Abstract
There seems to be a correlation between soluble amyloid beta protein (Aβ) accumulation in the main olfactory bulb (OB) and smell deterioration in both Alzheimer's disease (AD) patients and animal models. Moreover, this loss of smell appears to be related to alterations in neural network activity in several olfactory-related circuits, including the OB, as has been observed in anesthetized animals and brain slices. It is possible that there is a correlation between these two pathological phenomena, but a direct and simultaneous evaluation of the acute and direct effect of Aβ on OB activity while animals are actually smelling has not been performed. Thus, here, we tested the effects of acute intrabulbar injection of Aβ at a low dose (200 pmol) on the OB local field potential before and during the presence of a hidden piece of smelly food. Our results show that Aβ decreases the power of OB network activity while impairing the animal's ability to reach the hidden food. We found a strong relationship between the power of the OB oscillations and the correlation between OBs and the olfactory detection test scores. These findings provide a direct link between Aβ-induced OB network dysfunction and smell loss in rodents, which could be extrapolated to AD patients.
Highlights
Alzheimer’s disease (AD) is the most prevalent form of dementia [1]
Recent evidence in animal models has shown that amyloid beta (Aβ) accumulation in the olfactory bulb (OB) and other olfactory-related areas correlates with hyposmia [5,6,7,8,9], especially in the early stages of the AD-like pathology [9,10,11]
These findings strongly suggest that Aβ accumulation in the OB and the deterioration of its neural network activity is responsible, at least in part, for the hyposmia observed in AD
Summary
Alzheimer’s disease (AD) is the most prevalent form of dementia [1]. Aside from cognitive dysfunction, one of the earliest symptoms is hyposmia [2,3,4]. Accumulation of Aβ in a variety of circuits is associated with alterations in their synaptic function and intrinsic neural properties These alterations are reflected in population activity changes, which seem to underlie cognitive deterioration and other related symptoms in AD [8, 9, 12,13,14,15,16]. Our results show that a sudden Aβ application decreases the power of OB network activity and the correlation between both OBs while simultaneously impairing the olfactory function of rats These findings strongly suggest that Aβ accumulation in the OB and the deterioration of its neural network activity is responsible, at least in part, for the hyposmia observed in AD
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