School Of Basic And Applied Sciences

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Author: search.filters.author.Gopalakrishnan, Abilash Valsala

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    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, Balachandar
    Parkinson�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.
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    Molecular mechanisms of alcohol's effects on the human body: A review and update
    (John Wiley and Sons Inc, 2023-08-14T00:00:00) Renu, Kaviyarasi; Myakala, Haritha; Chakraborty, Rituraj; Bhattacharya, Sharmishtha; Abuwani, Asmita; Lokhandwala, Mariyam; Vellingiri, Balachandar; Gopalakrishnan, Abilash Valsala
    Alcohol consumption has been linked to numerous negative health outcomes although it has some beneficial effects on moderate dosages, the most severe of which being alcohol-induced hepatitis. The number of people dying from this liver illness has been shown to climb steadily over time, and its prevalence has been increasing. Researchers have found that alcohol consumption primarily affects the brain, leading to a wide range of neurological and psychological diseases. High-alcohol-consumption addicts not only experienced seizures, but also ataxia, aggression, social anxiety, and variceal hemorrhage that ultimately resulted in death, ascites, and schizophrenia. Drugs treating this liver condition are limited and can cause serious side effects like depression. Serine-threonine kinases, cAMP protein kinases, protein kinase C, ERK, RACK 1, Homer 2, and more have all been observed to have their signaling pathways disrupted by alcohol, and alcohol has also been linked to epigenetic changes. In addition, alcohol consumption induces dysbiosis by changing the composition of the microbiome found in the gastrointestinal tract. Although more studies are needed, those that have been done suggest that probiotics aid in keeping the various microbiota concentrations stable. It has been argued that reducing one's alcohol intake may seem less harmful because excessive drinking is a lifestyle disorder. � 2023 Wiley Periodicals LLC.
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    Epicardial adipose tissue and cardiac lipotoxicity: A review
    (Elsevier Inc., 2023-07-05T00:00:00) Mukherjee, Anirban Goutam; Renu, Kaviyarasi; Gopalakrishnan, Abilash Valsala; Jayaraj, Rama; Dey, Abhijit; Vellingiri, Balachandar; Ganesan, Raja
    Epicardial adipose tissue (EAT) has morphological and physiological contiguity with the myocardium and coronary arteries, making it a visceral fat deposit with some unique properties. Under normal circumstances, EAT exhibits biochemical, mechanical, and thermogenic cardioprotective characteristics. Under clinical processes, epicardial fat can directly impact the heart and coronary arteries by secreting proinflammatory cytokines via vasocrine or paracrine mechanisms. It is still not apparent what factors affect this equilibrium. Returning epicardial fat to its physiological purpose may be possible by enhanced local vascularization, weight loss, and focused pharmacological therapies. This review centers on EAT's developing physiological and pathophysiological dimensions and its various and pioneering clinical utilities. � 2023 Elsevier Inc.
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    Recent advances in understanding brain cancer metabolomics: a review
    (Springer, 2023-07-10T00:00:00) Mukherjee, Anirban Goutam; Gopalakrishnan, Abilash Valsala; Jayaraj, Rama; Ganesan, Raja; Renu, Kaviyarasi; Vellingiri, Balachandar; Dey, Abhijit; Parveen, Mohamudha
    Regardless of the significant progress made in surgical techniques and adjuvant therapies, brain tumors are a major contributor to cancer-related morbidity and mortality in both pediatric and adult populations. Gliomas represent a significant proportion of cerebral neoplasms, exhibiting diverse levels of malignancy. The etiology and mechanisms of resistance of this malignancy are inadequately comprehended, and the optimization of patient diagnosis and prognosis is a challenge due to the diversity of the disease and the restricted availability of therapeutic options. Metabolomics refers to the comprehensive analysis of endogenous and exogenous small molecules, both in a targeted and untargeted manner, that enables the characterization of an individual�s phenotype and offers valuable insights into cellular activity, particularly in the context of cancer biology, including brain tumor biology. Metabolomics has garnered attention in current years due to its potential to facilitate comprehension of the dynamic spatiotemporal regulatory network of enzymes and metabolites that enables cancer cells to adapt to their environment and foster the development of tumors. Metabolic changes are widely acknowledged as a significant characteristic for tracking the advancement of diseases, treatment efficacy, and identifying novel molecular targets for successful medical management. Metabolomics has emerged as an exciting area for personalized medicine and drug discovery, utilizing advanced analytical techniques such as nuclear magnetic resonance spectroscopy (MRS) and mass spectrometry (MS) to achieve high-throughput analysis. This review examines and highlights the latest developments in MRS, MS, and other technologies in studying human brain tumor metabolomics. � 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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    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, Balachandar
    Parkinson�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.
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    Onco-Pathogen Mediated Cancer Progression and Associated Signaling Pathways in Cancer Development
    (MDPI, 2023-05-28T00:00:00) Kannampuzha, Sandra; Gopalakrishnan, Abilash Valsala; Padinharayil, Hafiza; Alappat, Reema Rose; Anilkumar, Kavya V.; George, Alex; Dey, Abhijit; Vellingiri, Balachandar; Madhyastha, Harishkumar; Ganesan, Raja; Ramesh, Thiyagarajan; Jayaraj, Rama; Prabakaran, D.S.
    Infection with viruses, bacteria, and parasites are thought to be the underlying cause of about 8�17% of the world�s cancer burden, i.e., approximately one in every five malignancies globally is caused by an infectious pathogen. Oncogenesis is thought to be aided by eleven major pathogens. It is crucial to identify microorganisms that potentially act as human carcinogens and to understand how exposure to such pathogens occur as well as the following carcinogenic pathways they induce. Gaining knowledge in this field will give important suggestions for effective pathogen-driven cancer care, control, and, ultimately, prevention. This review will mainly focus on the major onco-pathogens and the types of cancer caused by them. It will also discuss the major pathways which, when altered, lead to the progression of these cancers. � 2023 by the authors.
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    The incidence of male breast cancer: from fiction to reality - correspondence
    (NLM (Medline), 2023-05-24T00:00:00) Mukherjee, Anirban Goutam; Gopalakrishnan, Abilash Valsala; Jayaraj, Rama; Renu, Kaviyarasi; Dey, Abhijit; Vellingiri, Balachandar; Malik, Tabarak
    [No abstract available]
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    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, Balachandar
    Growing 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.
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    Evolving strategies and application of proteins and peptide therapeutics in cancer treatment
    (Elsevier Masson s.r.l., 2023-05-05T00:00:00) Mukherjee, Anirban Goutam; Wanjari, Uddesh Ramesh; Gopalakrishnan, Abilash Valsala; Bradu, Pragya; Biswas, Antara; Ganesan, Raja; Renu, Kaviyarasi; Dey, Abhijit; Vellingiri, Balachandar; El Allali, Achraf; Alsamman, Alsamman M.; Zayed, Hatem; George Priya Doss, C.
    Several proteins and peptides have therapeutic potential and can be used for cancer therapy. By binding to cell surface receptors and other indicators uniquely linked with or overexpressed on tumors compared to healthy tissue, protein biologics enhance the active targeting of cancer cells, as opposed to the passive targeting of cells by conventional small-molecule chemotherapeutics. This study focuses on peptide medications that exist to slow or stop tumor growth and the spread of cancer, demonstrating the therapeutic potential of peptides in cancer treatment. As an alternative to standard chemotherapy, peptides that selectively kill cancer cells while sparing healthy tissue are developing. A mountain of clinical evidence supports the efficacy of peptide-based cancer vaccines. Since a single treatment technique may not be sufficient to produce favourable results in the fight against cancer, combination therapy is emerging as an effective option to generate synergistic benefits. One example of this new area is the use of anticancer peptides in combination with nonpeptidic cytotoxic drugs or the combination of immunotherapy with conventional therapies like radiation and chemotherapy. This review focuses on the different natural and synthetic peptides obtained and researched. Discoveries, manufacture, and modifications of peptide drugs, as well as their contemporary applications, are summarized in this review. We also discuss the benefits and difficulties of potential advances in therapeutic peptides. � 2023
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    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, Balachandar
    Amyloid 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.