Alzheimer’s disease (AD) is a neurodegenerative disease and the most common cause of dementia. Amyloidosis mediated by amyloid-beta(1-42) is a key factor in the pathophysiology of the disease. Braak staging of AD proposes that AD begins in the olfactory system, progressing then through the lateral entorhinal cortex to the hippocampus, whereupon symptoms of dementia become apparent. Intracerebral inoculation of healthy rodents with oligomeric amyloid-beta(1-42) results in impairments of hippocampal information processing and storage (doi: 10.3389/fnbeh.2015.00103).To what extent this also affects the primary olfactory (piriform) cortex is unclear.Here, we examined passive and active properties of principle cells of the piriform cortex (PC), in a period of months after intracerebral inoculation of healthy adult male rats with oligomeric amyloid-beta(1-42).Patch clamp recordings revealed that PC neurons from brains treated with amyloid-beta exhibited a progressive decline in input resistance in a time-period encompassing 1-6 months after treatment (compared to control peptide-treated brains). Action potential firing frequency was also significantly different in amyloid-beta-treated and control brains.Taken together, our results indicate that oligomeric amyloid-beta(1-42) progressively alters the information processing capacity of PC neurons and that this process may contribute to the staged debilitation of brain regions as AD progresses.Supported by the Deutsche Forschungsgemeinschaft (SFB 874/B1, project number: 122679504).