Therapeutic efficacy of amygdaline and amygdaline-loaded niosomes in a rat model of Alzheimer’s disease via oxidative stress, brain neurotransmitters, and apoptotic pathway

Background

Alzheimer’s disease (AD) is a specific form of neurodegeneration that is marked by impairments in memory and cognition. Exposure to some metal toxins, such as aluminum (AL), was directly linked to the onset of AD as it was hosted in the body via several exposure routes and can change the permeability and cross the blood–brain barrier. Due to amygdaline’s existence, apricot kernel therapy for AD is believed to have been established to be successful in numerous investigations. Amygdaline has been shown to have antioxidant effects that mitigate oxidative damage, and free radicals scavenger activity, as well as amygdaline niosomes as a nanoparticle has been found to improve the drug’s efficiency and selectivity. The objectives of this investigation are to study the neuroprotective role of amygdaline, and amygdaline-loaded niosomes formulation in the diminishment of the incidence of AD in neurotoxin (aluminum chloride; AlCl₃) AD animal model.

Results

Data revealed that AlCl₃ caused cognitive decline that was confirmed by cognitive behavioral tests (novel object and Y-maze); biochemical disturbances that include marked oxidative stress (elevated malondialdehyde and reduced total antioxidant capacity), reduced acetylcholinesterase, and brain monoamines levels (nor adrenalin; 4-dihydroxyphenylacetic acid; 5-hydroxytryptamine /serotonin; dopamine), and gene regulation upset (down-regulated transcript levels of acetylcholinesterase; monoamine oxidase; BCL-2 and up-regulated transcript levels of BAX), as well as neurodegenerative changes were observed in the hippocampus of AlCl₃-treated rats. Treatment with amygdaline and amygdaline-loaded niosomes formulation improved working memory and recognition, alleviated oxidative stress, and restored the levels of brain monoamines and neurotransmitters. Moreover, gene expression data showed a significant down-regulation of BAX, while BCL-2, acetylcholinesterase, and monoamine oxidase were significantly up-regulated. Additionally, the histopathological examination showed reduced neurodegeneration.

Conclusion

Conclusively, it was evident that amygdaline and amygdaline-loaded niosomes formulation possess a neuroprotective and cognitive enhancement role in AD via their potent antioxidant potential, neurotransmitters, and gene expression regulations, as well as neural damage reduction capability.

Graphical abstract