Abstract

Amyloid-β (Aβ) is a key pathological hallmark of Alzheimer's disease (AD), the most common form of dementia majorly occurring in the geriatrics. Aβ accumulation is observed in the brains of AD patients and is reported to produce long-term effects on cognitive functions leading to neurodegeneration and subsequently AD. Olfactory deficits are reported in AD and are proposed to be another consequence of these accumulations. The present study was performed to primarily investigate the olfactory behavior and neurochemical changes in olfactory bulb upon intracerebroventricular (i.c.v) injection of Aβ(1-42) in female C57BL/6 mice. The study also assessed the cognitive changes of i.c.v injected animals and recorded the subsequent changes in their hippocampus. All behavioral and neurochemical variations were noted separately on 7th,17th and 28th day after i.c.v injection. Results from the behavioral analysis indicated prominent olfactory deficit from the 7th day. Reactive oxygen species levels increased in both the tissues after Aβ injection. Neurotransmitter data showed that pathological accumulation of Aβ increases glutamate 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 neurochemical changes leading to these deficits in a non-transgenic model.

Key words: Amyloid beta (1-42), Alzheimer’s Disease, intracerebroventricular injection, olfactory dysfunction, non-transgenic model