Iman Jaljuli

All Publications

• Amygdala electrical-finger-print (AmygEFP) NeuroFeedback guided by individually-tailored Trauma script for post-traumatic stress disorder: Proof-of-concept NEUROIMAGE-CLINICAL Fruchtman-Steinbok, T., Keynan, J. N., Cohen, A., Jaljuli, I., Mermelstein, S., Drori, G., Routledge, E., Krasnoshtein, M., Playle, R., Linden, D. J., Hendler, T. 2021; 32: 102859

  Abstract

  Amygdala activity dysregulation plays a central role in post-traumatic stress disorder (PTSD). Hence learning to self-regulate one's amygdala activity may facilitate recovery. PTSD is further characterized by abnormal contextual processing related to the traumatic memory. Therefore, provoking the personal traumatic narrative while training amygdala down-regulation could enhance clinical efficacy. We report the results of a randomized controlled trial (NCT02544971) of a novel self-neuromodulation procedure (i.e. NeuroFeedback) for PTSD, aimed at down-regulating limbic activity while receiving feedback from an auditory script of a personal traumatic narrative. To scale-up applicability, neural activity was probed by an fMRI-informed EEG model of amygdala activity, termed Amygdala Electrical Finger-Print (AmygEFP).Fifty-nine adults meeting DSM-5 criteria for PTSD were randomized between three groups: Trauma-script feedback interface (Trauma-NF) or Neutral feedback interface (Neutral-NF), and a control group of No-NF (to control for spontaneous recovery). Before and immediately after 15 NF training sessions patients were blindly assessed for PTSD symptoms and underwent one session of amygdala fMRI-NF for transferability testing. Follow-up clinical assessment was performed at 3- and 6-months following NF treatment.Patients in both NF groups learned to volitionally down-regulate AmygEFP signal and demonstrated a greater reduction in PTSD symptoms and improved down-regulation of the amygdala during fMRI-NF, compared to the No-NF group. The Trauma-NF group presented the largest immediate clinical improvement.This proof-of-concept study indicates the feasibility of the AmygEFP-NF process-driven as a scalable intervention for PTSD and illustrates its clinical potential. Further investigation is warranted to elucidate the contribution of AmygEFP-NF beyond exposure and placebo effects.

  View details for DOI 10.1016/j.nicl.2021.102859

  View details for Web of Science ID 000712127900004

  View details for PubMedID 34689055

  View details for PubMedCentralID PMC8551212

• Single Cell ADNP Predictive of Human Muscle Disorders: Mouse Knockdown Results in Muscle Wasting. Cells Kapitansky, O., Karmon, G., Sragovich, S., Hadar, A., Shahoha, M., Jaljuli, I., Bikovski, L., Giladi, E., Palovics, R., Iram, T., Gozes, I. 2020; 9 (10)

  Abstract

  Activity-dependent neuroprotective protein (ADNP) mutations are linked with cognitive dysfunctions characterizing the autistic-like ADNP syndrome patients, who also suffer from delayed motor maturation. We thus hypothesized that ADNP is deregulated in versatile myopathies and that local ADNP muscle deficiency results in myopathy, treatable by the ADNP fragment NAP. Here, single-cell transcriptomics identified ADNP as a major constituent of the developing human muscle. ADNP transcript concentrations further predicted multiple human muscle diseases, with concentrations negatively correlated with the ADNP target interacting protein, microtubule end protein 1 (EB1). Reverting back to modeling at the single-cell level of the male mouse transcriptome, Adnp mRNA concentrations age-dependently correlated with motor disease as well as with sexual maturation gene transcripts, while Adnp expressing limb muscle cells significantly decreased with aging. Mouse Adnp heterozygous deficiency exhibited muscle microtubule reduction and myosin light chain (Myl2) deregulation coupled with motor dysfunction. CRISPR knockdown of adult gastrocnemius muscle Adnp in a Cas9 mouse resulted in treadmill (male) and gait (female) dysfunctions that were specifically ameliorated by treatment with the ADNP snippet, microtubule interacting, Myl2-regulating, NAP (CP201). Taken together, our studies provide new hope for personalized diagnosis/therapeutics in versatile myopathies.

  View details for DOI 10.3390/cells9102320

  View details for PubMedID 33086621