Study of the Effects of L-tryptophane Nanoparticles on Motor Behavior in Alzheimer's Experimental Models

Abstract

Background: Alzheimer's disease (AD) is a neurodegenerative disease characterized by the progressive and incapacitating decay of cognitive, neuropsychiatric, and behavioral manifestations. L-tryptophan is the precursor amino acid of serotonin, which is a neurotransmitter responsible for mood balance and the sense of well-being and can be administered in the form of nanoparticles. Objective: This study analyzed the effectiveness of L-tryptophan nanoparticles and L-tryptophan on behavioral physiological alterations resulting from AD in animal models. Methods: The sample consisted of 50 Rattus norvegicus rats, divided in 10 groups with 5 animals each: one negative control (NC), three positive control groups (C3, C7, and C21), three groups treated with L-tryptophan nanoparticles (T3N, T7N, and T21N) at the concentration of 1.5 mg, and three groups treated with L-tryptophan (T3L, T7L, and T21L) at the concentration of 1.5 mg. The rats underwent stereotactic surgery to induce AD through the injection of amyloid beta-amyloid peptide1-42 in the intracerebroventricular region. All rats were submitted to pre- and post-surgery and post-treatment motor behavior evaluation through the Later Water Maze (LWM) and elevated cross-labyrinth (ECL). Histological analysis was performed to verify the presence of senile plaques, and the statistical analysis used the unpaired T-test. Results: Significant intergroup differences were observed in some of the evaluated parameters between treated and untreated groups. Conclusion: It was concluded that the treatment with L-tryptophan nanoparticles was beneficial to improve behavioral reactions in the Alzheimer's model.

Effects of α-Humulene and its Nanoparticles in Experimental Model of Alzheimer's Disease: Behavioral Analysis and Anti-Inflammatory Activity

“…The animals were anesthetized with 80mg/Kg ketamine hydrochloride to 15mg/Kg xylazine hydrochloride via intraperitoneal. They were soon taken to an extereotaxic apparatus (David Kopf, USA) where their heads were fixed by the petrous temporal bone and upper incisors under coordinates AP= -3.0mm, ML= 1.6mm, -1.6mm and DV= 3.0mm, taking the bregma as reference, receiving 4µl of β-amyloid peptide via Hamilton syringe in the CA1 region of the hippocampus for the process of senile plaque development [14]. After the induction of the neuroinflammation and neurofibrillary process, the animals were rested for a period of 30 days for the inflammatory and neurodegenerative processes of hippocampal neurons to occur.…”