Honors & Awards

  • Dean of Medicine's Postdoctoral Fellowship, Stanford University (2018)

Professional Education

  • Doctor of Philosophy, McGill University (2016)
  • Master of Science, McGill University, Psychology (2011)
  • Bachelor of Science, Dalhousie University, Neuroscience and Biology (2008)

Stanford Advisors

Research & Scholarship

Current Research and Scholarly Interests

Single-cell transcriptomic profiling of immune cells in Alzheimer's disease brain

Alzheimer's disease, Parkinson's disease and multiple sclerosis biomarkers

Alzheimer?s disease experimental therapeutics


All Publications

  • Intraneuronal Amyloid Beta Accumulation Disrupts Hippocampal CRTC1-Dependent Gene Expression and Cognitive Function in a Rat Model of Alzheimer Disease CEREBRAL CORTEX Wilson, E. N., Abela, A. R., Do Carmo, S., Allard, S., Marks, A. R., Welikovitch, L. A., Ducatenzeiler, A., Chudasama, Y., Cuello, A. C. 2017; 27 (2): 1501-1511
  • BACE1 inhibition by microdose lithium formulation NP03 rescues memory loss and early stage amyloid neuropathology Translational Psychiatry Wilson, E. N., Do Carmo, S., Iulita, M., Hall, H., Ducatenzeiler, A., Marks, A. R., Allard, S., Jia, D., Windheim, J., Cuello, A. C. 2017; 7: 1-10

    View details for DOI 10.1038/tp.2017.169

  • PGE(2) signaling via the neuronal EP2 receptor increases injury in a model of cerebral ischemia PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA Liu, Q., Liang, X., Wang, Q., Wilson, E. N., Lam, R., Wang, J., Kong, W., Tsai, C., Pan, T., Larkin, P. B., Shamloo, M., Andreasson, K. I. 2019; 116 (20): 10019?24
  • Peripheral TREM1 responses to brain and intestinal immunogens amplify stroke severity Nature Immunology Liu, Q., Johnson, E., et al 2019
  • Microdose Lithium NP03 Diminishes Pre-Plaque Oxidative Damage and Neuroinflammation in a Rat Model of Alzheimer?s-like Amyloidosis Current Alzheimer Research Wilson, E. N., Do Carmo, S., Iulita, M., Hall, H., Austin, G. L., Jia, D., Malcolm, J. C., Foret, M. K., Marks, A. R., Butterfield, D., Cuello, A. 2018
  • Differential deregulation of NGF and BDNF neurotrophins in a transgenic rat model of Alzheimer's disease Neurobiology of Disease Iulita, M., Bistué Millón, M., Pentz, R., Aguilar, L., Do Carmo, S., Allard, S., Michalski, B., Wilson, E. N., Ducatenzeiler, A., Bruno, M. A., Fahnestock, M., Cuello, A. 2017: 307?23


    Evidence from human neuropathological studies indicates that the levels of the neurotrophins nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are compromised in Alzheimer's disease. However, the causes and temporal (pathology-dependent) evolution of these alterations are not completely understood. To elucidate these issues, we investigated the McGill-R-Thy1-APP transgenic rat, which exhibits progressive intracellular and extracellular amyloid-beta (A?) pathology and ensuing cognitive deficits. Neurochemical analyses revealed a differential dysregulation of NGF and BDNF transcripts and protein expression. While BDNF mRNA levels were significantly reduced at very early stages of amyloid pathology, before plaques appeared, there were no changes in NGF mRNA expression even at advanced stages. Paradoxically, the protein levels of the NGF precursor were increased. These changes in neurotrophin expression are identical to those seen during the progression of Alzheimer's disease. At advanced pathological stages, deficits in the protease cascade controlling the maturation and degradation of NGF were evident in McGill transgenic rats, in line with the paradoxical upregulation of proNGF, as seen in Alzheimer's disease, in the absence of changes in NGF mRNA. The compromise in NGF metabolism and BDNF levels was accompanied by downregulation of cortical cholinergic synapses; strengthening the evidence that neurotrophin dysregulation affects cholinergic synapses and synaptic plasticity. Our findings suggest a differential temporal deregulation of NGF and BDNF neurotrophins, whereby deficits in BDNF mRNA appear at early stages of intraneuronal A? pathology, before alterations in NGF metabolism and cholinergic synapse loss manifest.

    View details for DOI 10.1016/j.nbd.2017.08.019

  • Longitudinal testing of hippocampal plasticity reveals the onset and maintenance of endogenous human Aß-induced synaptic dysfunction in individual freely behaving pre-plaque transgenic rats: rapid reversal by anti-Aß agents. Acta neuropathologica communications Qi, Y., Klyubin, I., Harney, S. C., Hu, N., Cullen, W. K., Grant, M. K., Steffen, J., Wilson, E. N., Do Carmo, S., Remy, S., Fuhrmann, M., Ashe, K. H., Cuello, A. C., Rowan, M. J. 2014; 2: 175-?


    Long before synaptic loss occurs in Alzheimer's disease significant harbingers of disease may be detected at the functional level. Here we examined if synaptic long-term potentiation is selectively disrupted prior to extracellular deposition of Aß in a very complete model of Alzheimer's disease amyloidosis, the McGill-R-Thy1-APP transgenic rat. Longitudinal studies in freely behaving animals revealed an age-dependent, relatively rapid-onset and persistent inhibition of long-term potentiation without a change in baseline synaptic transmission in the CA1 area of the hippocampus. Thus the ability of a standard 200 Hz conditioning protocol to induce significant NMDA receptor-dependent short- and long-term potentiation was lost at about 3.5 months of age and this deficit persisted for at least another 2-3 months, when plaques start to appear. Consistent with in vitro evidence for a causal role of a selective reduction in NMDA receptor-mediated synaptic currents, the deficit in synaptic plasticity in vivo was associated with a reduction in the synaptic burst response to the conditioning stimulation and was overcome using stronger 400 Hz stimulation. Moreover, intracerebroventricular treatment for 3 days with an N-terminally directed monoclonal anti- human Aß antibody, McSA1, transiently reversed the impairment of synaptic plasticity. Similar brief treatment with the BACE1 inhibitor LY2886721 or the ?-secretase inhibitor MRK-560 was found to have a comparable short-lived ameliorative effect when tracked in individual rats. These findings provide strong evidence that endogenously generated human Aß selectively disrupts the induction of long-term potentiation in a manner that enables potential therapeutic options to be assessed longitudinally at the pre-plaque stage of Alzheimer's disease amyloidosis.

    View details for DOI 10.1186/s40478-014-0175-x

    View details for PubMedID 25540024

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