1Department of Pharmaceutics, KLE College of Pharmacy, Hubballi. KLE Academy of Higher Education and Research (Deemed to be University), Belagavi, Karnataka, INDIA.
2*Department of Pharmacy Practice, KLE College of Pharmacy, Hubballi. KLE Academy of Higher Education and Research (Deemed to be University), Belagavi, Karnataka, INDIA.
Neurodegenerative diseases are characterized by the progressive loss of neurons, leading to profound impairments in cognitive and motor functions. Conventional medical interventions often fail to impede disease progression and frequently result in enduring adverse effects. This study examined the neuroprotective properties of agmatine and its solid lipid nanoparticle (SLN) formulation in an animal model of induced neurodegeneration. Exposure to neurotoxic substances resulted in significant behavioral alterations. The neurotoxicant group exhibited substantial spatial learning impairments, evidenced by a prolonged escape latency in the Morris Water Maze (74.33 ± 0.70 seconds). Agmatine SLNs demonstrated superior neuroprotective efficacy compared to free agmatine. In the Elevated Plus Maze (EPM), agmatine SLNs significantly improved cognitive recovery by normalizing transfer latency to 59.13 ± 0.78 seconds, which was nearly identical to the normal control value (58.22 ± 0.84 seconds). Furthermore, while the neurotoxicant group showed significant motor impairment with only 185.3 ± 13.05 counts/5 min in locomotor activity, the agmatine SLN-treated group maintained significantly higher activity (270.3 ± 22.36 counts/5 min). These findings suggest that agmatine SLNs effectively ameliorate both motor and non-motor symptoms, offering a promising therapeutic strategy for progressive neuronal degeneration.
Keywords: Levodopa, Agmatine, 6-hydroxydopamine (6-OHDA), Solid Lipid Nanoparticles, Intracerebroventricular Injection, Neurodegeneration.
How to cite this article: Harish KH, Swamy AHV. Amelioration of Motor and Non-Motor Deficits by Agmatine-Loaded Solid Lipid Nanoparticles in a 6-OHDA Rat Model of Neurodegeneration. Int J Drug Deliv Technol. 2026;16(15s): 318-338. DOI: 10.25258/ijddt.16.15s.39
Source of support: Nil.
Conflict of interest: None