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Published on: June 17, 2015
Intranasal Aβ1-42 Exposure Led To Neurobehavioral Alteration, Neuroinflammatory and Neurodegenerative Molecular
Avtar Singh Gautam1, Mohammad Zunaid Akhtar1, Lasure Vaibhav Uttamrao1
1Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER) - Raebareli. Transit campus, 226002, Lucknow, Uttar Pradesh, India.
Abstract:
In this study, we aimed to evaluate the AD structural hallmarks along with brain biomarkers and neurobehavioral alterations in a repeated intranasal Aβ1-42 exposure mouse model. This model is a simple, non-invasive, and less stressful method and may allow direct access of Aβ to the brain. The results of this study showed a dose-dependent increase in the level of Aβ1-42 deposition, tau phosphorylation, neuroinflammatory and oxidative stress biomarkers in brain tissue, along with learning and memory deficits in mice. This model may be suitable for evaluating the biochemical, structural, functional histological alterations, along with the neurobehavioral deficits mimicking AD.
Insights
This study developed a mouse model for Alzheimer's disease (AD) using intranasal amyloid-beta (Aβ) exposure. The model successfully replicated AD hallmarks, including Aβ deposition, tau phosphorylation, and cognitive decline.
Area of Science:
- Neuroscience
- Biomedical Research
- Animal Models
Background:
- Alzheimer's disease (AD) is characterized by amyloid-beta (Aβ) plaques and neurofibrillary tangles.
- Developing accurate and less invasive animal models for AD research is crucial.
Purpose of the Study:
- To evaluate Alzheimer's disease (AD) structural hallmarks, brain biomarkers, and neurobehavioral changes.
- To assess a novel, non-invasive intranasal amyloid-beta (Aβ)1-42 exposure mouse model for AD research.
Main Methods:
- Repeated intranasal administration of Aβ1-42 in a mouse model.
- Analysis of brain tissue for Aβ1-42 deposition, tau phosphorylation, neuroinflammation, and oxidative stress biomarkers.
- Assessment of learning and memory deficits using neurobehavioral tests.
Main Results:
- A dose-dependent increase in Aβ1-42 deposition and tau phosphorylation was observed.
- Elevated levels of neuroinflammatory and oxidative stress biomarkers were detected in brain tissue.
- Mice exhibited significant learning and memory deficits, mimicking AD-related cognitive impairment.
Conclusions:
- The intranasal Aβ1-42 exposure mouse model effectively replicates key pathological and functional aspects of Alzheimer's disease.
- This model offers a simple, non-invasive approach for studying AD-related biochemical, structural, and neurobehavioral alterations.
- The model's suitability for evaluating therapeutic interventions targeting AD is suggested.
