1. Network-driven plasma proteomics expose molecular changes in the Alzheimer's brain.

    Molecular Neurodegeneration 11(1):31 (2016) PMID 27112350 PMCID PMC4845325

    Biological pathways that significantly contribute to sporadic Alzheimer's disease are largely unknown and cannot be observed directly. Cognitive symptoms appear only decades after the molecular disease onset, further complicating analyses. As a consequence, molecular research is often restricted...
  2. Maternal immune activation and abnormal brain development across CNS disorders.

    Nature Clinical Practice Neurology 10(11):643 (2014) PMID 25311587

    Epidemiological studies have shown a clear association between maternal infection and schizophrenia or autism in the progeny. Animal models have revealed maternal immune activation (mIA) to be a profound risk factor for neurochemical and behavioural abnormalities in the offspring. Microglial pri...
  3. Mind the gut: secretion of α-synuclein by enteric neurons.

    Journal of Neurochemistry 125(4):487 (2013) PMID 23448303

  4. Inflammation and α-synuclein's prion-like behavior in Parkinson's disease--is there a link?

    Molecular Neurobiology 47(2):561 (2013) PMID 22544647 PMCID PMC3589652

    Parkinson's disease patients exhibit progressive spreading of aggregated α-synuclein in the nervous system. This slow process follows a specific pattern in an inflamed tissue environment. Recent research suggests that prion-like mechanisms contribute to the propagation of α-synuclein pathology. ...
  5. Colony-stimulating factor 1 receptor (CSF1R) signaling in injured neurons facilitates protection and survival.

    Journal of Experimental Medicine 210(1):157 (2013) PMID 23296467 PMCID PMC3549715

    Colony-stimulating factor 1 (CSF1) and interleukin-34 (IL-34) are functional ligands of the CSF1 receptor (CSF1R) and thus are key regulators of the monocyte/macrophage lineage. We discovered that systemic administration of human recombinant CSF1 ameliorates memory deficits in a transgenic mouse...
  6. Post-marketing assessment of neuropsychiatric adverse events in influenza patients treated with oseltamivir: an updated review.

    Advances in Therapy 29(10):826 (2012) PMID 23054689

    A 2008 review by our group concluded that the risk of neuropsychiatric adverse events (NPAEs) in influenza patients was not increased by oseltamivir exposure, and did not identify any mechanism by which oseltamivir or its metabolites could cause or worsen such events. The current article reviews...
  7. Heparan sulfate subdomains that are degraded by Sulf accumulate in cerebral amyloid ß plaques of Alzheimer's disease: evidence from mouse models and patients.

    The American Journal of Pathology 180(5):2056 (2012) PMID 22429964

    Alzheimer's disease (AD) is characterized by extracellular cerebral accumulation of amyloid β peptide (Aβ). Heparan sulfate (HS) is a glycosaminoglycan that is abundant in the extracellular space. The state of sulfation within the HS chain influences its ability to interact with a variety of pro...
  8. Deficiency of terminal complement pathway inhibitor promotes neuronal tau pathology and degeneration in mice.

    Journal of neuroinflammation 9:220 (2012) PMID 22989354 PMCID PMC3511294

    The neuronal microtubule-associated protein tau becomes hyperphosphorylated and forms aggregates in tauopathies but the processes leading to this pathological hallmark are not understood. Because tauopathies are accompanied by neuroinflammation and the complement cascade forms a key innate immun...
  9. Modeling of pathological traits in Alzheimer's disease based on systemic extracellular signaling proteome.

    Molecular & Cellular Proteomics 10(10):M111.008862 (2011) PMID 21742799 PMCID PMC3205866

    The study of chronic brain diseases including Alzheimer's disease in patients is typically limited to brain imaging or psychometric testing. Given the epidemic rise and insufficient knowledge about pathological pathways in sporadic Alzheimer's disease, new tools are required to identify the mole...
  10. The ageing systemic milieu negatively regulates neurogenesis and cognitive function.

    Nature 477(7362):90 (2011) PMID 21886162 PMCID PMC3170097

    In the central nervous system, ageing results in a precipitous decline in adult neural stem/progenitor cells and neurogenesis, with concomitant impairments in cognitive functions. Interestingly, such impairments can be ameliorated through systemic perturbations such as exercise. Here, using hete...
  11. Complement receptor 2 is expressed in neural progenitor cells and regulates adult hippocampal neurogenesis.

    Journal of Neuroscience 31(11):3981 (2011) PMID 21411641 PMCID PMC3071463

    Injury and inflammation are potent regulators of adult neurogenesis. As the complement system forms a key immune pathway that may also exert critical functions in neural development and neurodegeneration, we asked whether complement receptors regulate neurogenesis. We discovered that complement ...
  12. Blood protein signature for the early diagnosis of Alzheimer disease.

    Archives of Neurology 66(2):161 (2009) PMID 19064741

    Alzheimer disease (AD) has become one of the main health concerns for the elderly population in the United States. Current treatments target symptoms only, but several advanced clinical trials are testing new drugs that are potentially disease modifying. Because AD is still difficult to diagnose...
  13. The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid beta accumulation in mice.

    Journal of Clinical Investigation 118(6):2190 (2008) PMID 18497889 PMCID PMC2391284

    Autophagy is the principal cellular pathway for degradation of long-lived proteins and organelles and regulates cell fate in response to stress. Recently, autophagy has been implicated in neurodegeneration, but whether it is detrimental or protective remains unclear. Here we report that beclin 1...
  14. P2-294: Microarray profiling reveals autoantibody reactivities against abnormal amyloid peptide conformations decline with age and in Alzheimer's disease

    Alzheimer's & Dementia 4(4):T458 (2008)

  15. Classification and prediction of clinical Alzheimer's diagnosis based on plasma signaling proteins.

    Nature Medicine 13(11):1359 (2007) PMID 17934472

    A molecular test for Alzheimer's disease could lead to better treatment and therapies. We found 18 signaling proteins in blood plasma that can be used to classify blinded samples from Alzheimer's and control subjects with close to 90% accuracy and to identify patients who had mild cognitive impa...
  16. Cross-reactivity patterns of T cells specific for iodinated contrast media.

    Journal of Allergy and Clinical Immunology 119(6):1529 (2007) PMID 17412404

    Approximately 3% of patients exposed to iodinated contrast media develop delayed hypersensitivity reactions. We wanted to better understand the molecular basis of contrast media cross-reactivity. Cross-reactivity was assessed by skin testing and measurement of T-cell activation (CD69 upregulatio...
  17. Immune cells may fend off Alzheimer disease.

    Nature Medicine 13(4):408 (2007) PMID 17415372

  18. Cross-reactivity patterns of T cells specific for iodinated contrast media

    Journal of Allergy and Clinical Immunology 119(6):1529 (2007)

    Background Approximately 3% of patients exposed to iodinated contrast media develop delayed hypersensitivity reactions.
  19. Systemic and Acquired Immune Responses in Alzheimer's Disease

    International Review of Neurobiology 82:205 (2007)

    Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by a progressive cognitive decline and dementia. AD brains are marked by amyloid plaques and neurofibrillary tangles, neuronal cell loss, and a prominent activation of glial cells, and innate immune respo...
  20. Systemic and acquired immune responses in Alzheimer's disease.

    International Review of Neurobiology 82:205 (2007) PMID 17678963

    Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by a progressive cognitive decline and dementia. AD brains are marked by amyloid plaques and neurofibrillary tangles, neuronal cell loss, and a prominent activation of glial cells, and innate immune responses. A gr...