Dr. Rita Christopher’s lab
A significant number of patients with progressive neurological symptoms are not diagnosed despite extensive workups. In order to facilitate the diagnosis, we conduct mass spectrometry-based targeted metabolomic studies leading to the diagnosis of several rare genetic metabolic disorders. In 2007, we have established the first state-of the-art, mass spectrometry facility for screening for inborn errors of intermediary metabolism (disorders of amino acid metabolism, fatty acid oxidation defects and organic acidemias). We measure a panel of 11 amino acids, free carnitine and 31 acylcarnitnes in a 3.2mm dried blood spot collected on filter paper, and, based on the characteristic profiles, we identify the specific disorder. We have tested >50,000 blood samples and identified more than 1300 cases. We have also established a high-throughput, mass spectrometry-based method to simultaneously measure a panel of lysosomal enzymes to screen for lysosomal storage disorders using dried blood spots collected on filter paper. The diseases selected in the panel include Gaucher disease, Pompe disease, Fabry disease, Niemann-Pick disease types A and B and Krabbe disease. Recently, we have developed low cost, robust and reliable, mass-spectrometry-based methods which can be used as first and second tier tests to screen, identify and confirm X-linked adrenoleukodystrophy using dried blood spots. Early diagnosis of these inherited neurometabolic disorders before the onset of irreversible pathologies would lead to better outcomes for current and proposed therapies.
Aneurysmal subarachnoid hemorrhage resulting from the rupture of an intracranial aneurysm is a major catastrophic event associated with high rate of mortality and morbidity in India. Consequently, our research is focused on evaluating the patho-mechanism of aneurysm formation, growth and rupture. Using microarray technique we have profiled the microRNA in aneurysmal tissues and controls and determined the differentially expressed miRNAs in order to identify their target genes and to decipher their role in aneurysm formation, growth and rupture. In addition, we are also evaluating the vasoprotective role of estrogen and the role of oestradiol deficiency in the aneurysm formation and rupture in postmenopausal women.
Primary brain tumors
Glioblastoma (GBM) is one of the most common and most malignant tumours of the central nervous system. It is notorious for its highly infiltrative and invasive behavior. Despite new diagnostic techniques and combined modality therapy prognosis remains dismal. Decades of surgical therapy, radiotherapy and chemotherapy have failed to drastically change survival. Glioma cells have exceptional ability to infiltrate normal brain, often along blood vessels or nerve fibres. This feature makes complete radical surgical resection virtually impossible and leading in almost all cases to tumor recurrence. Several factors are thought to contribute to the invasive and migratory properties of GBM cells, interacting with the microenvironment and enhancing motility and invasion. We aim at understanding glutamate excitotoxicity in GBM, glutamate receptor pathway, the role inflammatory and regulatory cytokines and its signaling on migration, proliferation and invasiveness of tumour and contribute to the understanding of the complex biological interactions that regulate glioblastoma growth, invasion and recurrence.
Dr. Ravish H. MBBS MD (ASST PROF)
Dr. Ravish H. MBBS MD (ASST PROF)
For any kind of discomfort or trauma body responds well by briefing certain chemicals or secretions as indicators. This response could be predominantly in the form of stress and pain, which could be an unpleasant sensory and emotional experience associated with actual or potential tissue damage leading to disorder/syndrome or disease.
Thrust Area of Research
Dr. Sarada Subramanian’s lab
We focus on the development of therapeutic strategies to Alzheimer’s disease (AD). AD is one of the leading causes of dementia in the elderly, with more than 40 million individuals currently affected worldwide. AD is caused by the selective loss/ dysfunction of neurons particularly those expressing nicotinic acetylcholine receptors in specific brain regions including the neocortex and hippocampus. Spatial learning, working memory, and long-term memory impairments are some of the earliest symptoms expressed in AD. The pathological hallmarks of AD include intracellular neurofibrillary tangles (NFT) consisting of hyperphosphorylated form of the microtubule associated protein tau and senile plaques comprising of the aggregated peptide amyloid ß (Aß). An increase in acetylcholinesterase (AChE), a key enzyme in the cholinergic nervous system, around the senile plaques and NFT is a common feature of AD neuropathology. Aß (1-42) is generated from a lager precursor protein (APP) by the proteolytic action of specific cleavage enzymes called ß- and γ-secretases. Mutations in either the Aß precursor protein or the processing enzymes account for familial cases of AD (<5%). However, vast majority of AD cases (>95%) are sporadic, significantly influenced by the presence of an apolipoprotein allele E4, dietary lifestyle and more importantly, the metabolic disorders such as diabetes and obesity.
We address the multiple targets of AD as therapeutic strategies. The methodology involves bacterial expression of the culprit peptides of Aβ, Tau and their analogs, immunotherapeutic interventions using peptide- and DNA vaccines in combination with adjuvants approved for use in humans, multiple antigenic peptide systems and conformational antibodies, development of non-transgenic rodent model systems, assessment of their suitability for AD research by physiological and by biochemical means, evaluation of metabolic (dys)function and the reversal on cognitive functions, selection of nootropic herbal extracts containing anti-Alzheimer effects and the development of relevant in vitro and in vivo assay methods.
Dr. Gokulakrishnan, Assistant Professor of Neurochemistry
Dr Gokul’s lab
Research Specialization: Disease Biology; Clinical significance and subclinical relevance of cellular and molecular alterations in metabolic diseases/ Psychiatric disorders; gut microbiome, epigenetics and metabolomics aspects of gestational diabetes & Schizophrenia, Unraveling mechanisms of Proinflammation, Oxidative stress, and biomarker(s) identification for early disease prediction.
He is presently working on certain unique programmes such as understanding ‘metabolic obesity’ in Indians; gut microbiome, epigenetics and metabolomics aspects of gestational diabetes, Schizophrenia & other Psychiatric disorders; novel biomarker(s) identification for early disease prediction; complementary medicine including molecular benefits of lifestyle intervention and Non-invasive point-of-care (POC) – clinical measures & medical devices.
The long term goal of his lab is to understand the molecular mechanisms of metabolic diseases/Psychiatric disorders and to identify diagnostic/predictive biomarkers of disease, identify drug targets and develop precision intervention strategies.