Depression is a known risk factor for dementia. Antidepressants are the most commonly used treatment for this condition, and are effective in at least half to two-thirds of cases. Extensive evidence from in vitro and animal models suggests that antidepressants have anti-inflammatory and neuroprotective properties. These effects have been shown to reduce the oxidative damage, amyloid aggregation, and expression of pro-inflammatory genes associated with animal models of neurodegenerative disorders. However, longitudinal research in humans has shown that antidepressants do not protect against dementia, and may even be associated with a risk of cognitive deterioration over time in older adults. The contrast between two sets of findings represents a paradox of significant clinical and public health significance, particularly when treating depression in late life. This review paper attempts to resolve this paradox by critically reviewing the medium- and long-term effects of antidepressants on peripheral immune-inflammatory responses, infection risk, gut microbiota, and neuroendocrine responses to stress, and how these effects may influence the risk of neurodegeneration. Briefly stated, it is possible that the peripheral actions of antidepressant medications may antagonize their beneficial effects against neuroinflammation. The implications of these findings are then explored with a particular focus on the development and testing of multimodal neuroprotective and anti-inflammatory treatments that could reduce the risk of Alzheimer’s and related dementias in patients suffering from depression.
{"title":"Resolving a paradox: antidepressants, neuroinflammation, and neurodegeneration","authors":"R. Rajkumar","doi":"10.37349/ent.2024.00068","DOIUrl":"https://doi.org/10.37349/ent.2024.00068","url":null,"abstract":"Depression is a known risk factor for dementia. Antidepressants are the most commonly used treatment for this condition, and are effective in at least half to two-thirds of cases. Extensive evidence from in vitro and animal models suggests that antidepressants have anti-inflammatory and neuroprotective properties. These effects have been shown to reduce the oxidative damage, amyloid aggregation, and expression of pro-inflammatory genes associated with animal models of neurodegenerative disorders. However, longitudinal research in humans has shown that antidepressants do not protect against dementia, and may even be associated with a risk of cognitive deterioration over time in older adults. The contrast between two sets of findings represents a paradox of significant clinical and public health significance, particularly when treating depression in late life. This review paper attempts to resolve this paradox by critically reviewing the medium- and long-term effects of antidepressants on peripheral immune-inflammatory responses, infection risk, gut microbiota, and neuroendocrine responses to stress, and how these effects may influence the risk of neurodegeneration. Briefly stated, it is possible that the peripheral actions of antidepressant medications may antagonize their beneficial effects against neuroinflammation. The implications of these findings are then explored with a particular focus on the development and testing of multimodal neuroprotective and anti-inflammatory treatments that could reduce the risk of Alzheimer’s and related dementias in patients suffering from depression.","PeriodicalId":502664,"journal":{"name":"Exploration of Neuroprotective Therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140436813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Carlos Forner-Álvarez, Carlos Zanón-Chanzá, F. Cuenca‐Martínez, N. Sempere-Rubio
Fibromyalgia syndrome (FMS) is characterised by the presence of distributed pain in different areas of the body accompanied by the alteration of some functions such as the activity of the neurovegetative system, the sleep quality, or the presence of fatigue. The present narrative review aims to evaluate some key studies regarding the effects of different therapeutic exercise (TE) modalities on clinical variables of interest in patients with FMS, as well as to discuss some of the possible mechanisms of action of TE in improving pain intensity in patients with FMS. All aerobic, strengthening, and body-mind exercises were shown to bring about changes in the improvement of clinical variables of interest in patients with FMS. In addition, with regard to the improvement of pain intensity, there are different arguments that could explain the hypoalgesic effect of TE (structured in physical, neurophysiological, and psychosocial mechanisms). In conclusion, TE is a clinical tool with great potential for patients with FMS as it may produce hypoalgesia through physical, neurophysiological, and psychosocial mechanisms. All these TE modalities have demonstrated in isolation a remarkable effectiveness in the overall improvement of patients with FMS. However, more research is needed in this field especially on the long-term effects and on the combination of the different training modalities.
纤维肌痛综合征（FMS）的特征是身体不同部位出现分布式疼痛，并伴有某些功能的改变，如神经肌能系统的活动、睡眠质量或疲劳。本综述旨在评估有关不同治疗性运动（TE）模式对 FMS 患者临床相关变量影响的一些重要研究，并讨论 TE 在改善 FMS 患者疼痛强度方面的一些可能作用机制。结果表明，所有有氧运动、强化运动和身心运动都能改善 FMS 患者的临床相关变量。此外，关于疼痛强度的改善，有不同的论点可以解释 TE 的镇痛效果（在物理、神经生理和社会心理机制方面）。总之，TE 是一种对 FMS 患者具有巨大潜力的临床工具，因为它可以通过物理、神经生理学和社会心理机制产生低痛感。所有这些 TE 方式都单独显示出在全面改善 FMS 患者方面的显著效果。然而，在这一领域还需要更多的研究，特别是对长期效果和不同训练模式的组合进行研究。
{"title":"Therapeutic exercise in fibromyalgia syndrome: a narrative review","authors":"Carlos Forner-Álvarez, Carlos Zanón-Chanzá, F. Cuenca‐Martínez, N. Sempere-Rubio","doi":"10.37349/ent.2024.00067","DOIUrl":"https://doi.org/10.37349/ent.2024.00067","url":null,"abstract":"Fibromyalgia syndrome (FMS) is characterised by the presence of distributed pain in different areas of the body accompanied by the alteration of some functions such as the activity of the neurovegetative system, the sleep quality, or the presence of fatigue. The present narrative review aims to evaluate some key studies regarding the effects of different therapeutic exercise (TE) modalities on clinical variables of interest in patients with FMS, as well as to discuss some of the possible mechanisms of action of TE in improving pain intensity in patients with FMS. All aerobic, strengthening, and body-mind exercises were shown to bring about changes in the improvement of clinical variables of interest in patients with FMS. In addition, with regard to the improvement of pain intensity, there are different arguments that could explain the hypoalgesic effect of TE (structured in physical, neurophysiological, and psychosocial mechanisms). In conclusion, TE is a clinical tool with great potential for patients with FMS as it may produce hypoalgesia through physical, neurophysiological, and psychosocial mechanisms. All these TE modalities have demonstrated in isolation a remarkable effectiveness in the overall improvement of patients with FMS. However, more research is needed in this field especially on the long-term effects and on the combination of the different training modalities.","PeriodicalId":502664,"journal":{"name":"Exploration of Neuroprotective Therapy","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140449405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：