Department of Biochemistry and Molecular Biomedicine, Faculty of Biology, University of Barcelona, 08028 Barcelona, Spain.
CiberNed, Network Center for Neurodegenerative Diseases, National Spanish Health Institute Carlos III, 28029 Madrid, Spain.
Cells. 2024 Apr 2;13(7):615. doi: 10.3390/cells13070615.
Alterations in olfactory functions are proposed as possible early biomarkers of neurodegenerative diseases. Parkinson's and Alzheimer's diseases manifest olfactory dysfunction as a symptom, which is worth mentioning. The alterations do not occur in all patients, but they can serve to rule out neurodegenerative pathologies that are not associated with small deficits. Several prevalent neurodegenerative conditions, including impaired smell, arise in the early stages of Parkinson's and Alzheimer's diseases, presenting an attractive prospect as a snitch for early diagnosis. This review covers the current knowledge on the link between olfactory deficits and Parkinson's and Alzheimer's diseases. The review also covers the emergence of olfactory receptors as actors in the pathophysiology of these diseases. Olfactory receptors are not exclusively expressed in olfactory sensory neurons. Olfactory receptors are widespread in the human body; they are expressed, among others, in the testicles, lungs, intestines, kidneys, skin, heart, and blood cells. Although information on these ectopically expressed olfactory receptors is limited, they appear to be involved in cell recognition, migration, proliferation, wound healing, apoptosis, and exocytosis. Regarding expression in non-chemosensory regions of the central nervous system (CNS), future research should address the role, in both the glia and neurons, of olfactory receptors. Here, we review the limited but relevant information on the altered expression of olfactory receptor genes in Parkinson's and Alzheimer's diseases. By unraveling how olfactory receptor activation is involved in neurodegeneration and identifying links between olfactory structures and neuronal death, valuable information could be gained for early diagnosis and intervention strategies in neurodegenerative diseases.
嗅觉功能的改变被认为是神经退行性疾病的早期生物标志物。帕金森病和阿尔茨海默病的表现为嗅觉功能障碍,这一点值得一提。这些改变并非发生在所有患者中,但它们可以用来排除与小缺陷无关的神经退行性病变。几种常见的神经退行性疾病,包括嗅觉受损,出现在帕金森病和阿尔茨海默病的早期阶段,作为早期诊断的线索具有很大的吸引力。本文综述了嗅觉缺陷与帕金森病和阿尔茨海默病之间的联系的最新知识。本文还涵盖了嗅觉受体作为这些疾病病理生理学中参与者的出现。嗅觉受体不仅在嗅觉感觉神经元中表达。嗅觉受体在人体中广泛表达,除其他外,还在睾丸、肺、肠、肾、皮肤、心脏和血细胞中表达。尽管关于这些异位表达的嗅觉受体的信息有限,但它们似乎参与细胞识别、迁移、增殖、伤口愈合、细胞凋亡和胞吐作用。关于在中枢神经系统 (CNS) 的非化学感觉区域的表达,未来的研究应该解决嗅觉受体在神经胶质和神经元中的作用。在这里,我们综述了关于帕金森病和阿尔茨海默病中嗅觉受体基因表达改变的有限但相关的信息。通过阐明嗅觉受体激活如何参与神经退行性变,并确定嗅觉结构与神经元死亡之间的联系,可以为神经退行性疾病的早期诊断和干预策略提供有价值的信息。