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Article ; Online: Therapeutic potential of Hsp27 in neurological diseases

Anila Venugopal / Kasthuri Sundaramoorthy / Balachandar Vellingiri

Egyptian Journal of Medical Human Genetics, Vol 20, Iss 1, Pp 1-

2019 Volume 8

Abstract: Abstract Background Heat shock proteins (Hsps) are widely reported in normal cellular dynamics under stress and non-stress conditions, and parallelly, the studies regarding its role in disease condition are also progressing steadily. The function of Hsps ...

Abstract	Abstract Background Heat shock proteins (Hsps) are widely reported in normal cellular dynamics under stress and non-stress conditions, and parallelly, the studies regarding its role in disease condition are also progressing steadily. The function of Hsps in neurodegenerative disorders is puzzling and not fully understood. This review aims to focus on the role of Hsp27 in normal and diseased conditions and emphasize its therapeutic potential. Hsp27 Hsp27, in particular, has shown to be involved in cell viability and actin cytoskeleton remodeling and also shown to improve many disease conditions. Phosphorylated Hsp27 modulates the p53 pathway by downregulating cellular senescence and also lowers reactive oxygen species to protect TNFα-mediated apoptosis. Hsp27 is also known to interfere with mitochondria-dependent and mitochondria-independent cell apoptotic stimulation. Conclusion This article will highlight the various functions of Hsp27 especially as an anti-apoptotic factor and stress response factor and its therapeutic potential in preventing neuronal apoptosis in neurological diseases. This review also includes a comparison of the therapeutic potential of Hsp27 with regard to other small Hsps.
Keywords	Heat shock proteins ; Hsp27 ; Neurological diseases ; Therapeutic ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
Subject code	610
Language	English
Publishing date	2019-11-01T00:00:00Z
Publisher	SpringerOpen
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Drug Studies on Rett Syndrome: From Bench to Bedside.

Gomathi, Mohan / Padmapriya, Subramanian / Balachandar, Vellingiri

Journal of autism and developmental disorders

2020 Volume 50, Issue 8, Page(s) 2740–2764

Abstract: Drug studies on Rett syndrome (RTT) have drastically increased over the past few decades. This review aims to provide master data on bench-to-bedside drug studies involving RTT. A comprehensive literature review was performed by searching in PUBMED, ... ...

Abstract	Drug studies on Rett syndrome (RTT) have drastically increased over the past few decades. This review aims to provide master data on bench-to-bedside drug studies involving RTT. A comprehensive literature review was performed by searching in PUBMED, MEDLINE and Google Scholar, international, national and regional clinical trial registries and pharmaceutical companies using the keywords "Rett syndrome treatment and/or drug or compound or molecule". Seventy drugs were investigated in non-clinical (N = 65 animal/cell line-based studies; N = 5 iPSC-based study) and clinical trials (N = 34) for ameliorating the symptoms of RTT. Though there is good progress in both clinical and non-clinical studies, none of these drugs entered phase III/IV for being launched as a therapeutic agent for RTT.
MeSH term(s)	Animals ; Disease Models, Animal ; Female ; Humans ; Rett Syndrome/drug therapy
Language	English
Publishing date	2020-02-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	391999-7
ISSN	1573-3432 ; 0162-3257
ISSN (online)	1573-3432
ISSN	0162-3257
DOI	10.1007/s10803-020-04381-y
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Article ; Online: Purinergic signalling pathway

Nisha Chandran / Mahalaxmi Iyer / Zothan Siama / Balachandar Vellingiri / Arul Narayanasamy

Egyptian Journal of Medical Human Genetics, Vol 21, Iss 1, Pp 1-

therapeutic target in ovarian cancer

2020 Volume 8

Abstract: Abstract Background The lack of early diagnostic tools and the development of chemoresistance have made ovarian cancer (OC) one of the deadliest gynaecological cancers. The tumour microenvironment is characterised by the extracellular release of high ... ...

Abstract	Abstract Background The lack of early diagnostic tools and the development of chemoresistance have made ovarian cancer (OC) one of the deadliest gynaecological cancers. The tumour microenvironment is characterised by the extracellular release of high levels of ATP, which is followed by the activation of P1 adenosinergic and P2 purinergic signalling systems. The sequential hydrolysis of ATP by the ectonucleotidases CD39 and CD73 generates adenosine, which creates an immune suppressive microenvironment by inhibiting the T and NK cell responses via the A2A adenosine receptor. Main body of the abstract In OC, adenosine-induced pAMPK pathway leads to the inhibition of cell growth and proliferation, which offers new treatment options to prevent or overcome chemoresistance. The activation of P2Y12 and P2Y1 purinergic receptors expressed in the platelets promotes epithelial-mesenchymal transition (EMT). The inhibitors of these receptors will be the effective therapeutic targets in managing OC. Furthermore, research on these signalling systems indicates an expanding field of opportunities to specifically target the purinergic receptors for the treatment of OC. Short conclusion In this review, we have described the complex purinergic signalling mechanism involved in the development of OC and discussed the merits of targeting the components involved in the purinergic signalling pathway.
Keywords	Adenosine ; Ectonucleotidases ; Chemoresistance ; Platelets ; Purinergic signalling ; Ovarian cancer (OC) ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
Subject code	570
Language	English
Publishing date	2020-06-01T00:00:00Z
Publisher	SpringerOpen
Document type	Article ; Online
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Article ; Online: Leber's hereditary optic neuropathy: Current approaches and future perspectives on Mesenchymal stem cell-mediated rescue.

Mohana Devi, Subramaniam / Abishek Kumar, B / Mahalaxmi, Iyer / Balachandar, Vellingiri

Mitochondrion

2021 Volume 60, Page(s) 201–218

Abstract: Leber's Hereditary Optic Neuropathy (LHON) is an inherited optic nerve disorder. It is a mitochondrially inherited disease due to point mutation in the MT-ND1, MT-ND4, and MT-ND6 genes of mitochondrial DNA (mtDNA) coding for complex I subunit proteins. ... ...

Abstract	Leber's Hereditary Optic Neuropathy (LHON) is an inherited optic nerve disorder. It is a mitochondrially inherited disease due to point mutation in the MT-ND1, MT-ND4, and MT-ND6 genes of mitochondrial DNA (mtDNA) coding for complex I subunit proteins. These mutations affect the assembly of the mitochondrial complex I and hence the electron transport chain leading to mitochondrial dysfunction and oxidative damage. Optic nerve cells like retinal ganglion cells (RGCs) are more sensitive to mitochondrial loss and oxidative damage which results in the progressive degeneration of RGCs at the axonal region of the optic nerve leading to bilateral vision loss. Currently, gene therapy using Adeno-associated viral vector (AAV) is widely studied for the therapeutics application in LHON. Our review highlights the application of cell-based therapy for LHON. Mesenchymal stem cells (MSCs) are known to rescue cells from the pre-apoptotic stage by transferring healthy mitochondria through tunneling nanotubes (TNT) for cellular oxidative function. Empowering the transfer of healthy mitochondria using MSCs may replace the mitochondria with pathogenic mutation and possibly benefit the cells from progressive damage. This review discusses the ongoing research in LHON and mitochondrial transfer mechanisms to explore its scope in inherited optic neuropathy.
MeSH term(s)	Humans ; Mesenchymal Stem Cell Transplantation ; Optic Atrophy, Hereditary, Leber/therapy
Language	English
Publishing date	2021-08-26
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2056923-3
ISSN	1872-8278 ; 1567-7249
ISSN (online)	1872-8278
ISSN	1567-7249
DOI	10.1016/j.mito.2021.08.013
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Article: Novel therapeutic approaches: Rett syndrome and human induced pluripotent stem cell technology.

Gomathi, Mohan / Balachandar, Vellingiri

Stem cell investigation

2017 Volume 4, Page(s) 20

Abstract: Recent advances in induced pluripotent stem cell (iPSC) technology target screening and discovering of therapeutic agents for the possible cure of human diseases. Human induced pluripotent stem cells (hiPSC) are the right kind of platform for testing ... ...

Abstract	Recent advances in induced pluripotent stem cell (iPSC) technology target screening and discovering of therapeutic agents for the possible cure of human diseases. Human induced pluripotent stem cells (hiPSC) are the right kind of platform for testing potency of specific active compounds. Ayurveda, the Indian traditional system of medicine developed between 2,500 and 500 BC, is a science involving the intelligent formulations of herbs and minerals. It can serve as a "goldmine" for novel neuroprotective agents used for centuries to treat neurological disorders. This review discusses limitations in screening drugs for neurological disorders and the advantages offered by hiPSC integrated with Indian traditional system of medicine. We begin by describing the current state of hiPSC technology in research on Rett syndrome (RTT) followed by the current controversies in RTT research combined with the emergence of patient-specific hiPSC that indicate an urgent need for researchers to understand the etiology and drug mechanism. We conclude by offering recommendations to reinforce the screening of active compounds present in the ayurvedic medicines using the human induced pluripotent neural model system for research involving drug discovery for RTT. This integrative approach will fill the current knowledge gap in the traditional medicines and drug discovery.
Language	English
Publishing date	2017-03-02
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	2884645-X
ISSN	2313-0792 ; 2306-9759
ISSN (online)	2313-0792
ISSN	2306-9759
DOI	10.21037/sci.2017.02.11
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Article: Cell replacement therapy is the remedial solution for treating Parkinson's disease.

Dhivya, Venkatesan / Balachandar, Vellingiri

Stem cell investigation

2017 Volume 4, Page(s) 59

Abstract: The selective degeneration of dopaminergic (DA) neurons in Parkinson's disease (PD) has made an idol target for cell replacement therapies and other emerging surgical treatments. Certainly, by transplantation method, the therapeutic regimens such as ... ...

Abstract	The selective degeneration of dopaminergic (DA) neurons in Parkinson's disease (PD) has made an idol target for cell replacement therapies and other emerging surgical treatments. Certainly, by transplantation method, the therapeutic regimens such as human fetal ventral midbrain (hfVM) cells, human embryonic stem cells (hESCs), human neural stem/precursor/ progenitor cells (hNSCs/hNPCs), human mesenchymal stem cells (hMSCs), human induced neural stem cells (hiNSCs), and human induced pluripotent stem cells (hiPSCs) have been used into DA deficient striatum. In recent decades, surgical methods such as deep brain stimulation (DBS) and gene therapies have been used with the aim of treating PD. Though the technology has improved and many treating options arise, the permanent source for curing PD has not been identified yet. In this review, we examine how stem cell therapies have made advancement as a therapeutic source for PD when compared with surgical treatments.
Language	English
Publishing date	2017-06-30
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	2884645-X
ISSN	2313-0792 ; 2306-9759
ISSN (online)	2313-0792
ISSN	2306-9759
DOI	10.21037/sci.2017.06.08
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Article ; Online: Genetic Instability and Disease Progression of Indian Rett Syndrome Patients.

Gomathi, Mohan / Dhivya, Venkatesan / Padmavathi, Vijayakumar / Pradeepkumar, Murugasamy / Robert Wilson, S / Kumar, Nachimuthu Senthil / Balachandar, Vellingiri

Molecular neurobiology

2023

Abstract: Rett syndrome (RTT) is the rare neurodevelopmental disorder caused by mutations in methyl CpG binding protein 2 (MECP2) gene with a prevalence of 1:10,000 worldwide. The hallmark clinical features of RTT are developmental delay, microcephaly, repetitive ... ...

Abstract	Rett syndrome (RTT) is the rare neurodevelopmental disorder caused by mutations in methyl CpG binding protein 2 (MECP2) gene with a prevalence of 1:10,000 worldwide. The hallmark clinical features of RTT are developmental delay, microcephaly, repetitive behaviours, gait abnormalities, respiratory abnormalities and seizures. Still, the understanding on the diagnosis of RTT among clinicians are less. The aim of our work was to study various clinical manifestations and a spectrum of MECP2 genetic heterogeneity in RTT patients from South Indian population. We screened 208 autistic patients and diagnosed 20 RTT patients, who were further divided into classical RTT (group I; N = 11) and variant RTT (group II; N = 9). The clinical severity of RTT was measured using RSSS, RSBQ, SSI, SSS and RTT gross motor scale. The biochemical analysis showed that thyroid-stimulating hormone (TSH), plasma dopamine and cholesterol levels were higher in group I when compared to group II, whereas the level of blood pressure, calcium, ferritin and high-density lipoprotein levels were significantly decreased in both RTT groups, when compared to the control group. The genetic mutational spectrum of MECP2 mutations were found in 12/20 of RTT patients, which revealed the occurrence of 60% pathogenic mutation and 20% unknown mutation and it was correlated with the clinical finding of respiratory dysfunction, scoliosis and sleeping problems. The significant results of this study provided clinical and genetic aspects of RTT diagnosis and proposed the clinicians to screen abnormal cholesterol, calcium and TSH levels tailed with MECP2 gene mutations for early prognosis of disease severity.
Language	English
Publishing date	2023-12-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-023-03882-y
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Article ; Online: Excessive carbohydrate consumption and body mass index

Padmavathi Vijayakumar / Arul Narayanasamy / Balachandar Vellingiri

Journal of Basic and Applied Zoology, Vol 79, Iss 1, Pp 1-

the risk factors for type 2 diabetes mellitus in patients with Prader-Willi syndrome in Tamil Nadu population

2018 Volume 10

Abstract: Abstract Background Prader-Willi syndrome (PWS) is commonly associated with severe obesity and type 2 diabetes mellitus (T2DM) and is caused by excessive eating. Only very few studies have reported the relationship between excessive eating, weight gain, ... ...

Abstract	Abstract Background Prader-Willi syndrome (PWS) is commonly associated with severe obesity and type 2 diabetes mellitus (T2DM) and is caused by excessive eating. Only very few studies have reported the relationship between excessive eating, weight gain, and T2DM associated with PWS. The aim of the present study was to investigate the relationship between high carbohydrate intake, body mass index (BMI), and the associated risk factor of T2DM development in people with PWS. We collected data from 23 PWS patients along with obesity control (OC) in Tamil Nadu, India. All PWS patients had T2DM whereas only 7 of 23 OC subjects had T2DM. The physical and biochemical parameters were compared in both subjects. We estimated daily intake in grams of food and calories for each item consumed by both PWS and OC subjects (with and without T2DM). Additionally, we compared BMI values and macronutrients, to investigate the occurrence of T2DM in PWS. Results All statistical analyses were done using mean ± SD. PWS subjects showed BMI values that were extremely significant in both adolescent and adult (p value < 0.0001) compared to OC subjects. All biochemical parameters were extremely significant in the adolescent than in the adult group of PWS compared to OC subjects. The current study showed that PWS subjects consume significantly more carbohydrates from total white rice intake and they have exceeding BMI values when compared to OC subjects with and without T2DM (p value 0.05). Conclusion This is the first report on excessive carbohydrate consumption of > 300 g by PWS patients in Tamil Nadu with BMI ≥ 30 kg/m2 as a risk factor for T2DM. We highly recommend the optimal daily intake of white rice to prevent the development of T2DM in PWS.
Keywords	Prader-Willi syndrome ; Obesity control ; T2DM ; Carbohydrates ; Body mass index ; Zoology ; QL1-991
Subject code	796
Language	English
Publishing date	2018-12-01T00:00:00Z
Publisher	SpringerOpen
Document type	Article ; Online
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Article ; Online: Neurotoxicity of pesticides – A link to neurodegeneration

Balachandar Vellingiri / Mamatha Chandrasekhar / S. Sri Sabari / Abilash Valsala Gopalakrishnan / Arul Narayanasamy / Dhivya Venkatesan / Mahalaxmi Iyer / Kavindra Kesari / Abhijit Dey

Ecotoxicology and Environmental Safety, Vol 243, Iss , Pp 113972- (2022)

2022

Abstract: Parkinson’s disease (PD) is a neurodegenerative disorder which mainly targets motor symptoms such as tremor, rigidity, bradykinesia and postural instability. The physiological changes occur due to dopamine depletion in basal ganglia region of the brain. ... ...

Abstract	Parkinson’s disease (PD) is a neurodegenerative disorder which mainly targets motor symptoms such as tremor, rigidity, bradykinesia and postural instability. The physiological changes occur due to dopamine depletion in basal ganglia region of the brain. PD aetiology is not yet elucidated clearly but genetic and environmental factors play a prominent role in disease occurrence. Despite of various environmental factors, pesticides exposure has been convicted as major candidate in PD pathogenesis. Among various pesticides 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been widely investigated in PD following with paraquat (PQ), maneb (MB), organochlorines (OC) and rotenone. Effect of these pesticides has been suggested to be involved in oxidative stress, alterations in dopamine transporters, mitochondrial dysfunction, α-synuclein (αSyn) fibrillation, and neuroinflammation in PD. The present review discusses the influence of pesticides in neurodegeneration and its related epidemiological studies conducted in PD. Furthermore, we have deliberated the common pesticides involved in PD and its associated genetic alterations and the probable mechanism of them behind PD pathogenesis. Hence, we conclude that pesticides play a prominent role in PD pathogenesis and advance research is needed to investigate the alterations in genetic and mechanistic aspects of PD.
Keywords	Toxicity ; Residual toxicant ; Toxic pollutant ; Pesticides ; Parkinson’s disease (PD) ; Pesticide toxicology ; Environmental pollution ; TD172-193.5 ; Environmental sciences ; GE1-350
Subject code	333
Language	English
Publishing date	2022-09-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Mitochondrial dysfunction: A hidden trigger of autism?

Balachandar, Vellingiri / Rajagopalan, Kamarajan / Jayaramayya, Kaavya / Jeevanandam, Madesh / Iyer, Mahalaxmi

Genes & diseases

2020 Volume 8, Issue 5, Page(s) 629–639

Abstract: Autism is a heterogeneous neurodevelopmental and neuropsychiatric disorder with no precise etiology. Deficits in cognitive functions uncover at early stages and are known to have an environmental and genetic basis. Since autism is multifaceted and also ... ...

Abstract	Autism is a heterogeneous neurodevelopmental and neuropsychiatric disorder with no precise etiology. Deficits in cognitive functions uncover at early stages and are known to have an environmental and genetic basis. Since autism is multifaceted and also linked with other comorbidities associated with various organs, there is a possibility that there may be a fundamental cellular process responsible for this. These reasons place mitochondria at the point of interest as it is involved in multiple cellular processes predominantly involving metabolism. Mitochondria encoded genes were taken into consideration lately because it is inherited maternally, has its own genome and also functions the time of embryo development. Various researches have linked mitochondrial mishaps like oxidative stress, ROS production and mt-DNA copy number variations to autism. Despite dramatic advances in autism research worldwide, the studies focusing on mitochondrial dysfunction in autism is rather minimal, especially in India. India, owing to its rich diversity, may be able to contribute significantly to autism research. It is vital to urge more studies in this domain as it may help to completely understand the basics of the condition apart from a genetic standpoint. This review focuses on the worldwide and Indian scenario of autism research; mitochondrial abnormalities in autism and possible therapeutic approaches to combat it.
Language	English
Publishing date	2020-07-16
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	2821806-1
ISSN	2352-3042 ; 2352-3042
ISSN (online)	2352-3042
ISSN	2352-3042
DOI	10.1016/j.gendis.2020.07.002
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