Evaluating the olfactory dysfunction and cognitive deficits induced by intracerebroventricular injection of Amyloid beta (1–42) in female C57BL/6 mice

ABSTRACT

Amyloid-β (Aβ) is a key pathological hallmark of Alzheimer's disease (AD), the most common form of dementiamajorly occurring in the geriatrics. Aβ accumulation is observed in the brains of AD patients and is reported toproduce long-term effects on cognitive functions leading to neurodegeneration, and subsequently, to AD. Olfactorydeficits are reported in AD and are proposed to be another consequence of these accumulations. The present studywas performed to primarily investigate the olfactory behavior and neurochemical changes in olfactory bulb uponintracerebroventricular (i.c.v) injection of Aβ (1–42) in female C57BL/6 mice. The study also assessed the cognitivechanges of i.c.v injected animals and recorded the subsequent changes in their hippocampus. All behavioral andneurochemical variations were noted separately on 7th, 17th, and 28th day after i.c.v injection. Results from thebehavioral analysis indicated prominent olfactory deficit from the 7th day. Reactive oxygen species levels increasedin both the tissues after Aβ injection. Neurotransmitter data showed that pathological accumulation of Aβ increasesglutamate levels in bulb and hippocampus. Additionally, histopathological evidence supported the neurochemical data.Data from the present study confirmed an olfactory dysfunction associated with AD and reported the neurochemicalchanges leading to these deficits in a non-transgenic model.