scholarly journals Spirulina Microalgae and Brain Health: A Scoping Review of Experimental and Clinical Evidence

Marine Drugs ◽  
2021 ◽  
Vol 19 (6) ◽  
pp. 293
Author(s):  
Vincenzo Sorrenti ◽  
Davide Augusto Castagna ◽  
Stefano Fortinguerra ◽  
Alessandro Buriani ◽  
Giovanni Scapagnini ◽  
...  
Keyword(s):  
Cognitive Skills ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Vascular Wall ◽  
Endothelial Damage ◽  
Brain Health ◽  
Brain Vessels ◽  
Malnourished Children ◽  
The Brain

Spirulina microalgae contain a plethora of nutrient and non-nutrient molecules providing brain health benefits. Numerous in vivo evidence has provided support for the brain health potential of spirulina, highlighting antioxidant, anti-inflammatory, and neuroprotective mechanisms. Preliminary clinical studies have also suggested that spirulina can help to reduce mental fatigue, protect the vascular wall of brain vessels from endothelial damage and regulate internal pressure, thus contributing to the prevention and/or mitigating of cerebrovascular conditions. Furthermore, the use of spirulina in malnourished children appears to ameliorate motor, language, and cognitive skills, suggesting a reinforcing role in developmental mechanisms. Evidence of the central effect of spirulina on appetite regulation has also been shown. This review aims to understand the applicative potential of spirulina microalgae in the prevention and mitigation of brain disorders, highlighting the nutritional value of this “superfood”, and providing the current knowledge on relevant molecular mechanisms in the brain associated with its dietary introduction.

scholarly journals Unraveling the neurotoxicity of titanium dioxide nanoparticles: focusing on molecular mechanisms

2016 ◽  
Vol 7 ◽  
pp. 645-654 ◽  
Author(s):  
Bin Song ◽  
Yanli Zhang ◽  
Jia Liu ◽  
Xiaoli Feng ◽  
Ting Zhou ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Titanium Dioxide ◽  
Molecular Mechanisms ◽  
Titanium Dioxide Nanoparticles ◽  
Brain Dysfunction ◽  
In Vivo Studies ◽  
Cell Components ◽  
New Perspective ◽  
The Brain

Titanium dioxide nanoparticles (TiO2 NPs) possess unique characteristics and are widely used in many fields. Numerous in vivo studies, exposing experimental animals to these NPs through systematic administration, have suggested that TiO2 NPs can accumulate in the brain and induce brain dysfunction. Nevertheless, the exact mechanisms underlying the neurotoxicity of TiO2 NPs remain unclear. However, we have concluded from previous studies that these mechanisms mainly consist of oxidative stress (OS), apoptosis, inflammatory response, genotoxicity, and direct impairment of cell components. Meanwhile, other factors such as disturbed distributions of trace elements, disrupted signaling pathways, dysregulated neurotransmitters and synaptic plasticity have also been shown to contribute to neurotoxicity of TiO2 NPs. Recently, studies on autophagy and DNA methylation have shed some light on possible mechanisms of nanotoxicity. Therefore, we offer a new perspective that autophagy and DNA methylation could contribute to neurotoxicity of TiO2 NPs. Undoubtedly, more studies are needed to test this idea in the future. In short, to fully understand the health threats posed by TiO2 NPs and to improve the bio-safety of TiO2 NPs-based products, the neurotoxicity of TiO2 NPs must be investigated comprehensively through studying every possible molecular mechanism.

Postischemic Revascularization: From Cellular and Molecular Mechanisms to Clinical Applications

2013 ◽  
Vol 93 (4) ◽  
pp. 1743-1802 ◽  
Author(s):  
Jean-Sébastien Silvestre ◽  
David M. Smadja ◽  
Bernard I. Lévy
Keyword(s):  
Progenitor Cells ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Therapeutic Option ◽  
Vascular Wall ◽  
Arterial Disease ◽  
Cellular Mechanisms ◽  
Collateral Growth ◽  
Vessel Growth ◽  
Ischemic Diseases

After the onset of ischemia, cardiac or skeletal muscle undergoes a continuum of molecular, cellular, and extracellular responses that determine the function and the remodeling of the ischemic tissue. Hypoxia-related pathways, immunoinflammatory balance, circulating or local vascular progenitor cells, as well as changes in hemodynamical forces within vascular wall trigger all the processes regulating vascular homeostasis, including vasculogenesis, angiogenesis, arteriogenesis, and collateral growth, which act in concert to establish a functional vascular network in ischemic zones. In patients with ischemic diseases, most of the cellular (mainly those involving bone marrow-derived cells and local stem/progenitor cells) and molecular mechanisms involved in the activation of vessel growth and vascular remodeling are markedly impaired by the deleterious microenvironment characterized by fibrosis, inflammation, hypoperfusion, and inhibition of endogenous angiogenic and regenerative programs. Furthermore, cardiovascular risk factors, including diabetes, hypercholesterolemia, hypertension, diabetes, and aging, constitute a deleterious macroenvironment that participates to the abrogation of postischemic revascularization and tissue regeneration observed in these patient populations. Thus stimulation of vessel growth and/or remodeling has emerged as a new therapeutic option in patients with ischemic diseases. Many strategies of therapeutic revascularization, based on the administration of growth factors or stem/progenitor cells from diverse sources, have been proposed and are currently tested in patients with peripheral arterial disease or cardiac diseases. This review provides an overview from our current knowledge regarding molecular and cellular mechanisms involved in postischemic revascularization, as well as advances in the clinical application of such strategies of therapeutic revascularization.

scholarly journals Anti-Cancer Effects of Green Tea Polyphenols Against Prostate Cancer

Molecules ◽  
2019 ◽  
Vol 24 (1) ◽  
pp. 193 ◽  
Author(s):  
Yasuyoshi Miyata ◽  
Yohei Shida ◽  
Tomoaki Hakariya ◽  
Hideki Sakai
Keyword(s):  
Prostate Cancer ◽  
Green Tea ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Tea Polyphenols ◽  
Green Tea Polyphenols ◽  
Anti Cancer ◽  
Prevention And Treatment

Prostate cancer is the most common cancer among men. Green tea consumption is reported to play an important role in the prevention of carcinogenesis in many types of malignancies, including prostate cancer; however, epidemiological studies show conflicting results regarding these anti-cancer effects. In recent years, in addition to prevention, many investigators have shown the efficacy and safety of green tea polyphenols and combination therapies with green tea extracts and anti-cancer agents in in vivo and in vitro studies. Furthermore, numerous studies have revealed the molecular mechanisms of the anti-cancer effects of green tea extracts. We believe that improved understanding of the detailed pathological roles at the molecular level is important to evaluate the prevention and treatment of prostate cancer. Therefore, in this review, we present current knowledge regarding the anti-cancer effects of green tea extracts in the prevention and treatment of prostate cancer, with a particular focus on the molecular mechanisms of action, such as influencing tumor growth, apoptosis, androgen receptor signaling, cell cycle, and various malignant behaviors. Finally, the future direction for the use of green tea extracts as treatment strategies in patients with prostate cancer is introduced.

scholarly journals Brain manganese and the balance between essential roles and neurotoxicity

2020 ◽  
Vol 295 (19) ◽  
pp. 6312-6329 ◽  
Author(s):  
Rekha C. Balachandran ◽  
Somshuvra Mukhopadhyay ◽  
Danielle McBride ◽  
Jennifer Veevers ◽  
Fiona E. Harrison ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Normal Development ◽  
The Body ◽  
Neurological Dysfunction ◽  
Cellular Transport ◽  
Brain Health ◽  
Biochemical Mechanisms ◽  
Molecular And Biochemical Mechanisms ◽  
Neuronal Physiology ◽  
The Brain

Manganese (Mn) is an essential micronutrient required for the normal development of many organs, including the brain. Although its roles as a cofactor in several enzymes and in maintaining optimal physiology are well-known, the overall biological functions of Mn are rather poorly understood. Alterations in body Mn status are associated with altered neuronal physiology and cognition in humans, and either overexposure or (more rarely) insufficiency can cause neurological dysfunction. The resultant balancing act can be viewed as a hormetic U-shaped relationship for biological Mn status and optimal brain health, with changes in the brain leading to physiological effects throughout the body and vice versa. This review discusses Mn homeostasis, biomarkers, molecular mechanisms of cellular transport, and neuropathological changes associated with disruptions of Mn homeostasis, especially in its excess, and identifies gaps in our understanding of the molecular and biochemical mechanisms underlying Mn homeostasis and neurotoxicity.

scholarly journals Mecanismos Moleculares de Adesão e Colonização da Mucosa Gástrica pela Helicobacter pylori e suas Implicações Clínicas

2016 ◽  
Vol 29 (7-8) ◽  
pp. 476 ◽  
Author(s):  
Elisabete Coelho ◽  
Ana Magalhães ◽  
Mário Dinis-Ribeiro ◽  
Celso A. Reis
Keyword(s):  
Helicobacter Pylori ◽  
Virulence Factors ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Helicobacter Pylori Infection ◽  
Gastric Epithelium ◽  
Antibiotics Resistance ◽  
Gastric Disease ◽  
Preventive Strategy

Introduction: Helicobacter pylori infection is very prevalent worldwide and is associated with the progression of the gastriccarcinogenesis cascade, being one of the main risk factors for the development of gastric carcinoma. Several factors are determinant for the infection and for the development of gastric disease, including environmental factors, host genetic factors and virulence factors of the bacteria.Material and Methods: In this review, we present an overview of the current knowledge on the determinants of the infection and on the recently described molecular mechanisms of Helicobacter pylori adhesion to the gastric mucosa, as well as its possible future therapeutic application.Results: The adhesion of Helicobacter pylori to the gastric epithelium is critical for gastric pathogenesis, allowing bacterial access to nutrients and the action of bacterial virulence factors, promoting recurrence of the infection and the progression of the gastric carcinogenesis pathway.Discussion: Eradication of Helicobacter pylori infection is the best preventive strategy available against gastric cancer, mainly if it is achieved before the development of pre-neoplastic lesions. The increase in antibiotics resistance, together with the eradication failures in some patients, has promoted the development of alternative treatments.Conclusion: The new therapeutic strategies, focused on the molecular mechanism of Helicobacter pylori adhesion, are very promising; however, future studies are needed to evaluate its in vivo efficiency and toxicity.

scholarly journals Probiotics combined with rifaximin influence the neurometabolic changes in a rat model of type C HE

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Emmanuelle Flatt ◽  
Valérie A. McLin ◽  
Olivier Braissant ◽  
Katarzyna Pierzchala ◽  
Paola Mastromarino ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Brain Metabolism ◽  
Treatment Options ◽  
Multimodal Approach ◽  
Ultra High Field ◽  
Neuropsychiatric Disease ◽  
Important Challenge ◽  
Type C ◽  
The Brain

AbstractType C hepatic encephalopathy (HE) is a neuropsychiatric disease caused by chronic liver disease. Management of type C HE remains an important challenge because treatment options are limited. Both the antibiotic rifaximin and probiotics have been reported to reduce the symptoms of HE, but longitudinal studies assessing their effects on brain metabolism are lacking and the molecular mechanisms underpinning their effects are not fully understood. Therefore, we evaluated in detail the effects of these different treatments on the neurometabolic changes associated with type C HE using a multimodal approach including ultra-high field in vivo 1H MRS. We analyzed longitudinally the effect of rifaximin alone or in combination with the probiotic Vivomixx on the brain metabolic profile in the hippocampus and cerebellum of bile duct ligated (BDL) rats, an established model of type C HE. Overall, while rifaximin alone appeared to induce no significant effect on the neurometabolic profile of BDL rats, its association with the probiotic resulted in more attenuated neurometabolic alterations in BDL rats followed longitudinally (i.e. a smaller increase in Gln and milder decrease in Glu and Cr levels). Given that both rifaximin and some probiotics are used in the treatment of HE, the implications of these findings may be clinically relevant.

scholarly journals Bursting at the Seams: Molecular Mechanisms Mediating Astrocyte Swelling

2019 ◽  
Vol 20 (2) ◽  
pp. 330 ◽  
Author(s):  
Audrey Lafrenaye ◽  
J. Simard
Keyword(s):  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Predictors Of Outcome ◽  
Cell Type ◽  
Brain Swelling ◽  
Astrocyte Swelling ◽  
Health And Disease ◽  
The One ◽  
The Brain ◽  
Cellular Swelling

Brain swelling is one of the most robust predictors of outcome following brain injury, including ischemic, traumatic, hemorrhagic, metabolic or other injury. Depending on the specific type of insult, brain swelling can arise from the combined space-occupying effects of extravasated blood, extracellular edema fluid, cellular swelling, vascular engorgement and hydrocephalus. Of these, arguably the least well appreciated is cellular swelling. Here, we explore current knowledge regarding swelling of astrocytes, the most abundant cell type in the brain, and the one most likely to contribute to pathological brain swelling. We review the major molecular mechanisms identified to date that contribute to or mitigate astrocyte swelling via ion transport, and we touch upon the implications of astrocyte swelling in health and disease.

scholarly journals Adenosine A2AReceptors in Substance Use Disorders: A Focus on Cocaine

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1372 ◽  
Author(s):  
Karolina Wydra ◽  
Dawid Gawliński ◽  
Kinga Gawlińska ◽  
Małgorzata Frankowska ◽  
Dasiel O. Borroto-Escuela ◽  
...  
Keyword(s):  
Substance Use ◽  
Substance Use Disorders ◽  
Current Knowledge ◽  
Ex Vivo ◽  
D2 Receptors ◽  
Future Research ◽  
Receptor Complexes ◽  
Abused Drugs ◽  
The Brain

Several psychoactive drugs can evoke substance use disorders (SUD) in humans and animals, and these include psychostimulants, opioids, cannabinoids (CB), nicotine, and alcohol. The etiology, mechanistic processes, and the therapeutic options to deal with SUD are not well understood. The common feature of all abused drugs is that they increase dopamine (DA) neurotransmission within the mesocorticolimbic circuitry of the brain followed by the activation of DA receptors. D2 receptors were proposed as important molecular targets for SUD. The findings showed that D2 receptors formed heteromeric complexes with other GPCRs, which forced the addiction research area in new directions. In this review, we updated the view on the brain D2 receptor complexes with adenosine (A)2A receptors (A2AR) and discussed the role of A2AR in different aspects of addiction phenotypes in laboratory animal procedures that permit the highly complex syndrome of human drug addiction. We presented the current knowledge on the neurochemical in vivo and ex vivo mechanisms related to cocaine use disorder (CUD) and discussed future research directions for A2AR heteromeric complexes in SUD.

scholarly journals Genetic Mouse Models as In Vivo Tools for Cholangiocarcinoma Research

Cancers ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 1868 ◽  
Author(s):  
Oihane Erice ◽  
Adrian Vallejo ◽  
Mariano Ponz-Sarvise ◽  
Michael Saborowski ◽  
Arndt Vogel ◽  
...  
Keyword(s):  
Mouse Models ◽  
Molecular Mechanisms ◽  
Complex Disease ◽  
Current Knowledge ◽  
Genetic Alterations ◽  
In Vivo Model ◽  
In Vivo Models ◽  
Dismal Prognosis ◽  
Genetic Mouse Models

Cholangiocarcinoma (CCA) is a genetically and histologically complex disease with a highly dismal prognosis. A deeper understanding of the underlying cellular and molecular mechanisms of human CCA will increase our current knowledge of the disease and expedite the eventual development of novel therapeutic strategies for this fatal cancer. This endeavor is effectively supported by genetic mouse models, which serve as sophisticated tools to systematically investigate CCA pathobiology and treatment response. These in vivo models feature many of the genetic alterations found in humans, recapitulate multiple hallmarks of cholangiocarcinogenesis (encompassing cell transformation, preneoplastic lesions, established tumors and metastatic disease) and provide an ideal experimental setting to study the interplay between tumor cells and the surrounding stroma. This review is intended to serve as a compendium of CCA mouse models, including traditional transgenic models but also genetically flexible approaches based on either the direct introduction of DNA into liver cells or transplantation of pre-malignant cells, and is meant as a resource for CCA researchers to aid in the selection of the most appropriate in vivo model system.

scholarly journals Rhombencephalitis Caused byListeria monocytogenesin Humans and Ruminants: A Zoonosis on the Rise?

2010 ◽  
Vol 2010 ◽  
pp. 1-22 ◽  
Author(s):  
Anna Oevermann ◽  
Andreas Zurbriggen ◽  
Marc Vandevelde
Keyword(s):  
Listeria Monocytogenes ◽  
High Mortality ◽  
Host Species ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Therapeutic Strategies ◽  
Zoonotic Infection ◽  
Cns Disease ◽  
The Brain

Listeriosis is an emerging zoonotic infection of humans and ruminants worldwide caused byListeria monocytogenes(LM). In both host species, CNS disease accounts for the high mortality associated with listeriosis and includes rhombencephalitis, whose neuropathology is strikingly similar in humans and ruminants. This review discusses the current knowledge about listeric encephalitis, and involved host and bacterial factors. There is an urgent need to study the molecular mechanisms of neuropathogenesis, which are poorly understood. Such studies will provide a basis for the development of new therapeutic strategies that aim to prevent LM from invading the brain and spread within the CNS.

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