International review of neurobiology最新文献_第3页

Alcohol and the dopamine system. 酒精与多巴胺系统

International review of neurobiology Pub Date : 2024-01-01 Epub Date: 2024-03-13 DOI: 10.1016/bs.irn.2024.02.003

Bo Söderpalm, Mia Ericson

引用次数: 0

Current neuroprotective therapies and future prospects for motor neuron disease. 当前的神经保护疗法和运动神经元疾病的未来前景。

International review of neurobiology Pub Date : 2024-01-01 Epub Date: 2024-05-16 DOI: 10.1016/bs.irn.2024.04.003

Laura J Evans, David O'Brien, Pamela J Shaw

{"title":"Current neuroprotective therapies and future prospects for motor neuron disease.","authors":"Laura J Evans, David O'Brien, Pamela J Shaw","doi":"10.1016/bs.irn.2024.04.003","DOIUrl":"10.1016/bs.irn.2024.04.003","url":null,"abstract":"Four medications with neuroprotective disease-modifying effects are now in use for motor neuron disease (MND). With FDA approvals for tofersen, relyvrio and edaravone in just the past year, 2022 ended a quarter of a century when riluzole was the sole such drug to offer to patients. The acceleration of approvals may mean we are witnessing the beginning of a step-change in how MND can be treated. Improvements in understanding underlying disease biology has led to more therapies being developed to target specific and multiple disease mechanisms. Consideration for how the pipeline of new therapeutic agents coming through in clinical and preclinical development can be more effectively evaluated with biomarkers, advances in patient stratification and clinical trial design pave the way for more successful translation for this archetypal complex neurodegenerative disease. While it must be cautioned that only slowed rates of progression have so far been demonstrated, pre-empting rapid neurodegeneration by using neurofilament biomarkers to signal when to treat, as is currently being trialled with tofersen, may be more effective for patients with known genetic predisposition to MND. Early intervention with personalized medicines could mean that for some patients at least, in future we may be able to substantially treat what is considered by many to be one of the most distressing diseases in medicine.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"176 ","pages":"327-384"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141159323","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}

引用次数: 0

Cannabidiol and epilepsy. 大麻二酚与癫痫。

International review of neurobiology Pub Date : 2024-01-01 Epub Date: 2024-04-06 DOI: 10.1016/bs.irn.2024.03.009

Fabrício A Moreira, Antônio C P de Oliveira, Victor R Santos, Márcio F D Moraes

引用次数: 0

Molecular mechanisms of neuropathic pain. 神经性疼痛的分子机制

International review of neurobiology Pub Date : 2024-01-01 Epub Date: 2024-11-02 DOI: 10.1016/bs.irn.2024.10.002

Paola Pacifico, Daniela M Menichella

引用次数: 0

Ghrelin system and GLP-1 as potential treatment targets for alcohol use disorder. 胃泌素系统和 GLP-1 作为酒精使用障碍的潜在治疗目标。

International review of neurobiology Pub Date : 2024-01-01 Epub Date: 2024-08-03 DOI: 10.1016/bs.irn.2024.07.006

Elisabet Jerlhag

{"title":"Ghrelin system and GLP-1 as potential treatment targets for alcohol use disorder.","authors":"Elisabet Jerlhag","doi":"10.1016/bs.irn.2024.07.006","DOIUrl":"https://doi.org/10.1016/bs.irn.2024.07.006","url":null,"abstract":"Peptides of the gut-brain axis have gained recent attention as potential treatment targets for addiction. While the number of gut-brain peptides is vast, ghrelin and glucagon-like peptide-1 (GLP-1) have been suggested as important players. Ghrelin is traditionally considered an orexigenic peptide, but recent studies found that it increases alcohol intake in rodents and craving for alcohol in humans. Additionally, suppression of the ghrelin receptor attenuates alcohol-related responses in animal models reflecting alcohol use disorder (AUD). For instance, a lower alcohol intake, suppressed motivation to consume alcohol, and attenuated reward from alcohol is observed after ghrelin receptor antagonism treatment. On a similar note, a partial ghrelin receptor agonist prevents hangover symptoms in humans. When it comes to the anorexigenic peptide GLP-1, agonists of its receptor are approved to treat diabetes type 2 and obesity. Extensive preclinical studies have revealed that these GLP-1 receptor agonists reduce alcohol intake, suppress the motivation to consume alcohol, and prevent relapse drink, with effects tentatively associated with a reduced alcohol-induced reward. These preclinical findings have to some extent been varied in humans, as GLP-1 receptor agonists decrease alcohol intake in overweight patients with AUD. Furthermore, genetic variations in either the genes encoding for pre-pro-ghrelin, GHSR, GLP-1, or its receptor, are associated with AUD and heavy alcohol drinking. While central mechanisms appear to modulate the ability of either ghrelin or GLP-1 to regulate alcohol-related responses the exact mechanisms have not been defined. Taken together these preclinical and clinical data imply that gut-brain peptides participate in the addiction process and should be considered as potential targets for AUD treatment.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"178 ","pages":"401-432"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142635033","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}

引用次数: 0

The CRF/Urocortin systems as therapeutic targets for alcohol use disorders. CRF/Urocortin 系统作为酒精使用障碍的治疗目标。

International review of neurobiology Pub Date : 2024-01-01 Epub Date: 2024-08-28 DOI: 10.1016/bs.irn.2024.08.002

Cristiane Aparecida Favoretto, Natalia Bonetti Bertagna, Tarciso Tadeu Miguel, Isabel M H Quadros

{"title":"The CRF/Urocortin systems as therapeutic targets for alcohol use disorders.","authors":"Cristiane Aparecida Favoretto, Natalia Bonetti Bertagna, Tarciso Tadeu Miguel, Isabel M H Quadros","doi":"10.1016/bs.irn.2024.08.002","DOIUrl":"https://doi.org/10.1016/bs.irn.2024.08.002","url":null,"abstract":"Development and maintenance of alcohol use disorders have been proposed to recruit critical mechanisms involving Corticotropin Releasing Factor and Urocortins (CRF/Ucns). The CRF/Ucns system is comprised of a family of peptides (CRF, Ucn 1, Ucn 2, Ucn 3) which act upon two receptor subtypes, CRFR1 and CRFR2, each with different affinity profiles to the endogenous peptides and differential brain distribution. Activity of CRF/Ucn system is further modulated by CRF binding protein (CRF-BP), which regulates availability of CRF and Ucns to exert their actions. Extensive evidence in preclinical models support the involvement of CRF/Ucn targets in escalated alcohol drinking, as well as point to changes in CRF/Ucn brain function as a result of chronic alcohol exposure and/or withdrawal. It highlights the role of CRF and CRFR1-mediated signaling in conditions of excessive alcohol taking and seeking, including during various stages of withdrawal and relapse to alcohol. Besides its role in the hypothalamic-pituitary-adrenal (HPA) axis, the importance of extra-hypothalamic CRF pathways, especially in the extended amygdala, in the neurobiology of alcohol abuse and dependence is emphasized. Emerging roles for other targets of the CRF/Ucn system, such as CRF2 receptors, CRF-BP and Ucns in escalated alcohol drinking is also discussed. Finally, the limited translational value of CRF/Ucn interventions in stress-related and alcohol use disorders is discussed. So far, CRFR1 antagonists have shown little or no efficacy in human clinical trials, although a range of unexplored conditions and possibilities remain to be explored.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"178 ","pages":"97-152"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142635066","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}

引用次数: 0

A general clinical overview of the non-motor symptoms in Parkinson's disease: Neuropsychiatric symptoms. 帕金森病非运动症状临床概述：神经精神症状。

International review of neurobiology Pub Date : 2024-01-01 Epub Date: 2024-01-15 DOI: 10.1016/bs.irn.2023.11.001

Lucia Batzu, Aleksandra Podlewska, Lucy Gibson, K Ray Chaudhuri, Dag Aarsland

引用次数: 0

Setting the clinical context to non-motor symptoms reflected by Park-pain, Park-sleep, and Park-autonomic subtypes of Parkinson's disease. 为帕金森病的帕克疼痛亚型、帕克睡眠亚型和帕克自主神经亚型所反映的非运动症状设定临床背景。

International review of neurobiology Pub Date : 2024-01-01 Epub Date: 2023-12-01 DOI: 10.1016/bs.irn.2023.08.012

Mubasher A Qamar, Phoebe Tall, Daniel van Wamelen, Yi Min Wan, Katarina Rukavina, Anna Fieldwalker, Donna Matthew, Valentina Leta, Kirsty Bannister, K Ray Chaudhuri

引用次数: 0

Cannabidiol in experimental cerebral ischemia. 大麻二酚在实验性脑缺血中的作用。

International review of neurobiology Pub Date : 2024-01-01 Epub Date: 2024-07-09 DOI: 10.1016/bs.irn.2024.04.012

Rúbia Maria Weffort de Oliveira, Nathalia Akemi Kohara, Humberto Milani

引用次数: 0

Neuropathic pain - A clinical primer. 神经性疼痛--临床入门。

International review of neurobiology Pub Date : 2024-01-01 Epub Date: 2024-11-08 DOI: 10.1016/bs.irn.2024.10.014

Jan Rosner, Prasad Shirvalkar, Daniel Ciampi de Andrade

{"title":"Neuropathic pain - A clinical primer.","authors":"Jan Rosner, Prasad Shirvalkar, Daniel Ciampi de Andrade","doi":"10.1016/bs.irn.2024.10.014","DOIUrl":"https://doi.org/10.1016/bs.irn.2024.10.014","url":null,"abstract":"Neuropathic pain is used both as a mechanistic descriptor and a classification category of pain caused by a lesion or disease of the somatosensory nervous system and encompasses a vast array of possible diagnoses. The identification of neuropathic pain and diagnosis of specific syndromes relies on a detailed patient history. Standardized pain questionnaires can capture the patient`s symptoms, while the anatomical distribution of pain is often documented using pain drawings. Following this, a thorough clinical neurological examination is conducted to identify distinct sensory abnormalities, specifically sensory deficits and signs of increased sensitivity such as allodynia and hyperalgesia, within the pain-affected areas. Regardless of whether the lesion or disease is in the peripheral or central somatosensory nervous system, the presence of clinically overt sensory abnormalities is a key feature, distinguishing neuropathic pain from other types of pain, such as nociceptive pain, which likely coexist in neurological disorders. Extensive sensory deficits, as seen in certain stroke syndromes or following spinal cord injuries, may increase the likelihood of concomitant non-neuropathic pain within the same area of sensory loss. For this reason, differential diagnosis is essential when assessing patients with suspected neuropathic pain. Further diagnostic tests, including imaging or specific neurophysiological methods that assess nociceptive pathways, can provide objective evidence of a lesion or disease within the somatosensory nervous system. However, the causality between the lesion and the presence of neuropathic pain cannot be established definitively and always requires clinical judgment and interpretation within the broader context of the neurological disorder.","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"179 ","pages":"41-65"},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142696217","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}

引用次数: 0