Abstract
Alzheimer's disease (AD) could be considered a multifactorial neurodegenerative disorder characterized by the accumulation of the β-amyloid-peptide (Aβ) within the brain leading to cognitive deficits, oxidative stress, and neuroinflammation. The present work was carried out to investigate the neuroprotective effect of (-)-cis-carveol (1% and 3%, for 21 days) against the β-amyloid-peptide 1-42- (Aβ1-42-) induced AD. Twenty-five rats were divided into five groups (n = 5/group): the first group—control (sham-operated); the second group—Aβ1-42 (1 mM) that received donepezil treatment (5 mg/kg, as the positive reference drug in the Y-maze and the radial arm maze tests); the third group—Aβ1-42 (1 mM); the fourth and fifth groups—Aβ1-42 (1 mM) that received (-)-cis-carveol treatment groups (1% and 3%). The results of this study demonstrated that (-)-cis-carveol improved Aβ1-42-induced memory deficits examined by using Y-maze and radial arm maze in vivo tests. Also, the biochemical analyses of the hippocampus homogenates showed that (-)-cis-carveol reduced hippocampal oxidative stress caused by Aβ1-42. Our results suggested that the use of (-)-cis-carveol may be suitable for decreasing AD-related symptoms.
Highlights
Alzheimer’s disease (AD) could be considered a multifactorial neurodegenerative disorder characterized by the accumulation of the β-amyloid-peptide (Aβ) within the brain leading to cognitive deficits, oxidative stress, and neuroinflammation
Our results suggested that the use of (-)-cis-carveol may be suitable for decreasing AD-related symptoms
Alzheimer’s disease (AD) is considered an irreversible, progressive neurological disorder characterized by the accumulation of the extracellular β-amyloid-peptide (Aβ), intracellular neurofibrillary tangles, disruption of synapses, brain inflammation, and memory loss [1]
Summary
Alzheimer’s disease (AD) is considered an irreversible, progressive neurological disorder characterized by the accumulation of the extracellular β-amyloid-peptide (Aβ), intracellular neurofibrillary tangles, disruption of synapses, brain inflammation, and memory loss [1]. There is some evidence that neuropsychiatric symptoms, anxiety and depression, could be risk factors for cognitive impairment and AD dementia and are associated with cortical Aβ deposition [2, 3]. There is evidence between oxidative stress and neuronal dysfunction in AD [4]. Excessive Aβ may trigger stress-related signaling pathways through increasing Ca2+ influx, increasing oxidative stress, and impairing energy metabolism [4, 5]. Clinical drug treatments are limited to acetylcholinesterase inhibitors (AChEIs), such as donepezil and the antagonist of N-methylD-aspartic acid (NMDA) receptor, represented by memantine [6]. Recent failures and limited progress of therapeutics suggest that alternative strategies for AD treatment could be considered [7]
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call