Linalool Reverses Neuropathological and Behavioral Impairments in Old Triple Transgenic Alzheimer's Mice

Sabogal-Guáqueta, Angélica Maria; Osorio, Edison; Cardona-Gómez, Gloria Patricia

doi:10.1016/j.neuropharm.2015.11.002

Cited by 148Alzheimer's disease research and treatmentsMedicinal Plants and NeuroprotectionNeuroinflammation and Neurodegeneration Mechanisms

Linalool Reverses Neuropathological and Behavioral Impairments in Old Triple Transgenic Alzheimer's Mice

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Sabogal-Guáqueta, Angélica Maria, Osorio, Edison, Cardona-Gómez, Gloria Patricia·2016·Neuropharmacology

DOI 10.1016/j.neuropharm.2015.11.002PMC PMC4698173

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Abstract

Alzheimer's disease (AD) is an age-related progressive neurodegenerative disorder. Several types of treatments have been tested to block or delay the onset of the disease, but none have been completely successful. Diet, lifestyle and natural products are currently the main scientific focuses. Here, we evaluate the effects of oral administration of the monoterpene linalool (25 mg/kg), every 48 h for 3 months, on aged (21-24 months old) mice with a triple transgenic model of AD (3xTg-AD) mice. Linalool-treated 3xTg-AD mice showed improved learning and spatial memory and greater risk assessment behavior during the elevated plus maze. Hippocampi and amygdalae from linalool-treated 3xTg-AD mice exhibited a significant reduction in extracellular β-amyloidosis, tauopathy, astrogliosis and microgliosis as well as a significant reduction in the levels of the pro-inflammatory markers p38 MAPK, NOS2, COX2 and IL-1β. Together, our findings suggest that linalool reverses the histopathological hallmarks of AD and restores cognitive and emotional functions via an anti-inflammatory effect. Thus, linalool may be an AD prevention candidate for preclinical studies.

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The neuroprotective effects of linalool correlate with reduced levels of p38 MAPK, NOS2, COX-2, and IL-1β.
“These neuroprotective effects correlate with reduced levels of p38 MAPK, NOS2, COX-2, and IL-1β (Sabogal-Guáqueta et al., 2016).”
From Exploring the Therapeutic Potential of Phytochemicals in Alzheimer’s Disease: Focus on Polyphenols and Monoterpenes (2022) · cites this paper as Sabogal-Guáqueta et al., 2016

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Authors: Sabogal-Guáqueta, A. M., Osorio, E., & Cardona-Gómez, G. P.
Affiliations: Universidad de Antioquia (CO)
ORCID: Osorio, Edison
Cardona-Gómez, Gloria Patricia
Venue: Neuropharmacology
Publisher: Elsevier BV
Published: 2016-03
Volume: 102
Pages: 111-120
ISSN: 0028-3908 (ISSN-L)
DOI: 10.1016/j.neuropharm.2015.11.002
PMC: PMC4698173
OpenAlex: W2170522615
Cited by: 148
References: 54
Citations by year: 2026: 14 · 2025: 12 · 2024: 14 · 2023: 17 · 2022: 15 · 2021: 20 · 2020: 14 · 2019: 12 · 2018: 12 · 2017: 13 · 2016: 5
FWCI: 7.36
Type: journal article
Language: en
Open access: green
doi.org
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neuropharmacology (publishedVersion)
PubMed (publishedVersion)
Institutional Repository University of Antioquia (University of Antioquia) (publishedVersion, cc-by-nc-nd)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: COLCIENCIAS (11565740581 (GPC-G))
Topics: Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: linalool, Alzheimer's disease, triple transgenic mice, monoterpenes, cognitive impairment, spatial memory, risk assessment behavior, amyloid-beta, tauopathy, astrocyte activation, microglial activation, neuroinflammation, p38 MAPK, NOS2, cyclooxygenase-2, IL-1β, hippocampus, amygdala, anti-inflammatory activity, natural products
MeSH terms: Acyclic Monoterpenes, Alzheimer Disease, Animals, Behavior, Animal, Brain, Disease Models, Animal, Mice, Transgenic, Amyloid beta-Peptides, tau Proteins, Maze Learning, Monoterpenes, Mice, Spatial Memory

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Linalool Reverses Neuropathological and Behavioral Impairments in Old Triple Transgenic Alzheimer's Mice

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