Inflammation and olfactory loss are associated with at least 139 medical conditions.

IF 3.5 3区医学 Q2 NEUROSCIENCES

Frontiers in Molecular Neuroscience Pub Date : 2024-10-11 eCollection Date: 2024-01-01 DOI:10.3389/fnmol.2024.1455418

Michael Leon, Emily T Troscianko, Cynthia C Woo

引用次数: 0

Abstract

Olfactory loss accompanies at least 139 neurological, somatic, and congenital/hereditary conditions. This observation leads to the question of whether these associations are correlations or whether they are ever causal. Temporal precedence and prospective predictive power suggest that olfactory loss is causally implicated in many medical conditions. The causal relationship between olfaction with memory dysfunction deserves particular attention because this sensory system has the only direct projection to memory centers. Mechanisms that may underlie the connections between medical conditions and olfactory loss include inflammation as well as neuroanatomical and environmental factors, and all 139 of the medical conditions listed here are also associated with inflammation. Olfactory enrichment shows efficacy for both prevention and treatment, potentially mediated by decreasing inflammation.

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炎症和嗅觉丧失至少与 139 种疾病有关。

至少有 139 种神经性、躯体性和先天性/遗传性疾病会导致嗅觉丧失。这一观察结果引出了一个问题：这些关联是相关关系还是因果关系？时间优先性和前瞻性预测能力表明，嗅觉丧失与许多病症有因果关系。嗅觉与记忆功能障碍之间的因果关系值得特别关注，因为这一感觉系统是唯一直接投射到记忆中心的系统。医学症状与嗅觉丧失之间的关联机制可能包括炎症以及神经解剖学和环境因素，这里列出的 139 种医学症状也都与炎症有关。丰富嗅觉对预防和治疗都有疗效，这可能是通过减少炎症来实现的。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Frontiers in Molecular Neuroscience NEUROSCIENCES-

CiteScore

5.70

自引率

2.10%

发文量

669

审稿时长

14 weeks

期刊介绍： Frontiers in Molecular Neuroscience is a first-tier electronic journal devoted to identifying key molecules, as well as their functions and interactions, that underlie the structure, design and function of the brain across all levels. The scope of our journal encompasses synaptic and cellular proteins, coding and non-coding RNA, and molecular mechanisms regulating cellular and dendritic RNA translation. In recent years, a plethora of new cellular and synaptic players have been identified from reduced systems, such as neuronal cultures, but the relevance of these molecules in terms of cellular and synaptic function and plasticity in the living brain and its circuits has not been validated. The effects of spine growth and density observed using gene products identified from in vitro work are frequently not reproduced in vivo. Our journal is particularly interested in studies on genetically engineered model organisms (C. elegans, Drosophila, mouse), in which alterations in key molecules underlying cellular and synaptic function and plasticity produce defined anatomical, physiological and behavioral changes. In the mouse, genetic alterations limited to particular neural circuits (olfactory bulb, motor cortex, cortical layers, hippocampal subfields, cerebellum), preferably regulated in time and on demand, are of special interest, as they sidestep potential compensatory developmental effects.