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Article: State of the Art and Future of Stem Cell Therapy in Ischemic Stroke: Why Don't We Focus on Their Administration?

Valeri, Andrea / Mazzon, Emanuela

2023 Volume 10, Issue 1

Abstract: Stroke is one of the leading causes of death and disability worldwide, so there is an urgent need to find a therapy for the tragic outcomes of this cerebrovascular disease. Stem cells appeared to be a good solution for many conditions, so different ... ...

Abstract	Stroke is one of the leading causes of death and disability worldwide, so there is an urgent need to find a therapy for the tragic outcomes of this cerebrovascular disease. Stem cells appeared to be a good solution for many conditions, so different experiments were made to establish stem cells as a feasible therapy for stroke. The aim of this review is to analyze the state of the art of stem cell therapy for stroke and if the route of administration could represent a valid adjusting point for ameliorating the therapy's outcome. To obtain this, we searched the scientific literature of the last 10 years for relevant in vitro and in vivo evidence regarding stem cells' potential in stroke therapy. In vitro evidence points to hypoxia, among the preconditioning strategies, as the most used and probably efficient method to enhance cells qualities, while in vivo results raise the question if it is the type of cells or how they are administrated which can make the difference in terms of efficiency. Unfortunately, despite the number of clinical trials, only a few were successfully concluded, demonstrating how urgent the necessity is to translate pre-clinical results into clinics. Since any type of stem cell seems suitable for therapy, the chosen route of administration corresponds to different engraftment rates, distribution and efficiency in terms of the beneficial effects of stem cells. Intravenous administration was widely used for delivering stem cells into the human body, but recently intranasal administration has given promising results in vivo. It allows stem cells to efficiently reach the brain that was precluded to intravenous administration, so it is worth further investigation.
Language	English
Publishing date	2023-01-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2746191-9
ISSN	2306-5354
ISSN	2306-5354
DOI	10.3390/bioengineering10010118
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Innovative Insights into Traumatic Brain Injuries: Biomarkers and New Pharmacological Targets.

Silvestro, Serena / Raffaele, Ivana / Quartarone, Angelo / Mazzon, Emanuela

International journal of molecular sciences

2024 Volume 25, Issue 4

Abstract: A traumatic brain injury (TBI) is a major health issue affecting many people across the world, causing significant morbidity and mortality. TBIs often have long-lasting effects, disrupting daily life and functionality. They cause two types of damage to ... ...

Abstract	A traumatic brain injury (TBI) is a major health issue affecting many people across the world, causing significant morbidity and mortality. TBIs often have long-lasting effects, disrupting daily life and functionality. They cause two types of damage to the brain: primary and secondary. Secondary damage is particularly critical as it involves complex processes unfolding after the initial injury. These processes can lead to cell damage and death in the brain. Understanding how these processes damage the brain is crucial for finding new treatments. This review examines a wide range of literature from 2021 to 2023, focusing on biomarkers and molecular mechanisms in TBIs to pinpoint therapeutic advancements. Baseline levels of biomarkers, including neurofilament light chain (NF-L), ubiquitin carboxy-terminal hydrolase-L1 (UCH-L1), Tau, and glial fibrillary acidic protein (GFAP) in TBI, have demonstrated prognostic value for cognitive outcomes, laying the groundwork for personalized treatment strategies. In terms of pharmacological progress, the most promising approaches currently target neuroinflammation, oxidative stress, and apoptotic mechanisms. Agents that can modulate these pathways offer the potential to reduce a TBI's impact and aid in neurological rehabilitation. Future research is poised to refine these therapeutic approaches, potentially revolutionizing TBI treatment.
MeSH term(s)	Humans ; Brain Injuries, Traumatic/drug therapy ; Brain Injuries ; Brain ; Biomarkers ; Glial Fibrillary Acidic Protein ; Ubiquitin Thiolesterase
Chemical Substances	Biomarkers ; Glial Fibrillary Acidic Protein ; Ubiquitin Thiolesterase (EC 3.4.19.12)
Language	English
Publishing date	2024-02-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25042372
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Article: The Role of Cannabinoid Type 2 Receptors in Parkinson's Disease.

Basile, Maria Sofia / Mazzon, Emanuela

Biomedicines

2022 Volume 10, Issue 11

Abstract: Parkinson's disease (PD) is the second most frequent neurodegenerative disease and currently represents a clear unmet medical need. Therefore, novel preventive and therapeutic strategies are needed. Cannabinoid type 2 (CB2) receptors, one of the ... ...

Abstract	Parkinson's disease (PD) is the second most frequent neurodegenerative disease and currently represents a clear unmet medical need. Therefore, novel preventive and therapeutic strategies are needed. Cannabinoid type 2 (CB2) receptors, one of the components of the endocannabinoid system, can regulate neuroinflammation in PD. Here, we review the current preclinical and clinical studies investigating the CB2 receptors in PD with the aim to clarify if these receptors could have a role in PD. Preclinical data show that CB2 receptors could have a neuroprotective action in PD and that the therapeutic targeting of CB2 receptors could be promising. Indeed, it has been shown that different CB2 receptor-selective agonists exert protective effects in different PD models. Moreover, the alterations in the expression of CB2 receptors observed in brain tissues from PD animal models and PD patients suggest the potential value of CB2 receptors as possible novel biomarkers for PD. However, to date, there is no direct evidence of the role of CB2 receptors in PD. Further studies are strongly needed in order to fully clarify the role of CB2 receptors in PD and thus pave the way to novel possible diagnostic and therapeutic opportunities for PD.
Language	English
Publishing date	2022-11-20
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines10112986
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Article ; Online: MiRNAs as Promising Translational Strategies for Neuronal Repair and Regeneration in Spinal Cord Injury.

Silvestro, Serena / Mazzon, Emanuela

Cells

2022 Volume 11, Issue 14

Abstract: Spinal cord injury (SCI) represents a devastating injury to the central nervous system (CNS) that is responsible for impaired mobility and sensory function in SCI patients. The hallmarks of SCI include neuroinflammation, axonal degeneration, neuronal ... ...

Abstract	Spinal cord injury (SCI) represents a devastating injury to the central nervous system (CNS) that is responsible for impaired mobility and sensory function in SCI patients. The hallmarks of SCI include neuroinflammation, axonal degeneration, neuronal loss, and reactive gliosis. Current strategies, including stem cell transplantation, have not led to successful clinical therapy. MiRNAs are crucial for the differentiation of neural cell types during CNS development, as well as for pathological processes after neural injury including SCI. This makes them ideal candidates for therapy in this condition. Indeed, several studies have demonstrated the involvement of miRNAs that are expressed differently in CNS injury. In this context, the purpose of the review is to provide an overview of the pre-clinical evidence evaluating the use of miRNA therapy in SCI. Specifically, we have focused our attention on miRNAs that are widely associated with neuronal and axon regeneration. "MiRNA replacement therapy" aims to transfer miRNAs to diseased cells and improve targeting efficacy in the cells, and this new therapeutic tool could provide a promising technique to promote SCI repair and reduce functional deficits.
MeSH term(s)	Axons/metabolism ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Nerve Regeneration/genetics ; Neurons/metabolism ; Spinal Cord Injuries/genetics ; Spinal Cord Injuries/pathology ; Spinal Cord Injuries/therapy
Chemical Substances	MicroRNAs
Language	English
Publishing date	2022-07-12
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11142177
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Network Analysis Performed on Transcriptomes of Parkinson's Disease Patients Reveals Dysfunction in Protein Translation.

D'Angiolini, Simone / Lui, Maria / Mazzon, Emanuela / Calabrò, Marco

International journal of molecular sciences

2024 Volume 25, Issue 2

Abstract: Parkinson's disease (PD) is a prevalent neurodegenerative disorder characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra region of the brain. The hallmark pathological feature of PD is the accumulation of misfolded ...

Abstract	Parkinson's disease (PD) is a prevalent neurodegenerative disorder characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra region of the brain. The hallmark pathological feature of PD is the accumulation of misfolded proteins, leading to the formation of intracellular aggregates known as Lewy bodies. Recent data evidenced how disruptions in protein synthesis, folding, and degradation are events commonly observed in PD and may provide information on the molecular background behind its etiopathogenesis. In the present study, we used a publicly available transcriptomic microarray dataset of peripheral blood of PD patients and healthy controls (GSE6613) to investigate the potential dysregulation of elements involved in proteostasis-related processes at the transcriptomic level. Our bioinformatics analysis revealed 375 differentially expressed genes (DEGs), of which 281 were down-regulated and 94 were up-regulated. Network analysis performed on the observed DEGs highlighted a cluster of 36 elements mainly involved in the protein synthesis processes. Different enriched ontologies were related to translation initiation and regulation, ribosome structure, and ribosome components nuclear export. Overall, this data consistently points to a generalized impairment of the translational machinery and proteostasis. Dysregulation of these mechanics has been associated with PD pathogenesis. Understanding the precise regulation of such processes may shed light on the molecular mechanisms of PD and provide potential data for early diagnosis.
MeSH term(s)	Humans ; Parkinson Disease/metabolism ; Transcriptome ; Lewy Bodies/metabolism ; Gene Expression Profiling ; Protein Biosynthesis ; Substantia Nigra/metabolism
Language	English
Publishing date	2024-01-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25021299
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Article ; Online: Multiple Sclerosis: Roles of miRNA, lcnRNA, and circRNA and Their Implications in Cellular Pathways.

Cipriano, Giovanni Luca / Schepici, Giovanni / Mazzon, Emanuela / Anchesi, Ivan

International journal of molecular sciences

2024 Volume 25, Issue 4

Abstract: Multiple sclerosis (MS) is a degenerative condition characterized by axonal damage and demyelination induced by autoreactive immune cells that occur in the Central Nervous System (CNS). The interaction between epigenetic changes and genetic factors can ... ...

Abstract	Multiple sclerosis (MS) is a degenerative condition characterized by axonal damage and demyelination induced by autoreactive immune cells that occur in the Central Nervous System (CNS). The interaction between epigenetic changes and genetic factors can be widely involved in the onset, development, and progression of the disease. Although numerous efforts were made to discover new therapies able to prevent and improve the course of MS, definitive curative treatments have not been found yet. However, in recent years, it has been reported that non-coding RNAs (ncRNAs), including microRNAs (miRNAs), long ncRNAs (lncRNAs), and circular RNAs (circRNAs), acting as gene expression regulators, could be used as potential therapeutic targets or biomarkers to diagnose and fight MS. In this review, we discussed the role of miRNAs, lncRNAs, and circRNAs, as well as their expression level changes and signaling pathways that are related to preclinical and human MS studies. Hence, the investigation of ncRNAs could be important to provide additional information regarding MS pathogenesis as well as promote the discovery of new therapeutic strategies or biomarkers.
MeSH term(s)	Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; RNA, Circular/genetics ; RNA, Circular/metabolism ; RNA, Long Noncoding/genetics ; Multiple Sclerosis/genetics ; RNA, Untranslated/genetics ; Biomarkers
Chemical Substances	MicroRNAs ; RNA, Circular ; RNA, Long Noncoding ; RNA, Untranslated ; Biomarkers
Language	English
Publishing date	2024-02-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25042255
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Article ; Online: In Silico Analysis Highlights Potential Predictive Indicators Associated with Secondary Progressive Multiple Sclerosis.

Calabrò, Marco / Lui, Maria / Mazzon, Emanuela / D'Angiolini, Simone

International journal of molecular sciences

2024 Volume 25, Issue 6

Abstract: Multiple sclerosis (MS) is a complex inflammatory disease affecting the central nervous system. Most commonly, it begins with recurrent symptoms followed by partial or complete recovery, known as relapsing-remitting MS (RRMS). Over time, many RRMS ... ...

Abstract	Multiple sclerosis (MS) is a complex inflammatory disease affecting the central nervous system. Most commonly, it begins with recurrent symptoms followed by partial or complete recovery, known as relapsing-remitting MS (RRMS). Over time, many RRMS patients progress to secondary progressive MS (SPMS), marked by gradual symptom deterioration. The factors triggering this transition remain unknown, lacking predictive biomarkers. This study aims to identify blood biomarkers specific to SPMS. We analyzed six datasets of SPMS and RRMS patients' blood and brain tissues, and compared the differential expressed genes (DEGs) obtained to highlight DEGs reflecting alterations occurring in both brain and blood tissues and the potential biological processes involved. We observed a total of 38 DEGs up-regulated in both blood and brain tissues, and their interaction network was evaluated through network analysis. Among the aforementioned DEGs, 21 may be directly involved with SPMS transition. Further, we highlighted three biological processes, including the calcineurin-NFAT pathway, related to this transition. The investigated DEGs may serve as a promising means to monitor the transition from RRMS to SPMS, which is still elusive. Given that they can also be sourced from blood samples, this approach could offer a relatively rapid and convenient method for monitoring MS and facilitating expedited assessments.
MeSH term(s)	Humans ; Multiple Sclerosis, Chronic Progressive/genetics ; Multiple Sclerosis/diagnosis ; Multiple Sclerosis, Relapsing-Remitting/metabolism ; Brain/metabolism ; Biomarkers
Chemical Substances	Biomarkers
Language	English
Publishing date	2024-03-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25063374
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Article ; Online: MicroRNAs and MAPKs: Evidence of These Molecular Interactions in Alzheimer's Disease.

Raffaele, Ivana / Silvestro, Serena / Mazzon, Emanuela

International journal of molecular sciences

2023 Volume 24, Issue 5

Abstract: Alzheimer's disease (AD) is a neurodegenerative disorder known to be the leading cause of dementia worldwide. Many microRNAs (miRNAs) were found deregulated in the brain or blood of AD patients, suggesting a possible key role in different stages of ... ...

Abstract	Alzheimer's disease (AD) is a neurodegenerative disorder known to be the leading cause of dementia worldwide. Many microRNAs (miRNAs) were found deregulated in the brain or blood of AD patients, suggesting a possible key role in different stages of neurodegeneration. In particular, mitogen-activated protein kinases (MAPK) signaling can be impaired by miRNA dysregulation during AD. Indeed, the aberrant MAPK pathway may facilitate the development of amyloid-beta (Aβ) and Tau pathology, oxidative stress, neuroinflammation, and brain cell death. The aim of this review was to describe the molecular interactions between miRNAs and MAPKs during AD pathogenesis by selecting evidence from experimental AD models. Publications ranging from 2010 to 2023 were considered, based on PubMed and Web of Science databases. According to obtained data, several miRNA deregulations may regulate MAPK signaling in different stages of AD and conversely. Moreover, overexpressing or silencing miRNAs involved in MAPK regulation was seen to improve cognitive deficits in AD animal models. In particular, miR-132 is of particular interest due to its neuroprotective functions by inhibiting Aβ and Tau depositions, as well as oxidative stress, through ERK/MAPK1 signaling modulation. However, further investigations are required to confirm and implement these promising results.
MeSH term(s)	Animals ; Alzheimer Disease/metabolism ; MicroRNAs/genetics ; Amyloid beta-Peptides/metabolism ; Signal Transduction ; Brain/metabolism ; Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	MicroRNAs ; Amyloid beta-Peptides ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2023-03-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24054736
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Article: Regenerative Effects of Exosomes-Derived MSCs: An Overview on Spinal Cord Injury Experimental Studies.

Schepici, Giovanni / Silvestro, Serena / Mazzon, Emanuela

Biomedicines

2023 Volume 11, Issue 1

Abstract: Spinal cord injury (SCI) is a devastating condition usually induced by the initial mechanical insult that can lead to permanent motor and sensory deficits. At present, researchers are investigating potential therapeutic strategies to ameliorate the neuro- ...

Abstract	Spinal cord injury (SCI) is a devastating condition usually induced by the initial mechanical insult that can lead to permanent motor and sensory deficits. At present, researchers are investigating potential therapeutic strategies to ameliorate the neuro-inflammatory cascade that occurs post-injury. Although the use of mesenchymal stromal/stem (MSCs) as a potential therapy in application to regenerative medicine promoted anti-inflammatory and neuroprotective effects, several disadvantages limit their use. Therefore, recent studies have reported the effects of exosomes-derived MSCs (MSC-EXOs) as an innovative therapeutic option for SCI patients. It is noteworthy that MSC-EXOs can maintain the integrity of the blood-spinal cord barrier (BSCB), promoting angiogenic, proliferative, and anti-oxidant effects, as well as immunomodulatory, anti-inflammatory, and antiapoptotic properties. Therefore, in this study, we summarized the preclinical studies reported in the literature that have shown the effects of MSC-EXOs as a new molecular target to counteract the devastating effects of SCI.
Language	English
Publishing date	2023-01-13
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines11010201
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Article: An In Silico Analysis Reveals Sustained Upregulation of Neuroprotective Genes in the Post-Stroke Human Brain.

Betto, Federica / Chiricosta, Luigi / Mazzon, Emanuela

Brain sciences

2023 Volume 13, Issue 7

Abstract: Ischemic stroke is a cerebrovascular disease caused by an interruption of blood flow to the brain, thus determining a lack of oxygen and nutrient supply. The ischemic event leads to the activation of several molecular signaling pathways involved in ... ...

Abstract	Ischemic stroke is a cerebrovascular disease caused by an interruption of blood flow to the brain, thus determining a lack of oxygen and nutrient supply. The ischemic event leads to the activation of several molecular signaling pathways involved in inflammation and the production of reactive oxygen species, causing irreversible neuronal damage. Several studies have focused on the acute phase of ischemic stroke. It is not clear if this traumatic event can influence some of the molecular processes in the affected area even years after the clinical event. In our study, we performed an in silico analysis using freely available raw data with the purpose of evaluating the transcriptomic state of post-mortem brain tissue. The samples were taken from non-fatal ischemic stroke patients, meaning that they suffered an ischemic stroke and lived for a period of about 2 years after the event. These samples were compared with healthy controls. The aim was to evaluate possible recovery processes useful to mitigating neuronal damage and the detrimental consequences of stroke. Our results highlighted differentially expressed genes codifying for proteins along with long non-coding genes with anti-inflammatory and anti-oxidant functions. This suggests that even after an amount of time from the ischemic insult, different neuroprotective mechanisms are activated to ameliorate brain conditions and repair post-stroke neuronal injury.
Language	English
Publishing date	2023-06-23
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2651993-8
ISSN	2076-3425
ISSN	2076-3425
DOI	10.3390/brainsci13070986
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