Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers

被引：3114

作者：

Jack, Clifford R., Jr. ^{[1
]}

Knopman, David S. ^{[2
]}

Jagust, William J. ^{[4
,5
]}

Petersen, Ronald C. ^{[2
]}

Weiner, Michael W. ^{[6
]}

Aisen, Paul S. ^{[7
]}

Shaw, Leslie M. ^{[8
,9
]}

Vemuri, Prashanthi ^{[1
]}

Wiste, Heather J. ^{[3
]}

Weigand, Stephen D. ^{[3
]}

Lesnick, Timothy G. ^{[3
]}

Pankratz, Vernon S. ^{[3
]}

Donohue, Michael C. ^{[7
]}

Trojanowski, John Q. ^{[8
,9
]}

机构：

[1] Mayo Clin, Dept Radiol, Rochester, MN 55905 USA

[2] Mayo Clin, Dept Neurol, Rochester, MN 55905 USA

[3] Mayo Clin, Dept Biomed Stat & Informat, Rochester, MN 55905 USA

[4] Univ Calif Berkeley, Sch Publ Hlth, Berkeley, CA 94720 USA

[5] Univ Calif Berkeley, Helen Wills Neurosci Inst, Berkeley, CA 94720 USA

[6] Vet Affairs, San Francisco, CA USA

[7] Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA

[8] Univ Penn, Sch Med, Dept Pathol & Lab Med, Philadelphia, PA 19104 USA

[9] Univ Penn, Sch Med, Inst Aging, Philadelphia, PA 19104 USA

来源：

LANCET NEUROLOGY | 2013年 / 12卷 / 02期

基金：

美国国家卫生研究院;

关键词：

MILD COGNITIVE IMPAIRMENT; POSITRON-EMISSION-TOMOGRAPHY; CEREBROSPINAL-FLUID A-BETA(42); AMYLOID DEPOSITION; A-BETA; APOLIPOPROTEIN-E; CSF BIOMARKERS; FUNCTIONAL CONNECTIVITY; HIPPOCAMPAL ATROPHY; EPSILON-4; STATUS;

D O I：

10.1016/S1474-4422(12)70291-0

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

In 2010, we put forward a hypothetical model of the major biomarkers of Alzheimer's disease (AD). The model was received with interest because we described the temporal evolution of AD biomarkers in relation to each other and to the onset and progression of clinical symptoms. Since then, evidence has accumulated that supports the major assumptions of this model. Evidence has also appeared that challenges some of our assumptions, which has allowed us to modify our original model. Refinements to our model indude indexing of individuals by time rather than clinical symptom severity; incorporation of interindividual variability in cognitive impairment associated with progression of AD pathophysiology; modifications of the specific temporal ordering of some biomarkers; and recognition that the two major proteinopathies underlying AD biomarker changes, amyloid beta (A beta) and tau, might be initiated independently in sporadic AD, in which we hypothesise that an incident A beta pathophysiology can accelerate antecedent limbic and brainstem tauopathy.

引用

页码：207 / 216

页数：10

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