International review of neurobiology最新文献

{"title":"Adenosine A_2A antagonists and Parkinson's disease.","authors":"Michelle Offit,&nbsp;Brian Nagle,&nbsp;Gonul Ozay,&nbsp;Irma Zhang,&nbsp;Anastassia Kerasidis,&nbsp;Yasar Torres-Yaghi,&nbsp;Fernando Pagan","doi":"10.1016/bs.irn.2023.06.004","DOIUrl":"https://doi.org/10.1016/bs.irn.2023.06.004","url":null,"abstract":"<p><p>Although there is no cure for Parkinson's disease (PD), there are several classes of medications with various mechanisms of action that can help improve the functionality of someone with PD. Dopamine derivatives are first line therapies for PD, hence dopamine receptor agonists (DAs) have been shown to improve functionality of symptoms in PD patients. The two main formulations of dopamine agonist medications in PD therapy are ergoline and non-ergoline derivatives. Additionally, it has been shown that PD can involve irregularities in other neurotransmitters, such as acetylcholine, norepinephrine, and serotonin, hence why non-dopaminergic medications are also vital in PD management. Examples include NMDA receptor antagonists, dopamine antagonists (i.e. neuroleptics), acetylcholine receptor antagonists, serotonin receptor 2A agonists, and adenosine A₂ antagonists. In general, dopaminergic medications are the most effective in improving motor involvement with PD, whereas non-dopaminergic medications tend to focus on the non-motor involvement of PD. In this chapter, we will focus on the chemistry and medication background on dopaminergic vs non-dopaminergic therapy, with a focus of adenosine A₂ antagonists at the end.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"170 ","pages":"105-119"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41158724","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}

{"title":"Sleep deprivation enhances amyloid beta peptide, p-tau and serotonin in the brain: Neuroprotective effects of nanowired delivery of cerebrolysin with monoclonal antibodies to amyloid beta peptide, p-tau and serotonin.","authors":"Aruna Sharma,&nbsp;Lianyuan Feng,&nbsp;Dafin F Muresanu,&nbsp;Z Ryan Tian,&nbsp;José Vicente Lafuente,&nbsp;Anca D Buzoianu,&nbsp;Ala Nozari,&nbsp;Igor Bryukhovetskiy,&nbsp;Igor Manzhulo,&nbsp;Lars Wiklund,&nbsp;Hari Shanker Sharma","doi":"10.1016/bs.irn.2023.05.009","DOIUrl":"10.1016/bs.irn.2023.05.009","url":null,"abstract":"<p><p>Sleep deprivation is quite frequent in military during combat, intelligence gathering or peacekeeping operations. Even one night of sleep deprivation leads to accumulation of amyloid beta peptide burden that would lead to precipitation of Alzheimer's disease over the years. Thus, efforts are needed to slow down or neutralize accumulation of amyloid beta peptide (AβP) and associated Alzheimer's disease brain pathology including phosphorylated tau (p-tau) within the brain fluid environment. Sleep deprivation also alters serotonin (5-hydroxytryptamine) metabolism in the brain microenvironment and impair upregulation of several neurotrophic factors. Thus, blockade or neutralization of AβP, p-tau and serotonin in sleep deprivation may attenuate brain pathology. In this investigation this hypothesis is examined using nanodelivery of cerebrolysin- a balanced composition of several neurotrophic factors and active peptide fragments together with monoclonal antibodies against AβP, p-tau and serotonin (5-hydroxytryptamine, 5-HT). Our observations suggest that sleep deprivation induced pathophysiology is significantly reduced following nanodelivery of cerebrolysin together with monoclonal antibodies to AβP, p-tau and 5-HT, not reported earlier.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"171 ","pages":"125-162"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41166410","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}

{"title":"A_2AR and traumatic brain injury.","authors":"Yan Zhao,&nbsp;Ya-Lei Ning,&nbsp;Yuan-Guo Zhou","doi":"10.1016/bs.irn.2023.07.006","DOIUrl":"https://doi.org/10.1016/bs.irn.2023.07.006","url":null,"abstract":"<p><p>Accumulating evidence has revealed the adenosine 2A receptor is a key tuner for neuropathological and neurobehavioral changes following traumatic brain injury by experimental animal models and a few clinical trials. Here, we highlight recent data involving acute/sub-acute and chronic alterations of adenosine and adenosine 2A receptor-associated signaling in pathological conditions after trauma, with an emphasis of traumatic brain injury, including neuroinflammation, cognitive and psychiatric disorders, and other severe consequences. We expect this would lead to the development of therapeutic strategies for trauma-related disorders with novel mechanisms of action.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"170 ","pages":"225-265"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41172179","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}

{"title":"Spinal cord injury induced exacerbation of Alzheimer's disease like pathophysiology is reduced by topical application of nanowired cerebrolysin with monoclonal antibodies to amyloid beta peptide, p-tau and tumor necrosis factor alpha.","authors":"Aruna Sharma, Lianyuan Feng, Dafin F Muresanu, Z Ryan Tian, José Vicente Lafuente, Anca D Buzoianu, Ala Nozari, Lars Wiklund, Hari Shanker Sharma","doi":"10.1016/bs.irn.2023.05.011","DOIUrl":"10.1016/bs.irn.2023.05.011","url":null,"abstract":"<p><p>Hallmark of Alzheimer's disease include amyloid beta peptide and phosphorylated tau deposition in brain that could be aggravated following traumatic of concussive head injury. However, amyloid beta peptide or p-tau in spinal cord following injury is not well known. In this investigation we measured amyloid beta peptide and p-tau together with tumor necrosis factor-alpha (TNF-α) in spinal cord and brain following 48 h after spinal cord injury in relation to the blood-spinal cord and blood-brain barrier, edema formation, blood flow changes and cell injury in perifocal regions of the spinal cord and brain areas. A focal spinal cord injury was inflicted over the right dorsal horn of the T10-11 segment (4 mm long and 2 mm deep) and amyloid beta peptide and p-tau was measured in perifocal rostral (T9) and caudal (T12) spinal cord segments as well as in the brain areas. Our observations showed a significant increase in amyloid beta peptide in the T9 and T12 segments as well as in remote areas of brain and spinal cord after 24 and 48 h injury. This is associated with breakdown of the blood-spinal cord (BSCB) and brain barriers (BBB), edema formation, reduction in blood flow and cell injury. After 48 h of spinal cord injury elevation of amyloid beta peptide, phosphorylated tau (p-tau) and tumor necrosis factor-alpha (TNF-α) was seen in T9 and T12 segments of spinal cord in cerebral cortex, hippocampus and brain stem regions associated with microglial activation as seen by upregulation of Iba1 and CD86. Repeated nanowired delivery of cerebrolysin topically over the traumatized segment repeatedly together with monoclonal antibodies (mAb) to amyloid beta peptide (AβP), p-tau and TNF-α significantly attenuated amyloid beta peptide, p-tau deposition and reduces Iba1, CD68 and TNF-α levels in the brain and spinal cord along with blockade of BBB and BSCB, reduction in blood flow, edema formation and cell injury. These observations are the first to show that spinal cord injury induces Alzheimer's disease like symptoms in the CNS, not reported earlier.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"172 ","pages":"3-35"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41224030","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}

{"title":"Co-administration of dl-3-n-butylphthalide and neprilysin is neuroprotective in Alzheimer disease associated with mild traumatic brain injury.","authors":"Zhenguo G Wang,&nbsp;Aruna Sharma,&nbsp;Lianyuan Feng,&nbsp;Dafin F Muresanu,&nbsp;Z Ryan Tian,&nbsp;José Vicente Lafuente,&nbsp;Anca D Buzoianu,&nbsp;Ala Nozari,&nbsp;Hongyun Huang,&nbsp;Lin Chen,&nbsp;Igor Manzhulo,&nbsp;Lars Wiklund,&nbsp;Hari Shanker Sharma","doi":"10.1016/bs.irn.2023.06.006","DOIUrl":"10.1016/bs.irn.2023.06.006","url":null,"abstract":"<p><p>dl-3-n-Butylphthalide is a potent synthetic Chinese celery extract that is highly efficient in inducing neuroprotection in concussive head injury (CHI), Parkinson's disease, Alzheimer's disease, stroke as well as depression, dementia, anxiety and other neurological diseases. Thus, there are reasons to believe that dl-3-n-butylphthalide could effectively prevent Alzheimer's disease brain pathology. Military personnel during combat operation or veterans are often the victims of brain injury that is a major risk factor for developing Alzheimer's disease in their later lives. In our laboratory we have shown that CHI exacerbates Alzheimer's disease brain pathology and reduces the amyloid beta peptide (AβP) inactivating enzyme neprilysin. We have used TiO₂ nanowired-dl-3-n-butylphthalide in attenuating Parkinson's disease brain pathology exacerbated by CHI. Nanodelivery of dl-3-n-butylphthalide appears to be more potent as compared to the conventional delivery of the compound. Thus, it would be interesting to examine the effects of nanowired dl-3-n-butylphthalide together with nanowired delivery of neprilysin in Alzheimer's disease model on brain pathology. In this investigation we found that nanowired delivery of dl-3-n-butylphthalide together with nanowired neprilysin significantly attenuated brain pathology in Alzheimer's disease model with CHI, not reported earlier. The possible mechanism and clinical significance is discussed based on the current literature.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"172 ","pages":"145-185"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41224105","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}

{"title":"The adenosine A_2A receptor in the basal ganglia: Expression, heteromerization, functional selectivity and signalling.","authors":"Rafael Franco,&nbsp;Gemma Navarro,&nbsp;Eva Martínez-Pinilla","doi":"10.1016/bs.irn.2023.04.008","DOIUrl":"https://doi.org/10.1016/bs.irn.2023.04.008","url":null,"abstract":"<p><p>Adenosine is a neuroregulatory nucleoside that acts through four G protein-coupled receptors (GPCRs), A₁, A_2A, A_2B and A₃, which are widely expressed in cells of the nervous system. The A_2A receptor (A_2AR), the GPCR with the highest expression in the striatum, has a similar role to that of receptors for dopamine, one of the main neurotransmitters. Neuronal and glial A_2ARs participate in the modulation of dopaminergic transmission and act in almost any action in which the basal ganglia is involved. This chapter revisits the expression of the A_2AR in the basal ganglia in health and disease, and describes the diversity of signalling depending on whether the receptors are expressed as monomer or as heteromer. The A_2AR can interact with other receptors as adenosine A₁, dopamine D₂, or cannabinoid CB₁ to form heteromers with relevant functions in the basal ganglia. Heteromerization, with these and other GPCRs, provides diversity to A_2AR-mediated signalling and to the modulation of neurotransmission. Thus, selective A_2AR antagonists have neuroprotective potential acting directly on neurons, but also through modulation of glial cell activation, for example, by decreasing neuroinflammatory events that accompany neurodegenerative diseases. In fact, A_2AR antagonists are safe and their potential in the therapy of Parkinson's disease has already led to the approval of one of them, istradefylline, in Japan and United States. The receptor also has a key role in reward circuits and, again, heteromers with dopamine receptors, but also with cannabinoid CB₁ receptors, participate in the events triggered by drugs of abuse.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"170 ","pages":"49-71"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41147780","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}

{"title":"Adenosine A_2A signals and dystonia.","authors":"Makio Takahashi","doi":"10.1016/bs.irn.2023.06.001","DOIUrl":"https://doi.org/10.1016/bs.irn.2023.06.001","url":null,"abstract":"<p><p>Dystonia is a movement disorder characterized by sustained or intermittent involuntary muscle contractions, which is also seen in an advanced stage of Parkinson's disease (PD) as camptocormia, torticollis, and Pisa syndrome. Istradefylline, an adenosine A_2A receptor antagonist, can be used for the treatment of PD to reduce 'off'-time period, and several clinical studies demonstrated the improvement of camptocormia, which have many similar features to dopa-responsive/non-responsive dystonia. Many animal models of dystonia showed that adenosine A_2A receptor colocalized with dopamine D2 positive spiny projection neurons in indirect pathway of basal ganglia circuit, and also in the cholinergic interneurons that affects the balance of indirect and direct pathway of basal ganglia. In this chapter, the potential effect of adenosine A_2A antagonism on dystonia was discussed in view of clinical studies of PD with postural abnormalities and the findings of dystonia mouse models.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"170 ","pages":"179-184"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41161388","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}

{"title":"Susac syndrome can be diagnosed by examination and cured by comprehensive therapy.","authors":"Feifei Jiang,&nbsp;Zhiming Ma,&nbsp;Zhizhi Chen,&nbsp;Ming Yang,&nbsp;Hongyun Huang,&nbsp;Lin Chen,&nbsp;Chao He","doi":"10.1016/bs.irn.2023.03.004","DOIUrl":"10.1016/bs.irn.2023.03.004","url":null,"abstract":"","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"171 ","pages":"329-337"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41169556","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}

{"title":"How and why the adenosine A_2A receptor became a target for Parkinson's disease therapy.","authors":"Peter Jenner,&nbsp;Tomoyuki Kanda,&nbsp;Akihisa Mori","doi":"10.1016/bs.irn.2023.04.005","DOIUrl":"https://doi.org/10.1016/bs.irn.2023.04.005","url":null,"abstract":"<p><p>Dopaminergic therapy for Parkinson's disease has revolutionised the treatment of the motor symptoms of the illness. However, it does not alleviate all components of the motor deficits and has only limited effects on non-motor symptoms. For this reason, alternative non-dopaminergic approaches to treatment have been sought and the adenosine A_2A receptor provided a novel target for symptomatic therapy both within the basal ganglia and elsewhere in the brain. Despite an impressive preclinical profile that would indicate a clear role for adenosine A_2A antagonists in the treatment of Parkinson's disease, the road to clinical use has been long and full of difficulties. Some aspects of the drugs preclinical profile have not translated into clinical effectiveness and not all the clinical studies undertaken have had a positive outcome. The reasons for this will be explored and suggestions made for the further development of this drug class in the treatment of Parkinson's disease. However, one adenosine A_2A antagonist, namely istradefylline has been introduced successfully for the treatment of late-stage Parkinson's disease in two major areas of the world and has become a commercial success through offering the first non-dopaminergic approach to the treatment of unmet need to be introduced in several decades.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"170 ","pages":"73-104"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41151025","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}

{"title":"Nose-to-brain drug delivery for the treatment of CNS disease: New development and strategies.","authors":"Li Du,&nbsp;Lin Chen,&nbsp;Fangfang Liu,&nbsp;Wenya Wang,&nbsp;Hongyun Huang","doi":"10.1016/bs.irn.2023.05.014","DOIUrl":"10.1016/bs.irn.2023.05.014","url":null,"abstract":"<p><p>Delivering drugs to the brain has always been a challenging task due to the restrictive properties of the blood-brain barrier (BBB). Intranasal delivery is therefore emerging as an efficient method of administration, making it easy to self-administration and thus provides a non-invasive and painless alternative to oral and parenteral administration for delivering therapeutics to the central nervous system (CNS). Recently, drug formulations have been developed to further enhance this nose-to-brain transport, primarily using nanoparticles (NPs). Therefore, the purposes of this review are to highlight and describe the anatomical basis of nasal-brain pathway and provide an overview of drug formulations and current drugs for intranasal administration in CNS disease.</p>","PeriodicalId":94058,"journal":{"name":"International review of neurobiology","volume":"171 ","pages":"255-297"},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41143367","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}