Minocycline augmentation significantly improved anhedonia in patients with melancholic MDD. Reducing pro-inflammatory cytokines (especially IL-1β) may play an important role in the potential mechanism for efficacy.
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
3 months 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
4 months ago
Trial completion date • Trial primary completion date