Brain injury biomarkers are not dependent on β‐amyloid in normal elderly

The new criteria for preclinical Alzheimer disease (AD) proposed 3 stages: abnormal levels of β‐amyloid (stage 1), stage 1 plus evidence of brain injury (stage 2), and stage 2 plus subtle cognitive changes (stage 3). However, a large group of subjects with normal β‐amyloid biomarkers have evidence of brain injury; we labeled them as the “suspected non‐Alzheimer pathophysiology” (sNAP) group. The characteristics of the sNAP group are poorly understood.

[1]  Michael J Leach,et al.  Longitudinal , 2015, The Medical journal of Australia.

[2]  D. Holtzman,et al.  Origins of Alzheimer's disease: reconciling cerebrospinal fluid biomarker and neuropathology data regarding the temporal sequence of amyloid-beta and tau involvement. , 2012, Current opinion in neurology.

[3]  A. Fagan,et al.  Toward a multifactorial model of Alzheimer disease , 2012, Neurobiology of Aging.

[4]  C. Jack,et al.  Multimodality imaging characteristics of dementia with Lewy bodies , 2012, Neurobiology of Aging.

[5]  C. Jack,et al.  Focal atrophy on MRI and neuropathologic classification of dementia with Lewy bodies , 2012, Neurology.

[6]  C. Jack,et al.  An operational approach to National Institute on Aging–Alzheimer's Association criteria for preclinical Alzheimer disease , 2012, Annals of neurology.

[7]  A. Dale,et al.  Amyloid-β--associated clinical decline occurs only in the presence of elevated P-tau. , 2012, Archives of neurology.

[8]  J. Gunter,et al.  Short-term clinical outcomes for stages of NIA-AA preclinical Alzheimer disease , 2012, Neurology.

[9]  E G Tangalos,et al.  The incidence of MCI differs by subtype and is higher in men , 2012, Neurology.

[10]  Elizabeth C Mormino,et al.  Not quite PIB-positive, not quite PIB-negative: Slight PIB elevations in elderly normal control subjects are biologically relevant , 2012, NeuroImage.

[11]  John L. Robinson,et al.  Neocortical and hippocampal amyloid-β and tau measures associate with dementia in the oldest-old. , 2011, Brain : a journal of neurology.

[12]  Dietmar R. Thal,et al.  Stages of the Pathologic Process in Alzheimer Disease: Age Categories From 1 to 100 Years , 2011, Journal of neuropathology and experimental neurology.

[13]  Alan E Hubbard,et al.  Longitudinal change of biomarkers in cognitive decline. , 2011, Archives of neurology.

[14]  M. Weiner,et al.  The dynamics of cortical and hippocampal atrophy in Alzheimer disease. , 2011, Archives of neurology.

[15]  B. Hyman,et al.  Amyloid-dependent and amyloid-independent stages of Alzheimer disease. , 2011, Archives of neurology.

[16]  Cindee M. Madison,et al.  Associations between cognitive, functional, and FDG-PET measures of decline in AD and MCI , 2011, Neurobiology of Aging.

[17]  Charles D. Smith,et al.  Hippocampal sclerosis in advanced age: clinical and pathological features. , 2011, Brain : a journal of neurology.

[18]  Denise C. Park,et al.  Toward defining the preclinical stages of Alzheimer’s disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease , 2011, Alzheimer's & Dementia.

[19]  D. Dickson,et al.  TDP-43 in aging and Alzheimer's disease - a review. , 2011, International journal of clinical and experimental pathology.

[20]  H. Braak,et al.  The pathological process underlying Alzheimer’s disease in individuals under thirty , 2011, Acta Neuropathologica.

[21]  E G Tangalos,et al.  Prevalence of mild cognitive impairment is higher in men , 2010, Neurology.

[22]  C. Jack,et al.  Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade , 2010, The Lancet Neurology.

[23]  A. Fagan,et al.  APOE predicts amyloid‐beta but not tau Alzheimer pathology in cognitively normal aging , 2010, Annals of neurology.

[24]  A. Fagan,et al.  Cerebrospinal fluid tau and ptau181 increase with cortical amyloid deposition in cognitively normal individuals: Implications for future clinical trials of Alzheimer's disease , 2009, EMBO molecular medicine.

[25]  E. Duchesnay,et al.  Longitudinal brain metabolic changes from amnestic Mild Cognitive Impairment to Alzheimer's disease , 2009, NeuroImage.

[26]  C. Jack,et al.  MRI and CSF biomarkers in normal, MCI, and AD subjects , 2009, Neurology.

[27]  Norbert Schuff,et al.  Measurement of MRI scanner performance with the ADNI phantom. , 2009, Medical physics.

[28]  Sirkka Goebeler,et al.  Apolipoprotein E–dependent accumulation of Alzheimer disease–related lesions begins in middle age , 2009, Annals of neurology.

[29]  G Forster,et al.  Hippocampal tau pathology is related to neuroanatomical connections: an ageing population-based study. , 2009, Brain : a journal of neurology.

[30]  Bedda L. Rosario,et al.  Consideration of Optimal Time Window for Pittsburgh Compound B PET Summed Uptake Measurements , 2009, Journal of Nuclear Medicine.

[31]  W. Jagust,et al.  An inverse association of cardiovascular risk and frontal lobe glucose metabolism , 2009, Neurology.

[32]  Scott A. Small,et al.  Linking Aβ and Tau in Late-Onset Alzheimer's Disease: A Dual Pathway Hypothesis , 2008, Neuron.

[33]  C. Jack,et al.  11C PiB and structural MRI provide complementary information in imaging of Alzheimer's disease and amnestic mild cognitive impairment. , 2008, Brain : a journal of neurology.

[34]  V. Pankratz,et al.  The Mayo Clinic Study of Aging: Design and Sampling, Participation, Baseline Measures and Sample Characteristics , 2008, Neuroepidemiology.

[35]  A. Fagan,et al.  Cerebrospinal fluid tau/beta-amyloid(42) ratio as a prediction of cognitive decline in nondemented older adults. , 2007, Archives of neurology.

[36]  Chris Zarow,et al.  Cognitive impact of subcortical vascular and Alzheimer's disease pathology , 2006, Annals of neurology.

[37]  S. DeKosky,et al.  Simplified quantification of Pittsburgh Compound B amyloid imaging PET studies: a comparative analysis. , 2005, Journal of nuclear medicine : official publication, Society of Nuclear Medicine.

[38]  C. Jack,et al.  Brain atrophy rates predict subsequent clinical conversion in normal elderly and amnestic MCI , 2005, Neurology.

[39]  Karl J. Friston,et al.  Unified segmentation , 2005, NeuroImage.

[40]  S. DeKosky,et al.  Kinetic Modeling of Amyloid Binding in Humans using PET Imaging and Pittsburgh Compound-B , 2005, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[41]  Keith A. Johnson,et al.  Neuropathology of Cognitively Normal Elderly , 2003, Journal of neuropathology and experimental neurology.

[42]  N. Tzourio-Mazoyer,et al.  Automated Anatomical Labeling of Activations in SPM Using a Macroscopic Anatomical Parcellation of the MNI MRI Single-Subject Brain , 2002, NeuroImage.

[43]  A. Dale,et al.  Whole Brain Segmentation Automated Labeling of Neuroanatomical Structures in the Human Brain , 2002, Neuron.

[44]  C. Jack,et al.  FLAIR histogram segmentation for measurement of leukoaraiosis volume , 2001, Journal of magnetic resonance imaging : JMRI.

[45]  Karl J. Friston,et al.  Voxel-Based Morphometry—The Methods , 2000, NeuroImage.

[46]  J. Morris,et al.  Tangles and plaques in nondemented aging and “preclinical” Alzheimer's disease , 1999, Annals of neurology.

[47]  C. Jack,et al.  MR‐based hippocampal volumetry in the diagnosis of Alzheimer's disease , 1992, Neurology.

[48]  Denise C. Park,et al.  Toward defining the preclinical stages of Alzheimer's disease: Recommendations from the National Institute on Aging and the Alzheimer's Association workgroup , 2011 .

[49]  A. Bonnet,et al.  [The Unified Parkinson's Disease Rating Scale]. , 2000, Revue neurologique.

[50]  H. Braak,et al.  Argyrophilic grain disease: frequency of occurrence in different age categories and neuropathological diagnostic criteria , 1998, Journal of Neural Transmission.