About

Dr. Alex Y. Bekker is an internationally recognized expert in neuroanesthesia, serving as Professor and Chair of the Department of Physiology and Pharmacology at Rutgers New Jersey Medical School, as well as Chief of Service at University Hospital's Department of Anesthesiology. His research has focused on perioperative brain protection, neuroinflammation, and clinical pharmacology, with a significant body of work including 92 peer-reviewed publications, 6 US patents, 32 educational reviews, and over 100 abstracts. Dr. Bekker has been a principal investigator in numerous clinical trials, including studies sponsored by the National Institute of Aging, and actively contributes to the scientific community through his role on the editorial board of the Journal of Neurosurgical Anesthesiology and as an ad hoc reviewer for several prestigious journals such as NEJM, Anesthesiology, Neurosurgery, and Anesthesia and Analgesia. His expertise encompasses anesthesia for neurosurgery, geriatric anesthesia, and postoperative pain management, and he is frequently invited to speak at Grand Rounds and scientific panels worldwide.

Research topics

• Medicine
• Anesthesia
• Neuroscience
• Biology
• Genetics
• Pharmacology
• Internal medicine
• Bioinformatics
• Physical therapy
• Endocrinology
• Chemistry
• Cancer research
• Cell biology
• Biochemistry

Selected publications

• Contribution of proneurotrophin-3 to nerve trauma-induced neuropathic pain through promoting TrkC-mediated increase of CCL2 in primary sensory neurons

  Brain Behavior and Immunity · 2026-01-06

  articleOpen access

  Neuropathic pain induced by nerve trauma remains a substantial and unresolved clinical challenge. Despite ongoing research, therapeutic options for this disorder remain inadequate. Here, we report that neurotrophin-3 (Nt3) mRNA and its encoded proneurotrophin-3 (proNT3) protein are upregulated in neurons of the injured dorsal root ganglion (DRG), but not in the spinal cord, following peripheral nerve trauma. Mature neurotrophin-3 (NT3) protein is undetectable in the DRG under both normal and nerve trauma conditions. Genetic blockage of Nt3 mRNA/proNT3 protein upregulation in the injured DRG attenuates the development and maintenance of nerve trauma-induced neuropathic pain, without impacting acute/basal pain responses or locomotor function. Conversely, mimicking nerve trauma-induced upregulation of DRG Nt3 mRNA/pro-NT3 produces neuropathic pain-like symptoms. These symptoms are mitigated by intrathecal injection of NT3 protein or by selective knockdown of tropomyosin receptor kinase C (TrkC), but not TrkA or TrkB, in the DRG. Notably, intrathecal injection of NT3 also alleviates nerve trauma-induced neuropathic pain. Mechanistically, upregulated proNT3 contributes to the nerve trauma-induced increases of C-C chemokine ligand 2 (Ccl2) mRNA and CCL2 protein through activating TrkC in the injured DRG. Given that CCL2 is a key driver in neuropathic pain genesis and that Nt3 mRNA co-expresses with TrkC and Ccl2 mRNA in DRG neurons, proNT3 likely participates in nerve trauma-induced neuropathic pain through promoting TrkC-mediated increase of CCL2 in DRG neurons, highlighting a potential therapeutic target for the treatment of this disorder.

  PublisherDOI

• STIM1 functionally couples to transient receptor potential ankyrin 1 contributing to nociception

  Pain · 2025-07-16

  articleOpen access

  ABSTRACT: STIM1 is a calcium sensor that can sense calcium level changes in the endoplasmic reticulum (ER) and respond to extracellular stimuli. We have reported that STIM1 is expressed in nociceptors. However, its functional significance remains unclear. Here, we show that STIM1 plays an important role in sensing cold, chemical, and noxious mechanical stimuli in both male and female mice. We found that activation of transient receptor potential ankyrin 1 (TRPA1) triggers ER Ca 2+ release, STIM1 translocation, and store-operated Ca 2+ entry (SOCE). Immunostaining and western blot results reveal that TRPA1 is expressed in the ER. In addition, STIM1 deficiency in the primary sensory neurons reduces cold-, allyl isothiocyanate (TRPA1 agonist)-, and bradykinin-induced Ca 2+ entry and nociception. Moreover, intraplantar injection of thapsigargin, an ER Ca 2+ -ATPase inhibitor, evokes nociception and increases pain hypersensitivity, which is significantly attenuated in STIM1 conditional knockout or L3/L4 dorsal root ganglia STIM1 knockdown mice. Mechanistic studies demonstrate that STIM1-mediated SOCE increases neuronal excitability and decreases potassium channel Kv4-mediated outward currents in small to medium-sized dorsal root ganglion neurons, which is abolished by inhibiting the mitogen-activated protein kinase/extracellular receptor kinase pathway. Our findings demonstrate that STIM1 acts as a transducer of nociception and uncover a novel link between STIM1 and TRPA1 ER . Our study also provides new insights into TRPA1-mediated nociception.

  PublisherOA PDFDOI

• Proneurotrophin-3 contributes to chemotherapy-induced neuropathic pain through TrkC-mediated CCL2 elevation in DRG neurons

  EMBO Reports · 2025-11-26 · 1 citations

  articleOpen access

  Cancer patients undergoing treatment with antineoplastic drugs often experience chemotherapy-induced neuropathic pain (CINP), and therapeutic options for managing CINP are limited. Here, we show that systemic paclitaxel administration upregulates the expression of neurotrophin-3 (Nt3) mRNA and its encoded proneurotrophin-3 (proNT3) protein in the neurons of dorsal root ganglia (DRG), but not in the spinal cord. Blocking this upregulation attenuates paclitaxel-induced mechanical, heat, and cold nociceptive hypersensitivities and spontaneous pain without altering acute pain and locomotor activity in male and female mice. Conversely, mimicking paclitaxel-induced upregulation of DRG proNT3 produces enhanced responses to mechanical, heat, and cold stimuli and spontaneous pain in naive male and female mice. Mechanistically, proNT3 triggers tropomyosin receptor kinase C (TrkC) activation and participates in the paclitaxel-induced increases of C-C chemokine ligand 2 (Ccl2) mRNA and CCL2 protein in the DRG. Given that CCL2 is an endogenous initiator of CINP and that Nt3 mRNA co-expresses with TrkC and Ccl2 mRNAs in DRG neurons, proNT3 likely contributes to CINP through TrkC-mediated activation of the Ccl2 gene in DRG neurons. Thus, proNT3 may be a potential target for CINP treatment.

  PublisherDOI

• Withdrawal Note: NT-3 contributes to chemotherapy-induced neuropathic pain through TrkC-mediated CCL2 elevation in DRG neurons

  EMBO Reports · 2025-11-26

  articleOpen access
  PublisherDOI

• Predicting and Mitigating Risk of Postoperative Cognitive Dysfunction: Is a Major Breakthrough on the Horizon?

  ASA Monitor · 2024-04-25

  article

  Your Patient's Brain| May 2024 Predicting and Mitigating Risk of Postoperative Cognitive Dysfunction: Is a Major Breakthrough on the Horizon? George Tewfik, MD, MBA, FASA; George Tewfik, MD, MBA, FASA Search for other works by this author on: This Site PubMed Google Scholar Alex Bekker, MD, PhD; Alex Bekker, MD, PhD Search for other works by this author on: This Site PubMed Google Scholar Daniel J. Cole, MD, FASA Daniel J. Cole, MD, FASA Search for other works by this author on: This Site PubMed Google Scholar ASA Monitor May 2024, Vol. 88, 1–6. https://doi.org/10.1097/01.ASM.0001016780.82092.72 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Cite Icon Cite Get Permissions Search Site Citation George Tewfik, Alex Bekker, Daniel J. Cole; Predicting and Mitigating Risk of Postoperative Cognitive Dysfunction: Is a Major Breakthrough on the Horizon?. ASA Monitor 2024; 88:1–6 doi: https://doi.org/10.1097/01.ASM.0001016780.82092.72 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll PublicationsASA Monitor Search Advanced Search Topics: postoperative cognitive dysfunction Postoperative cognitive dysfunction (POCD) – also referred to as perioperative neurocognitive disorders – and delirium are pathologic states that may develop after surgery and often result in distress to the patient, family members, medical practitioners, and the health care system. Patients who suffer from POCD may experience short- or long-term physical or emotional disturbances. These may require supportive care such as home health aides or, in extreme cases, institutionalization in a nursing facility. Given the potential for significant financial and health care-related consequences, there has been great interest regarding research into POCD. Such research includes inquest of contributing factors, strategies to mitigate risk, and (importantly) the ability to predict increased risks for patients undergoing a surgical procedure under anesthesia. Past studies have shown that both frailty and preexisting cognitive impairment are contributing risk factors toward the development of POCD. Nonetheless, patients who are neither frail nor explicitly cognitively impaired may... You do not currently have access to this content.

  PublisherDOI

• Psychedelics as novel therapeutic agents for chronic pain: mechanisms and future perspectives

  Exploration of neuroscience · 2024-09-24 · 2 citations

  articleOpen accessSenior author

  Chronic neuropathic pain is a significant public health issue affecting an estimated 1.5 billion individuals worldwide. The mechanisms underlying chronic pain are multifaceted and not fully understood. Chronic pain amplifies specific neural pathways through peripheral and central sensitization triggered by repeated exposure to noxious stimuli, ultimately resulting in physical and emotional pain. Traditional treatment options targeting these mechanisms, such as opioid and non-opioid analgesics, are associated with adverse effects, addiction, and suboptimal pain relief. Using psychedelics to treat chronic pain is an area of growing interest. While psychedelic substances, such as psilocybin, lysergic acid diethylamide, mescaline, and 3,4-methylenedioxymethamphetamine are primarily associated with recreational use or spiritual practices, emerging evidence suggests their potential therapeutic benefits for various mental health disorders, including chronic pain. Psychedelics alter pain perception by directly activating serotonin receptors, exerting anti-inflammatory effects, enhancing descending inhibition, opening a window of neuroplasticity, and facilitating synaptic remodeling. This review mainly elucidates the ongoing research regarding the psychedelic mechanisms of action, pharmacology, clinical applications, and therapeutic potential in treating neuropathic pain.

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• RETRACTED

  WITHDRAWN ARTICLE: NT-3 contributes to chemotherapy-induced neuropathic pain through TrkC-mediated CCL2 elevation in DRG neurons

  EMBO Reports · 2024-04-09 · 18 citations

  article

  Cancer patients undergoing treatment with antineoplastic drugs often experience chemotherapy-induced neuropathic pain (CINP), and the therapeutic options for managing CINP are limited. Here, we show that systemic paclitaxel administration upregulates the expression of neurotrophin-3 (Nt3) mRNA and NT3 protein in the neurons of dorsal root ganglia (DRG), but not in the spinal cord. Blocking NT3 upregulation attenuates paclitaxel-induced mechanical, heat, and cold nociceptive hypersensitivities and spontaneous pain without altering acute pain and locomotor activity in male and female mice. Conversely, mimicking this increase produces enhanced responses to mechanical, heat, and cold stimuli and spontaneous pain in naive male and female mice. Mechanistically, NT3 triggers tropomyosin receptor kinase C (TrkC) activation and participates in the paclitaxel-induced increases of C-C chemokine ligand 2 (Ccl2) mRNA and CCL2 protein in the DRG. Given that CCL2 is an endogenous initiator of CINP and that Nt3 mRNA co-expresses with TrkC and Ccl2 mRNAs in DRG neurons, NT3 likely contributes to CINP through TrkC-mediated activation of the Ccl2 gene in DRG neurons. NT3 may be thus a potential target for CINP treatment.

  PublisherOA PDFDOI

• RNA-binding protein SYNCRIP contributes to neuropathic pain through stabilising CCR2 expression in primary sensory neurones

  British Journal of Anaesthesia · 2024-09-07 · 7 citations

  articleOpen access
  PublisherOA PDFDOI

• Transcription factor EBF1 mitigates neuropathic pain by rescuing Kv1.2 expression in primary sensory neurons

  Translational research · 2023-08-20 · 16 citations

  articleOpen access
  PublisherOA PDFDOI

• FUS Contributes to Nerve Injury-Induced Nociceptive Hypersensitivity by Activating NF-κB Pathway in Primary Sensory Neurons

  Journal of Neuroscience · 2023-01-10 · 20 citations

  articleOpen access

  Dysregulation of pain-associated genes in the dorsal root ganglion (DRG) is considered to be a molecular basis of neuropathic pain genesis. Fused in sarcoma (FUS), a DNA/RNA-binding protein, is a critical regulator of gene expression. However, whether it contributes to neuropathic pain is unknown. This study showed that peripheral nerve injury caused by the fourth lumbar (L4) spinal nerve ligation (SNL) or chronic constriction injury (CCI) of the sciatic nerve produced a marked increase in the expression of FUS protein in injured DRG neurons. Blocking this increase through microinjection of the adeno-associated virus (AAV) 5-expressing Fus shRNA into the ipsilateral L4 DRG mitigated the SNL-induced nociceptive hypersensitivities in both male and female mice. This microinjection also alleviated the SNL-induced increases in the levels of phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and glial fibrillary acidic protein (GFAP) in the ipsilateral L4 dorsal horn. Furthermore, mimicking this increase through microinjection of AAV5 expressing full-length Fus mRNA into unilateral L3/4 DRGs produced the elevations in the levels of p-ERK1/2 and GFAP in the dorsal horn, enhanced responses to mechanical, heat and cold stimuli, and induced the spontaneous pain on the ipsilateral side of both male and female mice in the absence of SNL. Mechanistically, the increased FUS activated the NF-κB signaling pathway by promoting the translocation of p65 into the nucleus and phosphorylation of p65 in the nucleus from injured DRG neurons. Our results indicate that DRG FUS contributes to neuropathic pain likely through the activation of NF-κB in primary sensory neurons. SIGNIFICANCE STATEMENT In the present study, we reported that fused in sarcoma (FUS), a DNA/RNA-binding protein, is upregulated in injured dorsal root ganglion (DRG) following peripheral nerve injury. This upregulation is responsible for nerve injury-induced translocation of p65 into the nucleus and phosphorylation of p65 in the nucleus from injured DRG neurons. Because blocking this upregulation alleviates nerve injury-induced nociceptive hypersensitivity, DRG FUS participates in neuropathic pain likely through the activation of NF-κB in primary sensory neurons. FUS may be a potential target for neuropathic pain management.

  PublisherOA PDFDOI

Frequent coauthors

• Yuan‐Xiang Tao

  Rutgers, The State University of New Jersey

  68 shared

• Herman Turndorf

  New York University

  48 shared

• S. Wolk

  New Jersey Institute of Technology

  44 shared

• Shaogen Wu

  Stanford University

  41 shared

• Michael Haile

  39 shared

• Wanhong Zuo

  37 shared

• Rao Fu

  Central South University

  29 shared

• Arthur Ritter

  Stevens Institute of Technology

  27 shared

Education

• M.D.

  UMDNJ-NJMS

  1991

• Ph.D.

  New Jersey Institute of Technology

  1987

• M.S.

  New Jersey Institute of Technology

  1983

• B.S.

  Tbilisi State University

  1974