Jonathan M. Packer

ORCID: 0000-0001-9564-2695
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About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Tryptophan and brain disorders
  • S100 Proteins and Annexins
  • Stress Responses and Cortisol
  • Immune Response and Inflammation
  • interferon and immune responses
  • Inflammasome and immune disorders
  • Glioma Diagnosis and Treatment
  • Neonatal and fetal brain pathology
  • Brain Metastases and Treatment
  • Neuroendocrine regulation and behavior
  • Head and Neck Cancer Studies

The Ohio State University
2021-2025

The Ohio State University Wexner Medical Center
2022-2024

Institute for Behavioral Medicine
2022-2024

Traumatic brain injury (TBI) is associated with an increased risk of cognitive, psychiatric, and neurodegenerative complications that may develop after injury. Increased microglial reactivity following TBI underlie chronic neuroinflammation, neuropathology, exaggerated responses to immune challenges. Therefore, the goal this study was force turnover trauma-associated microglia diffuse determine whether alleviated inflammation, improved functional recovery attenuated reduced...

10.1523/jneurosci.1910-21.2022 article EN cc-by-nc-sa Journal of Neuroscience 2022-04-19

Traumatic brain injury (TBI) is associated with chronic psychiatric complications and increased risk for development of neurodegenerative pathology. Aged individuals account most TBI-related hospitalizations deaths. Nonetheless, neurobiological mechanisms that underlie worsened functional outcomes after TBI in the elderly remain unclear. Therefore, this study aimed to identify pathways govern differential responses age. Here, adult (2 months age) aged (16–18 male C57BL/6 mice were subjected...

10.1523/jneurosci.1377-22.2022 article EN cc-by-nc-sa Journal of Neuroscience 2022-10-18

Chronic stress is associated with increased anxiety, cognitive deficits, and post-traumatic disorder. Repeated social defeat (RSD) in mice causes long-term stress-sensitization microglia activation, monocyte accumulation, enhanced interleukin (IL)-1 signaling endothelia neurons. With stress-sensitization, have amplified neuronal, immune, behavioral responses to acute 24 days later. This clinically relevant as it shares key aspects The mechanisms underlying are unclear, but fear memory may be...

10.1038/s41380-024-02456-1 article EN cc-by Molecular Psychiatry 2024-03-08

Abstract Neuropsychiatric complications including depression and cognitive decline develop in the years after traumatic brain injury (TBI), negatively affecting quality of life. Microglial type 1 interferon (IFN‐I) responses are associated with transition from acute to chronic neuroinflammation diffuse TBI mice. Thus, purpose this study was determine if impaired neuronal homeostasis increased IFN‐I intersected cause impairment. Here, RNA profile neurons microglia (single nucleus...

10.1002/glia.24475 article EN Glia 2023-11-08

<title>Abstract</title> Neuropsychiatric complications including depression and cognitive impairment develop, persist, worsen in the years after traumatic brain injury (TBI), negatively affecting life lifespan. Inflammatory responses mediated by microglia are associated with transition from acute to chronic neuroinflammation TBI. Moreover, type I interferon (IFN-I) signaling is a key mediator of inflammation during this transition. Thus, purpose study was determine degree which...

10.21203/rs.3.rs-5960640/v1 preprint EN cc-by Research Square (Research Square) 2025-02-17
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