Structural, functional and behavioral impact of allergic rhinitis on olfactory pathway and prefrontal cortex

Rodrigues, Jorge; Rocha, Maria Inês; Teixeira, Francisco Lima Cruz; Resende, Beatriz; Cardoso, Armando; Sá, Susana I.; Vaz, Raquel; Raemdonck, Kristof

doi:10.1016/j.physbeh.2023.114171

Cited by 7 publications

(1 citation statement)

References 56 publications

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“…Olfaction transmits along the olfactory pathway, which originates within the olfactory neurons located in the olfactory epithelium of the nasal cavity; the signals are then conveyed to the primary olfactory center, the olfactory bulb (OB) before reaching higher brain centers such as the piriform cortex (PC), the hypothalamus, and the hippocampus. Damage, such as olfactory neuron loss [13] or nasal inflammation [14], including aseptic inflammation [15], to any part of this intricate network can potentially result in olfactory dysfunction [16]. In PD patients, the reasons for olfactory dysfunction are more complex [17], encompassing the deleterious effects of abnormally accumulated α-synuclein in the olfactory cortex [18], disruptions in olfactory transmission due to imbalances in secondary neurons [19], and exposure to environmental pollutants or toxins over a longer period compared to younger, healthy individuals, which can damage the olfactory epithelium [20,21].…”

Section: Introductionmentioning

confidence: 99%

A Pilot Study on a Possible Mechanism behind Olfactory Dysfunction in Parkinson’s Disease: The Association of TAAR1 Downregulation with Neuronal Loss and Inflammation along Olfactory Pathway

Zhang,

Hong,

Shi

et al. 2024

Brain Sciences

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Parkinson’s disease (PD) is characterized not only by motor symptoms but also by non-motor dysfunctions, such as olfactory impairment; the cause is not fully understood. Our study suggests that neuronal loss and inflammation in brain regions along the olfactory pathway, such as the olfactory bulb (OB) and the piriform cortex (PC), may contribute to olfactory dysfunction in PD mice, which might be related to the downregulation of the trace amine-associated receptor 1 (TAAR1) in these areas. In the striatum, although only a decrease in mRNA level, but not in protein level, of TAAR1 was detected, bioinformatic analyses substantiated its correlation with PD. Moreover, we discovered that neuronal death and inflammation in the OB and the PC in PD mice might be regulated by TAAR through the Bcl-2/caspase3 pathway. This manifested as a decrease of anti-apoptotic protein Bcl-2 and an increase of the pro-apoptotic protein cleaved caspase3, or through regulating astrocytes activity, manifested as the increase of TAAR1 in astrocytes, which might lead to the decreased clearance of glutamate and consequent neurotoxicity. In summary, we have identified a possible mechanism to elucidate the olfactory dysfunction in PD, positing neuronal damage and inflammation due to apoptosis and astrocyte activity along the olfactory pathway in conjunction with the downregulation of TAAR1.

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