scholarly journals Vitamin K2 Holds Promise for Alzheimer’s Prevention and Treatment

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2206
Author(s):  
Alexander Popescu ◽  
Monica German
Keyword(s):  
Mitochondrial Dysfunction ◽  
Clinical Studies ◽  
Basic Science ◽  
Cardiovascular Health ◽  
Science Research ◽  
Vitamin K2 ◽  
Prevention And Treatment ◽  
Growing Body ◽  
Antioxidant Effects

Recent studies have highlighted the importance of vitamin K2 (VK2) in human health. However, there have been no clinical studies investigating the role of VK2 in the prevention or treatment of Alzheimer’s disease (AD), a debilitating disease for which currently there is no cure. In reviewing basic science research and clinical studies that have connected VK2 to factors involved in AD pathogenesis, we have found a growing body of evidence demonstrating that VK2 has the potential to slow the progression of AD and contribute to its prevention. In our review, we consider the antiapoptotic and antioxidant effects of VK2 and its impact on neuroinflammation, mitochondrial dysfunction, cognition, cardiovascular health, and comorbidities in AD. We also examine the link between dysbiosis and VK2 in the context of the microbiome’s role in AD pathogenesis. Our review is the first to consider the physiological roles of VK2 in the context of AD, and, given the recent shift in AD research toward nonpharmacological interventions, our findings emphasize the timeliness and need for clinical studies involving VK2.

scholarly journals Mitochondrial Fusion/Fission, Transport and Autophagy in Parkinson's Disease: When Mitochondria Get Nasty

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Daniela M. Arduíno ◽  
A. Raquel Esteves ◽  
Sandra M. Cardoso
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mitochondrial Dysfunction ◽  
Molecular Basis ◽  
Molecular Mechanisms ◽  
Mitochondrial Dynamics ◽  
Growing Body ◽  
Parkinsonian Disorders ◽  
Mitochondrial Trafficking

Understanding the molecular basis of Parkinson's disease (PD) has proven to be a major challenge in the field of neurodegenerative diseases. Although several hypotheses have been proposed to explain the molecular mechanisms underlying the pathogenesis of PD, a growing body of evidence has highlighted the role of mitochondrial dysfunction and the disruption of the mechanisms of mitochondrial dynamics in PD and other parkinsonian disorders. In this paper, we comment on the recent advances in how changes in the mitochondrial function and mitochondrial dynamics (fusion/fission, transport, and clearance) contribute to neurodegeneration, specifically focusing on PD. We also evaluate the current controversies in those issues and discuss the role of fusion/fission dynamics in the mitochondrial lifecycle and maintenance. We propose that cellular demise and neurodegeneration in PD are due to the interplay between mitochondrial dysfunction, mitochondrial trafficking disruption, and impaired autophagic clearance.

scholarly journals MAPK signalling in cardiovascular health and disease: molecular mechanisms and therapeutic targets

2008 ◽  
Vol 115 (7) ◽  
pp. 203-218 ◽  
Author(s):  
Anthony J. Muslin
Keyword(s):  
Molecular Mechanisms ◽  
Cardiovascular Health ◽  
Mapk Pathway ◽  
Science Research ◽  
Pharmacological Therapy ◽  
Model Systems ◽  
Mitogen Activated Protein Kinase ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

Intracellular MAPK (mitogen-activated protein kinase) signalling cascades probably play an important role in the pathogenesis of cardiac and vascular disease. A substantial amount of basic science research has defined many of the details of MAPK pathway organization and activation, but the role of individual signalling proteins in the pathogenesis of various cardiovascular diseases is still being elucidated. In the present review, the role of the MAPKs ERK (extracellular signal-regulated kinase), JNK (c-Jun N-terminal kinase) and p38 MAPK in cardiac hypertrophy, cardiac remodelling after myocardial infarction, atherosclerosis and vascular restenosis will be examined, with attention paid to genetically modified murine model systems and to the use of pharmacological inhibitors of protein kinases. Despite the complexities of this field of research, attractive targets for pharmacological therapy are emerging.

scholarly journals A successful story of translational orthodontic research: Micro-osteoperforation-from experiments to clinical practice

2017 ◽  
Vol 7 ◽  
pp. 6-11 ◽  
Author(s):  
Michelle Yuching Chou ◽  
Mani Alikhani
Keyword(s):  
Clinical Practice ◽  
Translational Research ◽  
Clinical Application ◽  
Clinical Studies ◽  
Basic Science ◽  
Scientific Evidence ◽  
Science Research ◽  
Daily Practice ◽  
Research Projects ◽  
Basic Science Research

The gap between basic science research and clinical application has long existed and therefore translational research has emerged in recent years to bridge such gap. Consortium for Translational Orthodontic Research (CTOR) was established with missions to integrate resources from different entities and to provide a platform for interdisciplinary groups who share the same vision to exchange ideas and inspire innovations. During its short existence, CTOR has successfully carried out several research projects which led to various innovations. Micro-osteoperforation is by far one of the most successful examples of translational research in the orthodontic field. It exemplifies how translational research can benefit scientists, clinicians, and patients. In this article, the process of its development, the rationale and scientific evidence from animal and clinical studies, and how it can be applied in daily practice will be depicted.

scholarly journals Role of Chemokines in Endocrine Autoimmune Diseases

2007 ◽  
Vol 28 (5) ◽  
pp. 492-520 ◽  
Author(s):  
Mario Rotondi ◽  
Luca Chiovato ◽  
Sergio Romagnani ◽  
Mario Serio ◽  
Paola Romagnani
Keyword(s):  
Autoimmune Diseases ◽  
Clinical Studies ◽  
Basic Science ◽  
Serum Levels ◽  
Interferon Γ ◽  
Major Function ◽  
Chronic Autoimmune Thyroiditis ◽  
Ifn Γ

Chemokines are a group of peptides of low molecular weight that induce the chemotaxis of different leukocyte subtypes. The major function of chemokines is the recruitment of leukocytes to inflammation sites, but they also play a role in tumoral growth, angiogenesis, and organ sclerosis. In the last few years, experimental evidence accumulated supporting the concept that interferon-γ (IFN-γ) inducible chemokines (CXCL9, CXCL10, and CXCL11) and their receptor, CXCR3, play an important role in the initial stage of autoimmune disorders involving endocrine glands. The fact that, after IFN-γ stimulation, endocrine epithelial cells secrete CXCL10, which in turn recruits type 1 T helper lymphocytes expressing CXCR3 and secreting IFN-γ, thus perpetuating autoimmune inflammation, strongly supports the concept that chemokines play an important role in endocrine autoimmunity. This article reviews the recent literature including basic science, animal models, and clinical studies, regarding the role of these chemokines in autoimmune endocrine diseases. The potential clinical applications of assaying the serum levels of CXCL10 and the value of such measurements are reviewed. Clinical studies addressing the issue of a role for serum CXCL10 measurement in Graves’ disease, Graves’ ophthalmopathy, chronic autoimmune thyroiditis, type 1 diabetes mellitus, and Addison’s disease have been considered. The principal aim was to propose that chemokines, and in particular CXCL10, should no longer be considered as belonging exclusively to basic science, but rather should be used for providing new insights in the clinical management of patients with endocrine autoimmune diseases.

scholarly journals World Class Pioneering Clinical Innovations: Nobel Prize Committee’s Failures

2020 ◽  
Vol 1 (6) ◽  
pp. 246-248
Author(s):  
Aamir Jalal Al-Mosawi
Keyword(s):  
North America ◽  
Nobel Prize ◽  
Basic Science ◽  
Science Research ◽  
Autism Research ◽  
Basic Science Research ◽  
The World ◽  
World Class ◽  
The Universe

It is understandable even to the medical students, the undeniable role of Nobel Prize winners particularly in the clinical and therapeutic fields which included the discoveries that led to developing vaccines and therapies to combat potentially fatal infectious disease, and contributed to saving millions of lives throughout the world. However, there have been recent criticisms suggesting that the prize has been given unreasonably more to basic scientific research discoveries, while ignoring world class pioneering clinical achievements. Many of the basic science research may never have any impact of any magnitude outside North America, Europe and Japan, and thus will unlikely to really contribute to a noticeable benefit to humankind. In fact, many basic science research and discoveries, for the majority of mankind living outside North America, Europe and Japan, are like discovering new galaxies at the end of the universe. Therefore, ignoring research from developing countries that have the potential of conferring the greatest benefit to humankind is definitely associated with a serious ethical dilemma when giving the Prize. The aim of this paper is to highlight recent world class pioneering clinical innovations missed by the Nobel Prize committee. Examples of world class pioneering research that have the potential of conferring the greatest benefit to humankind including curing autism research, multi-factorial therapies for mental retardation, and brain damage including cerebral palsy and brain atrophy, and intestinal dialysis.

scholarly journals Emerging Roles of Dyslipidemia and Hyperglycemia in Diabetic Retinopathy: Molecular Mechanisms and Clinical Perspectives

2021 ◽  
Vol 12 ◽  
Author(s):  
Hussain Rao ◽  
Jonathan A. Jalali ◽  
Thomas P. Johnston ◽  
Peter Koulen
Keyword(s):  
Diabetic Retinopathy ◽  
Literature Review ◽  
Basic Science ◽  
Molecular Mechanisms ◽  
Clinical Evidence ◽  
Vision Loss ◽  
Science Research ◽  
Therapeutic Interventions ◽  
Research Subject

Diabetic retinopathy (DR) is a significant cause of vision loss and a research subject that is constantly being explored for new mechanisms of damage and potential therapeutic options. There are many mechanisms and pathways that provide numerous options for therapeutic interventions to halt disease progression. The purpose of the present literature review is to explore both basic science research and clinical research for proposed mechanisms of damage in diabetic retinopathy to understand the role of triglyceride and cholesterol dysmetabolism in DR progression. This review delineates mechanisms of damage secondary to triglyceride and cholesterol dysmetabolism vs. mechanisms secondary to diabetes to add clarity to the pathogenesis behind each proposed mechanism. We then analyze mechanisms utilized by both triglyceride and cholesterol dysmetabolism and diabetes to elucidate the synergistic, additive, and common mechanisms of damage in diabetic retinopathy. Gathering this research adds clarity to the role dyslipidemia has in DR and an evaluation of the current peer-reviewed basic science and clinical evidence provides a basis to discern new potential therapeutic targets.

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