Number of pages	11
Journal	Neurobiology of Aging
Volume	46
DOIs	https://doi.org/10.1016/j.neurobiolaging.2016.06.003
State	Published - Oct 1 2016

Keywords

Alzheimer's disease
FDG PET imaging
Longitudinal study
MR imaging
PIB PET imaging

ASJC Scopus subject areas

Clinical Neurology
Neuroscience(all)
Aging
Developmental Biology
Geriatrics and Gerontology

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Knopman, D. S., Jack, C. R. J., Lundt, E. S., Weigand, S. D., Vemuri, P. D., Lowe, V., Kantarci, K. M., Gunter, J. L., Senjem, M. L., Mielke, M. M., Machulda, M. M., Roberts, R. O., Boeve, B. F., Jones, D. T., & Petersen, R. C. (2016). Evolution of neurodegeneration-imaging biomarkers from clinically normal to dementia in the Alzheimer disease spectrum. Neurobiology of Aging, 46, 32-42. https://doi.org/10.1016/j.neurobiolaging.2016.06.003

Evolution of neurodegeneration-imaging biomarkers from clinically normal to dementia in the Alzheimer disease spectrum. / Knopman, David S ; Jack, Clifford R Jr.; Lundt, Emily S.; Weigand, Stephen D.; Vemuri, Prashanthi D ; Lowe, Val ; Kantarci, Kejal M; Gunter, Jeffrey L.; Senjem, Matthew L.; Mielke, Michelle M ; Machulda, Mary Margaret; Roberts, Rosebud O; Boeve, Bradley F ; Jones, David T ; Petersen, Ronald Carl.

In: Neurobiology of Aging, Vol. 46, 01.10.2016, p. 32-42.

Research output: Contribution to journal › Article

Knopman, DS , Jack, CRJ, Lundt, ES, Weigand, SD, Vemuri, PD , Lowe, V , Kantarci, KM, Gunter, JL, Senjem, ML, Mielke, MM , Machulda, MM, Roberts, RO, Boeve, BF , Jones, DT & Petersen, RC 2016, 'Evolution of neurodegeneration-imaging biomarkers from clinically normal to dementia in the Alzheimer disease spectrum', Neurobiology of Aging, vol. 46, pp. 32-42. https://doi.org/10.1016/j.neurobiolaging.2016.06.003

Knopman, David S ; Jack, Clifford R Jr. ; Lundt, Emily S. ; Weigand, Stephen D. ; Vemuri, Prashanthi D ; Lowe, Val ; Kantarci, Kejal M ; Gunter, Jeffrey L. ; Senjem, Matthew L. ; Mielke, Michelle M ; Machulda, Mary Margaret ; Roberts, Rosebud O ; Boeve, Bradley F ; Jones, David T ; Petersen, Ronald Carl. / Evolution of neurodegeneration-imaging biomarkers from clinically normal to dementia in the Alzheimer disease spectrum. In: Neurobiology of Aging. 2016 ; Vol. 46. pp. 32-42.

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abstract = "The availability of antemortem biomarkers for Alzheimer's disease (AD) enables monitoring the evolution of neurodegenerative processes in real time. Pittsburgh compound B (PIB) positron emission tomography (PET) was used to select participants in the Mayo Clinic Study of Aging and the Mayo Alzheimer's Disease Research Center with elevated β-amyloid, designated as “A+,” and hippocampal volume and 18fluorodeoxyglucose (FDG) positron emission tomography were used to characterize participants as having evidence of neurodegeneration (“N+”) at the baseline evaluation. There were 145 clinically normal (CN) A+ individuals, 62 persons with mild cognitive impairment (MCI) who were A+ and 20 with A+ AD dementia. Over a period of 1–6 years, MCI A+N+ individuals showed declines in medial temporal, lateral temporal, lateral parietal, and to a lesser extent, medial parietal regions for both FDG standardized uptake value ratio and gray matter volume that exceeded declines seen in the CN A+N+ group. The AD dementia group showed declines in the same regions on FDG standardized uptake value ratio and gray matter volume with rates that exceeded that in MCI A+N+. Expansion of regional involvement and faster rate of neurodegeneration characterizes progression in the AD pathway.",

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