Interventions targeting astrocyte phenotypes, including minocycline and Lcn2 knockdown, normalized the posterior piriform cortex neurochemistry and alleviated both nociceptive and affective symptoms. These findings define a mechanistic framework in which astrocytic dysfunction orchestrates pain and depression, and highlight astrocyte-directed strategies for treating cancer pain-depression comorbidity.
Interventions to correct glial dysfunction-e.g., anti-inflammatory medication (e.g., minocycline, ibudilast), gene therapy, and stem cell therapy-are investigated for their potential to restore glia to normal and diminish ASD symptoms. Understanding glial-neuronal communication mechanisms and their role in neuroinflammation offers a hopeful future for accurate, target-specific treatment. Advances in the elucidation of these processes will foretell an enormous increase in therapeutic efficacy and quality of life for individuals with ASD.
P1, N=30, Not yet recruiting, University of Cincinnati | Trial completion date: Dec 2026 --> Jun 2028 | Trial primary completion date: May 2026 --> Dec 2027
27 days ago
Trial completion date • Trial primary completion date
Furthermore, intraperitoneal injection of minocycline (40 mg/kg) with ACR reduced the levels of MDA, IL-1β, and caspase-3-cleaved proteins in the cerebral cortex. Administration of minocycline exhibits both prophylactic and therapeutic properties against ACR-induced neurotoxicity primarily through anti-oxidant, anti-apoptotic, and anti-inflammatory properties.
This study aimed to investigate the anticancer potential of three tetracycline analogues chemically modified tetracycline-3 (COL-3), doxycycline (DOX), and minocycline (MIN) in leukemia models, with a particular focus on their cytotoxic effects and modulation of the JAK2/STAT3 signaling pathway. Among them, COL-3 emerges as the most potent analogue and acts through both JAK/STAT-dependent and -independent mechanisms. This work supports further investigation of COL-3 as a candidate for drug repurposing strategies in hematological malignancies.
Furthermore, the anxiety-like behaviors in NSUN5-deficient mice were also relieved by rmFGF2 or minocycline treatments. Taken together, our study unveils a previously unknown effect of NSUN5 on anxiety disorders and a role of NSUN5 in regulating OPCs-microglia interaction and synaptic plasticity of BLA.
P4, N=42, Not yet recruiting, Stony Brook University | Trial completion date: Jan 2031 --> Jan 2032 | Trial primary completion date: Jun 2030 --> Jun 2031
2 months ago
Trial completion date • Trial primary completion date