Early neuroinflammation is associated with lower amyloid and tau levels in cognitively normal older adults

[1]  D. Wilcock,et al.  The Important Interface Between Apolipoprotein E and Neuroinflammation in Alzheimer’s Disease , 2020, Frontiers in Immunology.

[2]  A. Fagan,et al.  APOE4 leads to blood-brain barrier dysfunction predicting cognitive decline , 2020, Nature.

[3]  Muhammad Naveed Iqbal Qureshi,et al.  Association of Apolipoprotein E ε4 With Medial Temporal Tau Independent of Amyloid-β. , 2019, JAMA neurology.

[4]  David T. Jones,et al.  Tau-positron emission tomography correlates with neuropathology findings , 2019, Alzheimer's & Dementia.

[5]  O. Hansson,et al.  Staging β-Amyloid Pathology With Amyloid Positron Emission Tomography. , 2019, JAMA neurology.

[6]  William J. Jagust,et al.  Effect of Off-Target Binding on 18F-Flortaucipir Variability in Healthy Controls Across the Life Span , 2019, The Journal of Nuclear Medicine.

[7]  P. Selnes,et al.  Glial activation and inflammation along the Alzheimer’s disease continuum , 2019, Journal of Neuroinflammation.

[8]  A. Fagan,et al.  Blood-brain barrier breakdown is an early biomarker of human cognitive dysfunction , 2018, Nature Medicine.

[9]  I. Marriott,et al.  The Interleukin-10 Family of Cytokines and Their Role in the CNS , 2018, Front. Cell. Neurosci..

[10]  H. Pereira,et al.  The role of neutrophil granule proteins in neuroinflammation and Alzheimer’s disease , 2018, Journal of Neuroinflammation.

[11]  K. Blennow,et al.  CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early Alzheimer disease , 2018, Neurology.

[12]  D. Brooks,et al.  Microglial activation correlates in vivo with both tau and amyloid in Alzheimer’s disease , 2018, Brain : a journal of neurology.

[13]  A. Robinson,et al.  Inflammatory pathology markers (activated microglia and reactive astrocytes) in early and late onset Alzheimer disease: a post mortem study , 2018, Neuropathology and applied neurobiology.

[14]  F. Jessen,et al.  Characterization and clinical use of inflammatory cerebrospinal fluid protein markers in Alzheimer’s disease , 2018, Alzheimer's Research & Therapy.

[15]  R. Bazinet,et al.  Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review , 2017, Molecular Psychiatry.

[16]  G. Chételat,et al.  Increased florbetapir binding in the temporal neocortex from age 20 to 60 years , 2017, Neurology.

[17]  B. Pollock,et al.  Imaging microglial activation and amyloid burden in amnestic mild cognitive impairment , 2017, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[18]  Keith A. Johnson,et al.  Lessons learned about [F-18]-AV-1451 off-target binding from an autopsy-confirmed Parkinson’s case , 2017, Acta Neuropathologica Communications.

[19]  W. Jagust,et al.  Considerations and code for partial volume correcting [18F]-AV-1451 tau PET data , 2017, Data in brief.

[20]  A. Fagan,et al.  ApoE4 markedly exacerbates tau-mediated neurodegeneration in a mouse model of tauopathy , 2017, Nature.

[21]  Paul Edison,et al.  Brain inflammation accompanies amyloid in the majority of mild cognitive impairment cases due to Alzheimer’s disease , 2017, Brain : a journal of neurology.

[22]  Wei Tang,et al.  APOE ε4 allele elevates the expressions of inflammatory factors and promotes Alzheimer’s disease progression: A comparative study based on Han and She populations in the Wenzhou area , 2017, Brain Research Bulletin.

[23]  Paul Edison,et al.  An early and late peak in microglial activation in Alzheimer’s disease trajectory , 2017, Brain : a journal of neurology.

[24]  A. Nobre,et al.  Sex and APOE: A memory advantage in male APOE ε4 carriers in midlife , 2017, Cortex.

[25]  M. Mintun,et al.  Relationships between flortaucipir PET tau binding and amyloid burden, clinical diagnosis, age and cognition , 2017, Brain : a journal of neurology.

[26]  U. Sengupta,et al.  Tau Oligomers Associate with Inflammation in the Brain and Retina of Tauopathy Mice and in Neurodegenerative Diseases , 2016, Journal of Alzheimer's disease : JAD.

[27]  A. Fagan,et al.  Evaluation of Tau Imaging in Staging Alzheimer Disease and Revealing Interactions Between β-Amyloid and Tauopathy. , 2016, JAMA neurology.

[28]  Olivier Colliot,et al.  Early and protective microglial activation in Alzheimer's disease: a prospective study using 18F-DPA-714 PET imaging. , 2016, Brain : a journal of neurology.

[29]  Daniel R. Schonhaut,et al.  PET Imaging of Tau Deposition in the Aging Human Brain , 2016, Neuron.

[30]  D. Bredesen,et al.  Direct Transcriptional Effects of Apolipoprotein E , 2016, The Journal of Neuroscience.

[31]  S. Gabbita,et al.  Oral TNFα Modulation Alters Neutrophil Infiltration, Improves Cognition and Diminishes Tau and Amyloid Pathology in the 3xTgAD Mouse Model , 2015, PloS one.

[32]  D. Catalucci,et al.  Neutrophils promote Alzheimer's disease–like pathology and cognitive decline via LFA-1 integrin , 2015, Nature Medicine.

[33]  Guixiang Xu,et al.  Reactive microglia drive tau pathology and contribute to the spreading of pathological tau in the brain. , 2015, Brain : a journal of neurology.

[34]  P. Blackshear,et al.  APOε4 is associated with enhanced in vivo innate immune responses in human subjects. , 2014, The Journal of allergy and clinical immunology.

[35]  M. Heneka,et al.  Body Fluid Cytokine Levels in Mild Cognitive Impairment and Alzheimer’s Disease: a Comparative Overview , 2014, Molecular Neurobiology.

[36]  W. Jagust,et al.  Apolipoprotein E, Not Fibrillar β-Amyloid, Reduces Cerebral Glucose Metabolism in Normal Aging , 2012, The Journal of Neuroscience.

[37]  W. Bowers,et al.  Ablation of TNF-RI/RII expression in Alzheimer's disease mice leads to an unexpected enhancement of pathology: implications for chronic pan-TNF-α suppressive therapeutic strategies in the brain. , 2011, The American journal of pathology.

[38]  Ashutosh,et al.  CXCL8 protects human neurons from amyloid-β-induced neurotoxicity: relevance to Alzheimer's disease. , 2011, Biochemical and biophysical research communications.

[39]  N. Zilka,et al.  Misfolded Truncated Protein τ Induces Innate Immune Response via MAPK Pathway , 2011, The Journal of Immunology.

[40]  Arno Klein,et al.  A reproducible evaluation of ANTs similarity metric performance in brain image registration , 2011, NeuroImage.

[41]  K. Blennow,et al.  Soluble TNF receptors are associated with Aβ metabolism and conversion to dementia in subjects with mild cognitive impairment , 2010, Neurobiology of Aging.

[42]  Brian B. Avants,et al.  The optimal template effect in hippocampus studies of diseased populations , 2010, NeuroImage.

[43]  D. Dickson,et al.  Massive gliosis induced by interleukin‐6 suppresses Aβ deposition in vivo: evidence against inflammation as a driving force for amyloid deposition , 2010, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[44]  M. Fasshauer,et al.  Amyloid precursor protein expression is induced by tumor necrosis factor α in 3T3‐L1 adipocytes , 2009, Journal of cellular biochemistry.

[45]  J. M. Gatt,et al.  The contribution of apolipoprotein E alleles on cognitive performance and dynamic neural activity over six decades , 2007, Biological Psychology.

[46]  J. Morris,et al.  The Uniform Data Set (UDS): Clinical and Cognitive Variables and Descriptive Data From Alzheimer Disease Centers , 2006, Alzheimer disease and associated disorders.

[47]  R. Elkon,et al.  Apolipoprotein E4 enhances brain inflammation by modulation of the NF-κB signaling cascade , 2005, Neurobiology of Disease.

[48]  S. Miller,et al.  Microglia Initiate Central Nervous System Innate and Adaptive Immune Responses through Multiple TLRs1 , 2004, The Journal of Immunology.

[49]  R. Maccioni,et al.  Interleukin-6 induces Alzheimer-type phosphorylation of tau protein by deregulating the cdk5/p35 pathway. , 2004, Experimental cell research.

[50]  K. Blennow,et al.  Intrathecal inflammation precedes development of Alzheimer’s disease , 2003, Journal of neurology, neurosurgery, and psychiatry.

[51]  Brian J Cummings,et al.  The Induction of the TNFα Death Domain Signaling Pathway in Alzheimer's Disease Brain , 2003, Neurochemical Research.

[52]  H. Hampel,et al.  Inflammatory repertoire of Alzheimer's disease and nondemented elderly microglia in vitro , 2001, Glia.

[53]  G L Shulman,et al.  INAUGURAL ARTICLE by a Recently Elected Academy Member:A default mode of brain function , 2001 .

[54]  K. Blennow,et al.  Intracerebral Production of Tumor Necrosis Factor-α, a Local Neuroprotective Agent, in Alzheimer Disease and Vascular Dementia , 1999, Journal of Clinical Immunology.

[55]  B. Sommer,et al.  Association of microglia with amyloid plaques in brains of APP23 transgenic mice. , 1999, The American journal of pathology.

[56]  Shuxian Hu,et al.  Cytokine regulation of human microglial cell IL-8 production. , 1998, Journal of immunology.

[57]  D. Dickson,et al.  The Pathogenesis of Senile Plaques , 1997, Journal of neuropathology and experimental neurology.

[58]  B. Hyman,et al.  Interleukin-8 receptor B immunoreactivity in brain and neuritic plaques of Alzheimer's disease. , 1997, The American journal of pathology.

[59]  M. Hüll,et al.  Occurrence of Interleukin‐6 in Cortical Plaques of Alzheimer's Disease Patients May Precede Transformation of Diffuse into Neuritic Plaques a , 1996, Annals of the New York Academy of Sciences.

[60]  W. März,et al.  Apolipoprotein E polymorphism influences not only cerebral senile plaque load but also Alzheimer-type neurofibrillary tangle formation , 1995, Neuroscience.

[61]  G. Forloni,et al.  Reciprocal control of inflammatory cytokines, IL-1 and IL-6, and β-amyloid production in cultures , 1995, Neuroscience Letters.

[62]  Paul L. Wood,et al.  Cytokine indices in Alzheimer's temporal cortex: no changes in mature IL-1β or IL-1RA but increases in the associated acute phase proteins IL-6, α2-macroglobulin and C-reactive protein , 1993, Brain Research.

[63]  J. Haines,et al.  Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families. , 1993, Science.

[64]  C. Cotman,et al.  Trophic effects of interleukin-4, -7 and -8 on hippocampal neuronal cultures: potential involvement of glial-derived factors , 1993, Brain Research.

[65]  R. Strieter,et al.  Interleukin-8 as a macrophage-derived mediator of angiogenesis. , 1992, Science.

[66]  A. Carè,et al.  Production of hemolymphopoietic cytokines (IL-6, IL-8, colony-stimulating factors) by normal human astrocytes in response to IL-1 beta and tumor necrosis factor-alpha. , 1992, Journal of immunology.

[67]  U. Schreiter-Gasser,et al.  Interleukin‐6 and α‐2‐macroglobulin indicate an acute‐phase state in Alzheimer's disease cortices , 1991, FEBS letters.

[68]  Keith A. Johnson,et al.  18F-Flortaucipir Binding in Choroid Plexus: Related to Race and Hippocampus Signal. , 2018, Journal of Alzheimer's disease : JAD.

[69]  Christopher G Schwarz,et al.  Widespread brain tau and its association with ageing, Braak stage and Alzheimer's dementia. , 2018, Brain : a journal of neurology.

[70]  Sterling C. Johnson,et al.  Cerebrospinal Fluid and Plasma Levels of Inflammation Differentially Relate to CNS Markers of Alzheimer's Disease Pathology and Neuronal Damage. , 2018, Journal of Alzheimer's disease : JAD.

[71]  Brian J Cummings,et al.  The induction of the TNFalpha death domain signaling pathway in Alzheimer's disease brain. , 2003, Neurochemical research.