Abstract

Alzheimer’s disease is the main reason for dementia, which increases with age. Cholinesterase inhibition and antioxidant potentials of extracts and essential oils from bulbs of A. tuncelianum (Kollmann) Özhatay & al., an endemic species to Tunceli (easthern Turkey), were evaluated. The fraction extracted of ethyl acetate had the highest phenolics level, 1,1-diphenyl-2-picrylhydrazyl, and thiobarbituric acid antioxidant capacity. Also, the ethyl acetate fraction presented the highest acetylcholinesterase (15.98 ± 2.76%), and butyrylcholinesterase inhibition (47.33 ± 3.27%). Diallyl disulfide (49.8%), diallyl trisulfide (27.9%) and allyl methyl trisulfide (6.9%) were found to be the major components of essential oil. This paper shows that the ethyl acetate fraction of A. tuncelianum could be a potent source of antioxidant and anticholinesterase components.

Highlights

  • Alzheimer’s disease (AD) is a neurodegenerative disease characterized by an accumulation of extracellular amyloid-beta peptide (Aβ) and intracellular neurofibrils resulting in a loss of memory

  • This paper shows that the ethyl acetate fraction of A. tuncelianum could be a potent source of antioxidant and anticholinesterase components

  • Other research found a substantial correlation between antioxidant capacity and total phenolic content (Sytar & al. 2015; Granato & al. 2018) as well

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Summary

Introduction

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by an accumulation of extracellular amyloid-beta peptide (Aβ) and intracellular neurofibrils resulting in a loss of memory. Aβ is the principal constituent of senile plaques that are thought to play a central role in the healing and progression of oligomer and fibril forms of AD. Many studies have shown that oxidative stress and mitochondrial dysfunction might have a substantial role in AD and that they are suppressed or reduced by using antioxidant agents, suggesting a therapeutic intervention for AD patients. It is reported that numerous antioxidant components protect the brain from Aβ neurotoxicity Pharmacological treatments available for AD occur by relaxation of the symptoms rather than targeting the etiological mechanisms

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