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Article: Molecular and Cellular Involvement in CIPN.

Kacem, Housem / Cimini, Annamaria / d'Angelo, Michele / Castelli, Vanessa

2024 Volume 12, Issue 4

Abstract: Many anti-cancer drugs, such as taxanes, platinum compounds, vinca alkaloids, and proteasome inhibitors, can cause chemotherapy-induced peripheral neuropathy (CIPN). CIPN is a frequent and harmful side effect that affects the sensory, motor, and ... ...

Abstract	Many anti-cancer drugs, such as taxanes, platinum compounds, vinca alkaloids, and proteasome inhibitors, can cause chemotherapy-induced peripheral neuropathy (CIPN). CIPN is a frequent and harmful side effect that affects the sensory, motor, and autonomic nerves, leading to pain, numbness, tingling, weakness, and reduced quality of life. The causes of CIPN are not fully known, but they involve direct nerve damage, oxidative stress, inflammation, DNA damage, microtubule dysfunction, and altered ion channel activity. CIPN is also affected by genetic, epigenetic, and environmental factors that modulate the risk and intensity of nerve damage. Currently, there are no effective treatments or prevention methods for CIPN, and symptom management is mostly symptomatic and palliative. Therefore, there is a high demand for better understanding of the cellular and molecular mechanisms involved in CIPN, as well as the development of new biomarkers and therapeutic targets. This review gives an overview of the current knowledge and challenges in the field of CIPN, focusing on the biological and molecular mechanisms underlying this disorder.
Language	English
Publishing date	2024-03-28
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines12040751
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Organoids Modeling Stroke in a Petri Dish.

Giorgi, Chiara / Castelli, Vanessa / d'Angelo, Michele / Cimini, Annamaria

Biomedicines

2024 Volume 12, Issue 4

Abstract: Stroke is a common neurological disorder, the second leading cause of death, and the third leading cause of disability. Unfortunately, the only approved drug for it is tissue plasminogen, but the therapeutic window is limited. In this context, ... ...

Abstract	Stroke is a common neurological disorder, the second leading cause of death, and the third leading cause of disability. Unfortunately, the only approved drug for it is tissue plasminogen, but the therapeutic window is limited. In this context, preclinical studies are relevant to better dissect the underlying mechanisms of stroke and for the drug screening of potential therapies. Brain organoids could be relevant in this setting. They are derived from pluripotent stem cells or isolated organ progenitors that differentiate to form an organ-like tissue, exhibiting multiple cell types that self-organize to form a structure not unlike the organ in vivo. Brain organoids mimic many key features of early human brain development at molecular, cellular, structural, and functional levels and have emerged as novel model systems that can be used to investigate human brain diseases including stroke. Brain organoids are a promising and powerful tool for ischemic stroke studies; however, there are a few concerns that need to be addressed, including the lack of vascularization and the many cell types that are typically present in the human brain. The aim of this review is to discuss the potential of brain organoids as a novel model system for studying ischemic stroke, highlighting both the advantages and disadvantages in the use of this technology.
Language	English
Publishing date	2024-04-16
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines12040877
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Cell Rearrangement and Oxidant/Antioxidant Imbalance in Huntington's Disease.

D'Egidio, Francesco / Castelli, Vanessa / Cimini, Annamaria / d'Angelo, Michele

Antioxidants (Basel, Switzerland)

2023 Volume 12, Issue 3

Abstract: Huntington's Disease (HD) is a hereditary neurodegenerative disorder caused by the expansion of a CAG triplet repeat in ... ...

Abstract	Huntington's Disease (HD) is a hereditary neurodegenerative disorder caused by the expansion of a CAG triplet repeat in the
Language	English
Publishing date	2023-02-24
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox12030571
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Therapeutic potential of saffron in brain disorders: From bench to bedside.

Bej, Erjola / Volpe, Anna Rita / Cesare, Patrizia / Cimini, Annamaria / d'Angelo, Michele / Castelli, Vanessa

Phytotherapy research : PTR

2024 Volume 38, Issue 5, Page(s) 2482–2495

Abstract: Saffron is a spice derived from the flower of Crocus sativus L., which has been used for centuries as a coloring and flavoring agent, as well as a source of medicinal compounds. Saffron contains various bioactive constituents, such as crocin, crocetin, ... ...

Abstract	Saffron is a spice derived from the flower of Crocus sativus L., which has been used for centuries as a coloring and flavoring agent, as well as a source of medicinal compounds. Saffron contains various bioactive constituents, such as crocin, crocetin, safranal, picrocrocin, and kaempferol, that have shown potential benefits for human health. Among them, crocin is the most abundant and characteristic constituent of saffron, responsible for its bright red color and antioxidant properties. One of the most promising applications of saffron and its constituents is in the prevention and treatment of neurological disorders, such as depression, anxiety, Alzheimer's disease, Parkinson's disease, and other brain disorders. Saffron and its constituents have been reported to exert neuroprotective effects through various mechanisms, such as modulating neurotransmitters, enhancing neurogenesis, reducing neuroinflammation, regulating oxidative stress, activating the Nrf2 signaling pathway, and modulating epigenetic factors. Several clinical and preclinical studies have demonstrated the efficacy and safety of saffron and its constituents in improving cognitive function, mood, and other neurological outcomes. In this review, we summarize the current evidence on the therapeutic potential of saffron and its constituents in neurological disorders, from bench to bedside. We also discuss the challenges and future directions for the development of saffron-based therapies for brain health.
MeSH term(s)	Crocus/chemistry ; Humans ; Animals ; Brain Diseases/drug therapy ; Neuroprotective Agents/pharmacology ; Neuroprotective Agents/therapeutic use ; Plant Extracts/pharmacology ; Plant Extracts/therapeutic use ; Antioxidants/pharmacology ; Antioxidants/therapeutic use ; Carotenoids/pharmacology ; Carotenoids/therapeutic use ; Oxidative Stress/drug effects
Chemical Substances	Neuroprotective Agents ; Plant Extracts ; Antioxidants ; Carotenoids (36-88-4) ; crocin (877GWI46C2)
Language	English
Publishing date	2024-03-06
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	639136-9
ISSN	1099-1573 ; 0951-418X
ISSN (online)	1099-1573
ISSN	0951-418X
DOI	10.1002/ptr.8169
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Probing Gut Participation in Parkinson's Disease Pathology and Treatment via Stem Cell Therapy.

Lee, Jea-Young / Castelli, Vanessa / Sanberg, Paul R / Borlongan, Cesar V

International journal of molecular sciences

2023 Volume 24, Issue 13

Abstract: Accumulating evidence suggests the critical role of the gut-brain axis (GBA) in Parkinson's disease (PD) pathology and treatment. Recently, stem cell transplantation in transgenic PD mice further implicated the GBA's contribution to the therapeutic ... ...

Abstract	Accumulating evidence suggests the critical role of the gut-brain axis (GBA) in Parkinson's disease (PD) pathology and treatment. Recently, stem cell transplantation in transgenic PD mice further implicated the GBA's contribution to the therapeutic effects of transplanted stem cells. In particular, intravenous transplantation of human umbilical-cord-blood-derived stem/progenitor cells and plasma reduced motor deficits, improved nigral dopaminergic neuronal survival, and dampened α-synuclein and inflammatory-relevant microbiota and cytokines in both the gut and brain of mouse and rat PD models. That the gut robustly responded to intravenously transplanted stem cells and prompted us to examine in the present study whether direct cell implantation into the gut of transgenic PD mice would enhance the therapeutic effects of stem cells. Contrary to our hypothesis, results revealed that intragut transplantation of stem cells exacerbated motor and gut motility deficits that corresponded with the aggravated expression of inflammatory microbiota, cytokines, and α-synuclein in both the gut and brain of transgenic PD mice. These results suggest that, while the GBA stands as a major source of inflammation in PD, targeting the gut directly for stem cell transplantation may not improve, but may even worsen, functional outcomes, likely due to the invasive approach exacerbating the already inflamed gut. The minimally invasive intravenous transplantation, which likely avoided worsening the inflammatory response of the gut, appears to be a more optimal cell delivery route to ameliorate PD symptoms.
MeSH term(s)	Humans ; Rats ; Animals ; Parkinson Disease/metabolism ; alpha-Synuclein/metabolism ; Substantia Nigra/metabolism ; Stem Cell Transplantation ; Cytokines/metabolism
Chemical Substances	alpha-Synuclein ; Cytokines
Language	English
Publishing date	2023-06-25
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/ijms241310600
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Neurotrophic factor-based pharmacological approaches in neurological disorders.

Alfonsetti, Margherita / d'Angelo, Michele / Castelli, Vanessa

Neural regeneration research

2022 Volume 18, Issue 6, Page(s) 1220–1228

Abstract: Aging is a physiological event dependent on multiple pathways that are linked to lifespan and processes leading to cognitive decline. This process represents the major risk factor for aging-related diseases such as Alzheimer's disease, Parkinson's ... ...

Abstract	Aging is a physiological event dependent on multiple pathways that are linked to lifespan and processes leading to cognitive decline. This process represents the major risk factor for aging-related diseases such as Alzheimer's disease, Parkinson's disease, and ischemic stroke. The incidence of all these pathologies increases exponentially with age. Research on aging biology has currently focused on elucidating molecular mechanisms leading to the development of those pathologies. Cognitive deficit and neurodegeneration, common features of aging-related pathologies, are related to the alteration of the activity and levels of neurotrophic factors, such as brain-derived neurotrophic factor, nerve growth factor, and glial cell-derived neurotrophic factor. For this reason, treatments that modulate neurotrophin levels have acquired a great deal of interest in preventing neurodegeneration and promoting neural regeneration in several neurological diseases. Those treatments include both the direct administration of neurotrophic factors and the induced expression with viral vectors, neurotrophins' binding with biomaterials or other molecules to increase their bioavailability but also cell-based therapies. Considering neurotrophins' crucial role in aging pathologies, here we discuss the involvement of several neurotrophic factors in the most common brain aging-related diseases and the most recent therapeutic approaches that provide direct and sustained neurotrophic support.
Language	English
Publishing date	2022-11-28
Publishing country	India
Document type	Journal Article ; Review
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.358619
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Are We What We Eat? Impact of Diet on the Gut-Brain Axis in Parkinson's Disease.

Alfonsetti, Margherita / Castelli, Vanessa / d'Angelo, Michele

Nutrients

2022 Volume 14, Issue 2

Abstract: Parkinson's disease is characterized by motor and non-motor symptoms, such as defects in the gut function, which may occur before the motor symptoms. To date, there are therapies that can improve these symptoms, but there is no cure to avoid the ... ...

Abstract	Parkinson's disease is characterized by motor and non-motor symptoms, such as defects in the gut function, which may occur before the motor symptoms. To date, there are therapies that can improve these symptoms, but there is no cure to avoid the development or exacerbation of this disorder. Dysbiosis of gut microbiota could have a crucial role in the gut-brain axis, which is a bidirectional communication between the central nervous system and the enteric nervous system. Diet can affect the microbiota composition, impacting gut-brain axis functionality. Gut microbiome restoration through probiotics, prebiotics, synbiotics or other dietary means could have the potential to slow PD progression. In this review, we will discuss the influence of diet on the bidirectional communication between gut and brain, thus supporting the hypothesis that this disorder could begin in the gut. We also focus on how food-based therapies might then have an influence on PD and could ameliorate non-motor as well as motor symptoms.
MeSH term(s)	Brain-Gut Axis/physiology ; Diet ; Disease Progression ; Gastrointestinal Microbiome/physiology ; Gastrointestinal Tract/microbiology ; Gastrointestinal Tract/physiopathology ; Humans ; Nutrition Therapy ; Parkinson Disease/physiopathology ; Parkinson Disease/therapy ; Prebiotics/administration & dosage ; Probiotics/therapeutic use ; Synbiotics/administration & dosage
Chemical Substances	Prebiotics
Language	English
Publishing date	2022-01-17
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu14020380
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Brain Organoids: A Game-Changer for Drug Testing.

Giorgi, Chiara / Lombardozzi, Giorgia / Ammannito, Fabrizio / Scenna, Marta Sofia / Maceroni, Eleonora / Quintiliani, Massimiliano / d'Angelo, Michele / Cimini, Annamaria / Castelli, Vanessa

Pharmaceutics

2024 Volume 16, Issue 4

Abstract: Neurological disorders are the second cause of death and the leading cause of disability worldwide. Unfortunately, no cure exists for these disorders, but the actual therapies are only able to ameliorate people's quality of life. Thus, there is an urgent ...

Abstract	Neurological disorders are the second cause of death and the leading cause of disability worldwide. Unfortunately, no cure exists for these disorders, but the actual therapies are only able to ameliorate people's quality of life. Thus, there is an urgent need to test potential therapeutic approaches. Brain organoids are a possible valuable tool in the study of the brain, due to their ability to reproduce different brain regions and maturation stages; they can be used also as a tool for disease modelling and target identification of neurological disorders. Recently, brain organoids have been used in drug-screening processes, even if there are several limitations to overcome. This review focuses on the description of brain organoid development and drug-screening processes, discussing the advantages, challenges, and limitations of the use of organoids in modeling neurological diseases. We also highlighted the potential of testing novel therapeutic approaches. Finally, we examine the challenges and future directions to improve the drug-screening process.
Language	English
Publishing date	2024-03-22
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527217-2
ISSN	1999-4923
ISSN	1999-4923
DOI	10.3390/pharmaceutics16040443
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Therapeutic advances in neural regeneration for Huntington's disease.

D'Egidio, Francesco / Castelli, Vanessa / Lombardozzi, Giorgia / Ammannito, Fabrizio / Cimini, Annamaria / d'Angelo, Michele

Neural regeneration research

2023 Volume 19, Issue 9, Page(s) 1991–1997

Abstract: Huntington's disease is a neurodegenerative disease caused by the expansion mutation of a cytosine-adenine-guanine triplet in the exon 1 of the HTT gene which is responsible for the production of the huntingtin (Htt) protein. In physiological conditions, ...

Abstract	Huntington's disease is a neurodegenerative disease caused by the expansion mutation of a cytosine-adenine-guanine triplet in the exon 1 of the HTT gene which is responsible for the production of the huntingtin (Htt) protein. In physiological conditions, Htt is involved in many cellular processes such as cell signaling, transcriptional regulation, energy metabolism regulation, DNA maintenance, axonal trafficking, and antiapoptotic activity. When the genetic alteration is present, the production of a mutant version of Htt (mHtt) occurs, which is characterized by a plethora of pathogenic activities that, finally, lead to cell death. Among all the cells in which mHtt exerts its dangerous activity, the GABAergic Medium Spiny Neurons seem to be the most affected by the mHtt-induced excitotoxicity both in the cortex and in the striatum. However, as the neurodegeneration proceeds ahead the neuronal loss grows also in other brain areas such as the cerebellum, hypothalamus, thalamus, subthalamic nucleus, globus pallidus, and substantia nigra, determining the variety of symptoms that characterize Huntington's disease. From a clinical point of view, Huntington's disease is characterized by a wide spectrum of symptoms spanning from motor impairment to cognitive disorders and dementia. Huntington's disease shows a prevalence of around 3.92 cases every 100,000 worldwide and an incidence of 0.48 new cases every 100,000/year. To date, there is no available cure for Huntington's disease. Several treatments have been developed so far, aiming to reduce the severity of one or more symptoms to slow down the inexorable decline caused by the disease. In this context, the search for reliable strategies to target the different aspects of Huntington's disease become of the utmost interest. In recent years, a variety of studies demonstrated the detrimental role of neuronal loss in Huntington's disease condition highlighting how the replacement of lost cells would be a reasonable strategy to overcome the neurodegeneration. In this view, numerous have been the attempts in several preclinical models of Huntington's disease to evaluate the feasibility of invasive and non-invasive approaches. Thus, the aim of this review is to offer an overview of the most appealing approaches spanning from stem cell-based cell therapy to extracellular vesicles such as exosomes in light of promoting neurogenesis, discussing the results obtained so far, their limits and the future perspectives regarding the neural regeneration in the context of Huntington's disease.
Language	English
Publishing date	2023-12-15
Publishing country	India
Document type	Journal Article
ZDB-ID	2388460-5
ISSN	1876-7958 ; 1673-5374
ISSN (online)	1876-7958
ISSN	1673-5374
DOI	10.4103/1673-5374.390969
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Are We What We Eat? Impact of Diet on the Gut–Brain Axis in Parkinson’s Disease

Alfonsetti, Margherita / Castelli, Vanessa / d’Angelo, Michele

Nutrients. 2022 Jan. 17, v. 14, no. 2

2022

Abstract: Parkinson’s disease is characterized by motor and non-motor symptoms, such as defects in the gut function, which may occur before the motor symptoms. To date, there are therapies that can improve these symptoms, but there is no cure to avoid the ... ...

Abstract	Parkinson’s disease is characterized by motor and non-motor symptoms, such as defects in the gut function, which may occur before the motor symptoms. To date, there are therapies that can improve these symptoms, but there is no cure to avoid the development or exacerbation of this disorder. Dysbiosis of gut microbiota could have a crucial role in the gut–brain axis, which is a bidirectional communication between the central nervous system and the enteric nervous system. Diet can affect the microbiota composition, impacting gut–brain axis functionality. Gut microbiome restoration through probiotics, prebiotics, synbiotics or other dietary means could have the potential to slow PD progression. In this review, we will discuss the influence of diet on the bidirectional communication between gut and brain, thus supporting the hypothesis that this disorder could begin in the gut. We also focus on how food-based therapies might then have an influence on PD and could ameliorate non-motor as well as motor symptoms.
Keywords	brain ; digestive system ; dysbiosis ; intestinal microorganisms ; prebiotics ; probiotics
Language	English
Dates of publication	2022-0117
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu14020380
Database	NAL-Catalogue (AGRICOLA)

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