Browsing by Author "Iyer, Mahalaxmi"
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Item Advantages of mesenchymal stem cell over the other stem cells(Elsevier GmbH, 2023-05-09T00:00:00) Gopalarethinam, Janani; Nair, Aswathy P.; Iyer, Mahalaxmi; Vellingiri, Balachandar; Subramaniam, Mohana DeviA stem cell is a particular group of cells that has the extraordinary potential to convert within the body into particular cell types. They are used to regenerate tissues and cells in the body that have been damaged or destroyed by the disease. Stem cells come in three different varieties: adult stem cells, embryonic stem cells and induced pluripotent stem cells (iPSCs). Embryonic stem cells have a high chance of immune rejection and also have ethical dilemmas and iPSCs have genetic instability. Adult stem cells are difficult to analyze and extract for research since they are frequently insufficient in native tissues. However, mesenchymal stem cells (MSC) one of the categories of adult stem cells are stromal cells with a variety of potentials that can differentiate into a wide range of cell types. MSCs can be transplanted into a variety of people without worrying about rejection because they have demonstrated the ability to prevent an adverse reaction from the immune system. These transplants have powerful anti-inflammatory and immunosuppressive effects and greatly enhance the body's inherent healing capacity. While MSCs do not offer treatment for illnesses, the idea behind them is to enable the body to recover sufficiently for a protracted reduction in symptoms. In many cases, this is sufficient to significantly enhance the patient's well-being. Inspite of several advantages some potential long-term concerns connected to MSC therapy are maldifferentiation, immunosuppression and cancerous tumor growth. In this review, we will compare the mesenchymal stem cells with other stem cells with respect to the source of origin, their properties and therapeutic applications, and discuss the MSC's disadvantages. � 2023 Elsevier GmbHItem Artificial intelligence in heavy metals detection: Methodological and ethical challenges(Elsevier B.V., 2023-07-02T00:00:00) Yadav, Nidhi; Maurya, Brij Mohan; Chettri, Dewan; Pooja; Pulwani, Chirag; Jajula, Mahesh; kanda, Savleen Singh; babu, Harysh Winster Suresh; Elangovan, Ajay; Velusamy, Parthasarathy; Iyer, Mahalaxmi; Vellingiri, BalachandarHeavy metals (HMs) are metallic substances. They enter biotic and abiotic systems through natural and human activities. These HMs have an impact on the atmosphere, soil, and groundwater, and they also affect all living things, especially humans, when they enter the food chain. Therefore, monitoring and removing HMs from the environment and humans are crucial for maintaining HMs-based toxicity. The detection of HMs from environmental and human samples has been performed by techniques such as atomic adsorption spectrometry (AAS) and inductively coupled plasma mass spectrometry (ICP-MS). With the advancement of AI-based technology, HMs are now detected and removed from the environment and human systems. This review discusses the impact of HMs on the environment and human health, their detection and removal techniques, and the integration of recent advancements in AI-based technology for the detection and removal of HMs from environmental and human samples. � 2023 The Author(s)Item Assessment of tRNAThr and tRNAGln Variants and Mitochondrial Functionality in Parkinson�s Disease (PD) Patients of Tamil Nadu Population(Springer, 2023-10-17T00:00:00) Venkatesan, Dhivya; Iyer, Mahalaxmi; Raj, Neethu; Gopalakrishnan, Abilash Valsala; Narayanasamy, Arul; Kumar, Nachimuthu Senthil; Vellingiri, BalachandarParkinson�s disease (PD) is speculated with genetic and environmental factors. At molecular level, the mitochondrial impact is stated to be one of the causative reasons for PD. In this study, we investigated the mitochondrial membrane potential (MMP), reactive oxygen species (ROS) and adenosine triphosphate (ATP) levels along with mitochondrial tRNA alterations among three age categories of PD. By determining the genetic and organellar functionality using molecular techniques, the ROS levels were reported to be high with decreased MMP and ATP in the late-onset age group than in other two age categories. Likewise, the tRNA significancy in tRNAThr and tRNAGln was noticed with C4335T and G15927A mutations in late-onset and early-onset PD groups respectively. Therefore, from the findings, ageing has shown a disruption in tRNA metabolism leading to critical functioning of ATP synthesis and MMP, causing oxidative stress in PD patients. These physiological outcomes show that ageing has a keen role in the divergence of mitochondrial function, thereby proving a correlation with ageing and maintenance of mitochondrial homeostasis in PD. � 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.Item Concurrent Assessment of Oxidative Stress and MT-ATP6 Gene Profiling to Facilitate Diagnosis of Autism Spectrum Disorder (ASD) in Tamil Nadu Population(Springer, 2023-03-27T00:00:00) Vellingiri, Balachandar; Venkatesan, Dhivya; Iyer, Mahalaxmi; Mohan, Gomathi; Krishnan, Padmavathi; Sai Krishna, Krothapalli; Sangeetha, R.; Narayanasamy, Arul; Gopalakrishnan, Abilash Valsala; Kumar, Nachimuthu Senthil; Subramaniam, Mohana DeviAutism spectrum disorder (ASD) is a neurodevelopmental disability that causes social impairment, debilitated verbal or nonverbal conversation, and restricted/repeated behavior. Recent research reveals that mitochondrial dysfunction and oxidative stress might play a pivotal role in ASD condition. The goal of this case�control study was to investigate oxidative stress and related alterations in ASD patients. In addition, the impact of mitochondrial DNA (mtDNA) mutations, particularly MT-ATP6, and its link with oxidative stress in ASD was studied. We found that ASD patient�s plasma had lower superoxide dismutase (SOD) and higher catalase (CAT) activity, resulting in lower SOD/CAT ratio. MT-ATP6 mutation analysis revealed that four variations, 8865 G>A, 8684 C>T, 8697 G>A, and 8836 A>G, have a frequency of more than 10% with missense and synonymous (silent) mutations. It was observed that abnormalities in mitochondrial complexes (I, III, V) are more common in ASD, and it may have resulted in MT-ATP6 changes or vice versa. In conclusion, our findings authenticate that oxidative stress and genetics both have an equal and potential role behind ASD and we recommend to conduct more such concurrent research to understand their unique mechanism for better diagnosis and therapeutic for ASD. Graphical Abstract: [Figure not available: see fulltext.] � 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.Item miRNA in Parkinson's disease:�From pathogenesis to theranostic approaches(John Wiley and Sons Inc, 2022-12-11T00:00:00) Elangovan, Ajay; Venkatesan, Dhivya; Selvaraj, Priyanka; Pasha, Md. Younus; Babu, Harysh Winster Suresh; Iyer, Mahalaxmi; Narayanasamy, Arul; Subramaniam, Mohana Devi; Valsala Gopalakrishnan, Abilash; Kumar, Nachimuthu Senthil; Vellingiri, BalachandarParkinson's disease (PD) is an age associated neurological disorder which is specified by cardinal motor symptoms such as tremor, stiffness, bradykinesia, postural instability, and non-motor symptoms. Dopaminergic neurons degradation in substantia nigra region and aggregation of ?Syn are the classic signs of molecular defects noticed in PD pathogenesis. The discovery of microRNAs (miRNA) predicted to have a pivotal part in various processes regarding regularizing the cellular functions. Studies on dysregulation of miRNA in PD pathogenesis has recently gained the concern where our review unravels the role of miRNA expression in PD and its necessity in clinical validation for therapeutic development in PD. Here, we discussed how miRNA associated with ageing process in PD through molecular mechanistic approach of miRNAs on sirtuins, tumor necrosis factor-alpha and interleukin-6, dopamine loss, oxidative stress and autophagic dysregulation. Further we have also conferred the expression of miRNAs affected by SNCA gene expression, neuronal differentiation and its therapeutic potential with PD. In conclusion, we suggest more rigorous studies should be conducted on understanding the mechanisms and functions of miRNA in PD which will eventually lead to discovery of novel and promising therapeutics for PD. � 2022 Wiley Periodicals LLC.Item Plausible Role of Mitochondrial DNA Copy Number in Neurodegeneration�a Need for Therapeutic Approach in Parkinson�s Disease (PD)(Springer, 2023-07-31T00:00:00) Venkatesan, Dhivya; Iyer, Mahalaxmi; Narayanasamy, Arul; Gopalakrishnan, Abilash Valsala; Vellingiri, BalachandarParkinson�s disease (PD) is an advancing age-associated progressive brain disorder which has various diverse factors, among them mitochondrial dysfunction involves in dopaminergic (DA) degeneration. Aging causes a rise in mitochondrial abnormalities which leads to structural and functional modifications in neuronal activity and cell death in PD. This ends in deterioration of mitochondrial function, mitochondrial alterations, mitochondrial DNA copy number (mtDNA CN) and oxidative phosphorylation (OXPHOS) capacity. mtDNA levels or mtDNA CN in PD have reported that mtDNA depletion would be a predisposing factor in PD pathogenesis. To maintain the mtDNA levels, therapeutic approaches have been focused on mitochondrial biogenesis in PD. The depletion of mtDNA levels in PD can be influenced by autophagic dysregulation, apoptosis, neuroinflammation, oxidative stress, sirtuins, and calcium homeostasis. The current review describes the regulation of mtDNA levels and discusses the plausible molecular pathways in mtDNA CN depletion in PD pathogenesis. We conclude by suggesting further research on mtDNA depletion which might show a promising effect in predicting and diagnosing PD. � 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.Item A review of chromium (Cr) epigenetic toxicity and health hazards(Elsevier B.V., 2023-04-17T00:00:00) Iyer, Mahalaxmi; Anand, Uttpal; Thiruvenkataswamy, Saranya; Babu, Harysh Winster Suresh; Narayanasamy, Arul; Prajapati, Vijay Kumar; Tiwari, Chandan Kumar; Gopalakrishnan, Abilash Valsala; Bontempi, Elza; Sonne, Christian; Barcel�, Dami�; Vellingiri, BalachandarCarcinogenic metals affect a variety of cellular processes, causing oxidative stress and cancer. The widespread distribution of these metals caused by industrial, residential, agricultural, medical, and technical activities raises concern for adverse environmental and human health effects. Of these metals, chromium (Cr) and its derivatives, including Cr(VI)-induced, are of a public health concern as they cause DNA epigenetic alterations resulting in heritable changes in gene expression. Here, we review and discuss the role of Cr(VI) in epigenetic changes, including DNA methylation, histone modifications, micro-RNA changes, biomarkers of exposure and toxicity, and highlight prevention and intervention strategies to protect susceptible populations from exposure and adverse occupational health effects. Cr(VI) is a ubiquitous toxin linked to cardiovascular, developmental, neurological, and endocrine diseases as well as immunologic disorders and a high number of cancer types in humans following inhalation and skin contact. Cr alters DNA methylation levels as well as global and gene-specific histone posttranslational modifications, emphasizing the importance of considering epigenetics as a possible mechanism underlying Cr(VI) toxicity and cell-transforming ability. Our review shows that determining the levels of Cr(VI) in occupational workers is a crucial first step in shielding health problems, including cancer and other disorders. More clinical and preventative measures are therefore needed to better understand the toxicity and safeguard employees against cancer. � 2023Item Role of Telomeres and Telomerase in Parkinson's Disease�A New Theranostics?(John Wiley and Sons Inc, 2023-08-21T00:00:00) Vellingiri, Balachandar; Balasubramani, Kiruthika; Iyer, Mahalaxmi; Raj, Neethu; Elangovan, Ajay; Song, Kwonwoo; Yeo, Han-Cheol; Jayakumar, Namitha; Kinoshita, Masako; Thangarasu, Ravimanickam; Narayanasamy, Arul; Dayem, Ahmed Abdal; Prajapati, Vijay Kumar; Gopalakrishnan, Abilash Valsala; Cho, Ssang-GooParkinson's disease (PD) is a complex condition that is significantly influenced by oxidative stress and inflammation. It is also suggested that telomere shortening (TS) is regulated by oxidative stress which leads to various diseases including age-related neurodegenerative diseases like PD. Thus, it is anticipated that PD would result in TS of peripheral blood mononuclear cells (PBMCs). Telomeres protect the ends of eukaryotic chromosomes preserving them against fusion and destruction. The TS is a normal process because DNA polymerase is unable to replicate the linear ends of the DNA due to end replication complications and telomerase activity in various cell types counteracts this process. PD is usually observed in the aged population and progresses over time therefore, disparities among telomere length in PBMCs of PD patients are recorded and it is still a question whether it has any useful role. Here, the likelihood of telomere attrition in PD and its implications concerning microglia activation, ageing, oxidative stress, and the significance of telomerase activators are addressed. Also, the possibility of telomeres and telomerase as a diagnostic and therapeutic biomarker in PD is discussed. � 2023 Wiley-VCH GmbH.Item Type 2 Diabetes (T2DM) and Parkinson�s Disease (PD): a Mechanistic Approach(Springer, 2023-04-28T00:00:00) Sabari, S. Sri; Balasubramani, Kiruthika; Iyer, Mahalaxmi; Sureshbabu, Harysh Winster; Venkatesan, Dhivya; Gopalakrishnan, Abilash Valsala; Narayanaswamy, Arul; Senthil Kumar, Nachimuthu; Vellingiri, BalachandarGrowing evidence suggest that there is a connection between Parkinson�s disease (PD) and insulin dysregulation in the brain, whilst the connection between PD and type 2 diabetes mellitus (T2DM) is still up for debate. Insulin is widely recognised to play a crucial role in neuronal survival and brain function; any changes in insulin metabolism and signalling in the central nervous system (CNS) can lead to the development of various brain disorders. There is accumulating evidence linking T2DM to PD and other neurodegenerative diseases. In fact, they have a lot in common patho-physiologically, including insulin dysregulation, oxidative stress resulting in mitochondrial dysfunction, microglial activation, and inflammation. As a result, initial research should focus on the role of insulin and its molecular mechanism in order to develop therapeutic outcomes. In this current review, we will look into the link between T2DM and PD, the function of insulin in the brain, and studies related to impact of insulin in causing T2DM and PD. Further, we have also highlighted the role of various insulin signalling pathway in both T2DM and PD. We have also suggested that T2DM-targeting pharmacological strategies as potential therapeutic approach for individuals with cognitive impairment, and we have demonstrated the effectiveness of T2DM-prescribed drugs through current PD treatment trials. In conclusion, this investigation would fill a research gap in T2DM-associated Parkinson�s disease (PD) with a potential therapy option. Graphical Abstract: [Figure not available: see fulltext.]. � 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.Item Untangle the mystery behind DS-associated AD � Is APP the main protagonist?(Elsevier Ireland Ltd, 2023-04-07T00:00:00) Elangovan, Ajay; Babu, Harysh Winster Suresh; Iyer, Mahalaxmi; Gopalakrishnan, Abilash Valsala; Vellingiri, BalachandarAmyloid precursor protein profusion in Trisomy 21, also called Down Syndrome (DS), is rooted in the genetic determination of Alzheimer's disease (AD). With the recent development in patient care, the life expectancy of DS patients has gradually increased, leading to the high prospect of AD development, consequently leading to the development of plaques of amyloid proteins and neurofibrillary tangles made of tau by the fourth decade of the patient leading to dementia. The altered gene expression resulted in cellular dysfunction due to impairment of autophagy, mitochondrial and lysosomal dysfunction, and copy number variation controlled by the additional genes in Trisomy 21. The cognitive impairment and mechanistic insights underlying DS-AD conditions have been reviewed in this article. Some recent findings regarding biomarkers and therapeutics of DS-AD conditions were highlighted in this review. � 2023 Elsevier B.V.