Biblio
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“APOE predicts amyloid-beta but not tau Alzheimer pathology in cognitively normal aging.”, Ann Neurol, vol. 67, no. 1, pp. 122-31, 2010.
, “APOE predicts amyloid-beta but not tau Alzheimer pathology in cognitively normal aging.”, Ann Neurol, vol. 67, no. 1, pp. 122-31, 2010.
, “Tau in Alzheimer disease and related tauopathies.”, Curr Alzheimer Res, vol. 7, no. 8, pp. 656-64, 2010.
, “Tau in Alzheimer disease and related tauopathies.”, Curr Alzheimer Res, vol. 7, no. 8, pp. 656-64, 2010.
, “18F-THK523: a novel in vivo tau imaging ligand for Alzheimer's disease.”, Brain, vol. 134, no. Pt 4, pp. 1089-100, 2011.
, “Anti-aβ therapeutics in Alzheimer's disease: the need for a paradigm shift.”, Neuron, vol. 69, no. 2, pp. 203-13, 2011.
, “Caspase signalling controls microglia activation and neurotoxicity.”, Nature, vol. 472, no. 7343, pp. 319-24, 2011.
, “Evidence for ordering of Alzheimer disease biomarkers.”, Arch Neurol, vol. 68, no. 12, pp. 1526-35, 2011.
, “Neuronal basis of age-related working memory decline.”, Nature, vol. 476, no. 7359, pp. 210-3, 2011.
, “Pathogenic protein seeding in Alzheimer disease and other neurodegenerative disorders.”, Ann Neurol, vol. 70, no. 4, pp. 532-40, 2011.
, “Report of the task force on designing clinical trials in early (predementia) AD.”, Neurology, vol. 76, no. 3, pp. 280-6, 2011.
, “Soluble amyloid beta-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration.”, Proc Natl Acad Sci U S A, vol. 108, no. 14, pp. 5819-24, 2011.
, “Stages of the pathologic process in Alzheimer disease: age categories from 1 to 100 years.”, J Neuropathol Exp Neurol, vol. 70, no. 11, pp. 960-9, 2011.
, “Cerebrospinal fluid levels of β-amyloid 1-42, but not of tau, are fully changed already 5 to 10 years before the onset of Alzheimer dementia.”, Arch Gen Psychiatry, vol. 69, no. 1, pp. 98-106, 2012.
, “Cerebrospinal fluid levels of β-amyloid 1-42, but not of tau, are fully changed already 5 to 10 years before the onset of Alzheimer dementia.”, Arch Gen Psychiatry, vol. 69, no. 1, pp. 98-106, 2012.
, “Exercise Engagement as a Moderator of the Effects of APOE Genotype on Amyloid Deposition.”, Arch Neurol, vol. 69, no. 5, pp. 636-43, 2012.
, “Neuroinflammation, hyperphosphorylated tau, diffuse amyloid plaques, and down-regulation of the cellular prion protein in air pollution exposed children and young adults.”, J Alzheimers Dis, vol. 28, no. 1, pp. 93-107, 2012.
, “An operational approach to National Institute on Aging-Alzheimer's Association criteria for preclinical Alzheimer disease.”, Ann Neurol, vol. 71, no. 6, pp. 765-75, 2012.
, “Propagation of tau pathology in a model of early Alzheimer's disease.”, Neuron, vol. 73, no. 4, pp. 685-97, 2012.
, “Propagation of tau pathology in a model of early Alzheimer's disease.”, Neuron, vol. 73, no. 4, pp. 685-97, 2012.
, “Anti-amyloid β autoantibodies in cerebral amyloid angiopathy-related inflammation: implications for amyloid-modifying therapies.”, Ann Neurol, vol. 73, no. 4, pp. 449-58, 2013.
, “Tracking pathophysiological processes in Alzheimer's disease: an updated hypothetical model of dynamic biomarkers.”, Lancet Neurol, vol. 12, no. 2, pp. 207-16, 2013.
, “C9orf72 nucleotide repeat structures initiate molecular cascades of disease.”, Nature, vol. 507, no. 7491, pp. 195-200, 2014.
, “Phase 3 trials of solanezumab for mild-to-moderate Alzheimer's disease.”, N Engl J Med, vol. 370, no. 4, pp. 311-21, 2014.
, “Phase 3 trials of solanezumab for mild-to-moderate Alzheimer's disease.”, N Engl J Med, vol. 370, no. 4, pp. 311-21, 2014.
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