Erica Jensen

All Publications

• Distinct predictors of short- versus long-term depression outcomes following electroconvulsive therapy. Journal of psychiatric research Mickey, B. J., Ginsburg, Y., Jensen, E., Maixner, D. F. 2022; 145: 159-166

  Abstract

  Patients and clinicians considering electroconvulsive therapy (ECT) for treatment-resistant depression are faced with limited information about the likely long-term outcomes, and the individual characteristics that predict those outcomes. We aimed to identify sociodemographic and clinical predictors of acute ECT response and subsequent long-term depression severity. This prospective longitudinal study followed adult patients at a single academic ECT center. Among 114 participants, 105 completed an index ECT series and 70 were classified as acute ECT responders. Over a 2-year follow-up period, 82 subjects provided data on depression severity (Patient Health Questionnaire; PHQ-9). Better acute ECT response was predicted by less medication resistance, shorter index episode, and psychotic features (p < 0.05). PHQ-9 scores during the two-year follow-up period improved from baseline at all time points (p < 0.000001) but individual scores varied widely. Lower long-term PHQ-9 scores were predicted by better acute therapeutic response to ECT (p = 0.004) but not by ECT adverse effects (p > 0.05). Married status and greater baseline clinician-rated severity were not associated with acute ECT response but those variables did predict lower PHQ-9 scores longitudinally (p < 0.001), independent of other baseline features, initial ECT response, or intensity of ongoing treatment. These findings confirm previously identified predictors of short-term ECT response and demonstrate that distinct individual characteristics predict long-term depression outcomes. An individual's social context appears to strongly influence long-term but not short-term outcomes, suggesting a potential target for post-ECT therapeutic interventions.

  View details for DOI 10.1016/j.jpsychires.2021.12.028

  View details for PubMedID 34923356

  View details for PubMedCentralID PMC9192826

• Long-term quality of life in treatment-resistant depression after electroconvulsive therapy. Journal of affective disorders Lex, H., Nevers, S. W., Jensen, E. L., Ginsburg, Y., Maixner, D. F., Mickey, B. J. 2021; 291: 135-139

  Abstract

  Electroconvulsive therapy (ECT) is highly effective for treatment-resistant depression (TRD), and previous studies have demonstrated short-term improvements in quality of life (QoL) after ECT.  However, long-term QoL after ECT has not been studied, and the baseline patient characteristics that predict long-term QoL remain unknown.Seventy-nine subjects with unipolar or bipolar TRD were enrolled in this prospective longitudinal observational study. Physical, psychological, social, and environmental QoL domains were measured with the abbreviated World Health Organization Quality of Life scale (WHOQOL-BREF) at baseline and every 6 months for up to 2 years after ECT.  Baseline sociodemographic and clinical features were tested for association with long-term QoL.Long-term follow-up data were available from 49 participants.  Relative to baseline, average psychological and physical QoL improved during the follow-up period (Hedges' effect size: 0.27-0.83).  About 40-50% of individuals experienced clinically meaningful improvement.  Subjects with better initial antidepressant response with ECT reported better QoL over the subsequent two years.  Long-term QoL improved most among individuals who were married, those without disability status, and those with psychotic features or shorter depressive episodes at baseline.Participants were from a single US academic center and mainly of European ancestry, so findings may not generalize to other settings or ethnicities.  The observational design does not allow causal inferences.Long-term psychological and physical QoL outcomes vary widely after ECT. Individuals with the best outcomes are those who respond well to ECT initially, married people, and those with a less chronic course of illness.

  View details for DOI 10.1016/j.jad.2021.05.012

  View details for PubMedID 34038830

  View details for PubMedCentralID PMC8628522

• Kinesin-1 regulates synaptic strength by mediating the delivery, removal, and redistribution of AMPA receptors. Neuron Hoerndli, F. J., Maxfield, D. A., Brockie, P. J., Mellem, J. E., Jensen, E., Wang, R., Madsen, D. M., Maricq, A. V. 2013; 80 (6): 1421-37

  Abstract

  A primary determinant of the strength of neurotransmission is the number of AMPA-type glutamate receptors (AMPARs) at synapses. However, we still lack a mechanistic understanding of how the number of synaptic AMPARs is regulated. Here, we show that UNC-116, the C. elegans homolog of vertebrate kinesin-1 heavy chain (KIF5), modifies synaptic strength by mediating the rapid delivery, removal, and redistribution of synaptic AMPARs. Furthermore, by studying the real-time transport of C. elegans AMPAR subunits in vivo, we demonstrate that although homomeric GLR-1 AMPARs can diffuse to and accumulate at synapses in unc-116 mutants, glutamate-gated currents are diminished because heteromeric GLR-1/GLR-2 receptors do not reach synapses in the absence of UNC-116/KIF5-mediated transport. Our data support a model in which ongoing motor-driven delivery and removal of AMPARs controls not only the number but also the composition of synaptic AMPARs, and thus the strength of synaptic transmission.

  View details for DOI 10.1016/j.neuron.2013.10.050

  View details for PubMedID 24360545

  View details for PubMedCentralID PMC3933021

• Cornichons control ER export of AMPA receptors to regulate synaptic excitability. Neuron Brockie, P. J., Jensen, M., Mellem, J. E., Jensen, E., Yamasaki, T., Wang, R., Maxfield, D., Thacker, C., Hoerndli, F., Dunn, P. J., Tomita, S., Madsen, D. M., Maricq, A. V. 2013; 80 (1): 129-42

  Abstract

  The strength of synaptic communication at central synapses depends on the number of ionotropic glutamate receptors, particularly the class gated by the agonist AMPA (AMPARs). Cornichon proteins, evolutionarily conserved endoplasmic reticulum cargo adaptors, modify the properties of vertebrate AMPARs when coexpressed in heterologous cells. However, the contribution of cornichons to behavior and in vivo nervous system function has yet to be determined. Here, we take a genetic approach to these questions by studying CNI-1--the sole cornichon homolog in C. elegans. cni-1 mutants hyperreverse, a phenotype associated with increased glutamatergic synaptic transmission. Consistent with this behavior, we find larger glutamate-gated currents in cni-1 mutants with a corresponding increase in AMPAR number. Furthermore, we observe opposite phenotypes in transgenic worms that overexpress CNI-1 or vertebrate homologs. In reconstitution studies, we provide support for an evolutionarily conserved role for cornichons in regulating the export of vertebrate and invertebrate AMPARs.

  View details for DOI 10.1016/j.neuron.2013.07.028

  View details for PubMedID 24094107

  View details for PubMedCentralID PMC3795439

• Wnt signaling regulates acetylcholine receptor translocation and synaptic plasticity in the adult nervous system. Cell Jensen, M., Hoerndli, F. J., Brockie, P. J., Wang, R., Johnson, E., Maxfield, D., Francis, M. M., Madsen, D. M., Maricq, A. V. 2012; 149 (1): 173-87

  Abstract

  The adult nervous system is plastic, allowing us to learn, remember, and forget. Experience-dependent plasticity occurs at synapses--the specialized points of contact between neurons where signaling occurs. However, the mechanisms that regulate the strength of synaptic signaling are not well understood. Here, we define a Wnt-signaling pathway that modifies synaptic strength in the adult nervous system by regulating the translocation of one class of acetylcholine receptors (AChRs) to synapses. In Caenorhabditis elegans, we show that mutations in CWN-2 (Wnt ligand), LIN-17 (Frizzled), CAM-1 (Ror receptor tyrosine kinase), or the downstream effector DSH-1 (disheveled) result in similar subsynaptic accumulations of ACR-16/α7 AChRs, a consequent reduction in synaptic current, and predictable behavioral defects. Photoconversion experiments revealed defective translocation of ACR-16/α7 to synapses in Wnt-signaling mutants. Using optogenetic nerve stimulation, we demonstrate activity-dependent synaptic plasticity and its dependence on ACR-16/α7 translocation mediated by Wnt signaling via LIN-17/CAM-1 heteromeric receptors.

  View details for DOI 10.1016/j.cell.2011.12.038

  View details for PubMedID 22464329

  View details for PubMedCentralID PMC3375111