TY - JOUR
T1 - Biomarker modeling of alzheimer's disease
AU - Jack, Clifford R.
AU - Holtzman, David M.
N1 - Funding Information:
C.R.J. was supported by NIH grants (R01 AG011378 and R01 AG041851) and the Alexander Family Professorship of Alzheimer’s Disease Research. D.M.H. was supported by NIH grants (P50-AG05681, P01-AG03991, P01-26276). D.M.H. is a cofounder, on the scientific advisory board, and has ownership interests in C2N Diagnostics, LLC. He has consulted for AstraZeneca, Genentech, and Eli Lilly.
PY - 2013/12/18
Y1 - 2013/12/18
N2 - Alzheimer's disease (AD) is a slowly progressing disorder in which pathophysiological abnormalities, detectable invivo by biomarkers, precede overt clinical symptoms by many years to decades. Five AD biomarkers are sufficiently validated to have been incorporated into clinical diagnostic criteria and commonly used in therapeutic trials. Current AD biomarkers fall into two categories: biomarkers of amyloid-β plaques and of tau-related neurodegeneration. Three of the five are imaging measures and two are cerebrospinal fluid analytes. AD biomarkers do not evolve in an identical manner but rather in a sequential but temporally overlapping manner. Models of the temporal evolution of AD biomarkers can take the form of plots of biomarker severity (degree of abnormality) versus time. In this Review, we discuss several time-dependent models of AD that take into consideration varying age of onset (early versus late) and the influence of aging and co-occurring brain pathologies that commonly arise in the elderly.
AB - Alzheimer's disease (AD) is a slowly progressing disorder in which pathophysiological abnormalities, detectable invivo by biomarkers, precede overt clinical symptoms by many years to decades. Five AD biomarkers are sufficiently validated to have been incorporated into clinical diagnostic criteria and commonly used in therapeutic trials. Current AD biomarkers fall into two categories: biomarkers of amyloid-β plaques and of tau-related neurodegeneration. Three of the five are imaging measures and two are cerebrospinal fluid analytes. AD biomarkers do not evolve in an identical manner but rather in a sequential but temporally overlapping manner. Models of the temporal evolution of AD biomarkers can take the form of plots of biomarker severity (degree of abnormality) versus time. In this Review, we discuss several time-dependent models of AD that take into consideration varying age of onset (early versus late) and the influence of aging and co-occurring brain pathologies that commonly arise in the elderly.
UR - http://www.scopus.com/inward/record.url?scp=84890528022&partnerID=8YFLogxK
U2 - 10.1016/j.neuron.2013.12.003
DO - 10.1016/j.neuron.2013.12.003
M3 - Review article
C2 - 24360540
AN - SCOPUS:84890528022
SN - 0896-6273
VL - 80
SP - 1347
EP - 1358
JO - Neuron
JF - Neuron
IS - 6
ER -