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Nicotine Modulates Cognitive Function in D-Galactose-Induced Senescence in Mice
Alireza Majdi1, Saeed Sadigh-Eteghad1, Mahnaz Talebi1
1Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Frontiers in Aging Neuroscience
|August 1, 2018
Summary
Nicotine may improve cognitive function and reduce brain aging markers in mice. Specific doses and intranasal administration show potential for cognitive enhancement without adverse effects.
Area of Science:
- Neuroscience
- Pharmacology
- Aging Research
Background:
- Brain aging is associated with cognitive decline and cellular dysfunction.
- D-galactose (DGal) is used to induce an animal model of brain aging.
- Nicotine's potential neuroprotective effects warrant investigation.
Purpose of the Study:
- To investigate nicotine's efficacy in attenuating D-galactose-induced brain dysfunction in mice.
- To evaluate the effects of different nicotine doses and administration routes on cognitive function and cellular markers.
- To determine optimal nicotine administration for mitigating age-related brain changes.
Main Methods:
- Mice received D-galactose (500 mg/kg s.c.) for 6 weeks to model brain aging.
- Nicotine was administered subcutaneously (0.1, 0.5, 1 mg/kg) or intranasally (0.1 mg/kg).
- Cognitive functions were assessed using Barnes maze, novel object recognition, elevated plus maze, and open field tests. Biochemical analyses included oxidative stress, apoptosis markers, and neurotrophic factors.
Main Results:
- Nicotine (0.5 mg/kg s.c. and 0.1 mg/kg i.n.) significantly improved spatial and episodic memory in DGal-treated mice.
- These effective nicotine doses reduced mito-oxidative damage and apoptosis.
- Neurotrophic factor levels (BDNF, NGF) were increased by effective nicotine doses.
- A higher subcutaneous dose (1 mg/kg) induced withdrawal signs.
Conclusions:
- Nicotine, at specific doses and via intranasal administration, can attenuate age-related cognitive impairment and cellular damage in a mouse model.
- Nicotine demonstrates potential in reducing oxidative stress and apoptosis while enhancing neurotrophic factors.
- Careful dose and route selection are crucial to avoid adverse effects like withdrawal symptoms.
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