Dr. Debprasad Dutta is a Research Scientist at Mazumdar Shaw Center for Translational Research, specializing in translational neuroscience, biomarker discovery, and stem cell-based therapies for neurological disorders. With an extensive academic background including a PhD in Human Genetics from NIMHANS and a Commonwealth Split-site Scholarship at the University of Liverpool, his career blends deep scientific rigor with global impact.
He has played key roles in multi-institutional research projects focusing on stroke, heart attack predictability, and neuroimmunology, managing BSL2 laboratories and collaborating across disciplines and continents. His scientific achievements are recognized by numerous awards, international fellowships, and active memberships in leading societies, such as the Royal Society of Biology (UK), American Society of Human Genetics, and the European Stroke Organization (ESO).
Dr. Dutta is passionate about mentorship, public science engagement, and fostering innovation among early-career researchers and startup founders. His outreach spans supervising international research internships, driving educational workshops in genetic data analysis, and advocating for equity, inclusion, and cross-sector collaboration. Beyond research, he channels creativity into poetry, science communication, and leadership initiatives, reflecting a holistic approach to advancing knowledge and societal progress.
1) Translational neurosciences: mechanisms biomarkers and therapies for neurological disorders including stroke Guillain-Barré syndrome and Alzheimer's and Parkinson's diseases. 2) Biomarker discovery and omics data analysis: utilizing transcriptomic tools for early diagnosis and personalized medicine. 3) Systematic reviews and meta-analysis: advancing methodological rigor and evidence synthesis in biomedical research. 4) Mentorship: mentoring early-career researchers and entrepreneurs in research strategy technical validation and commercialization of health technologies. 5) Science communication and outreach: promoting equity inclusion and public engagement through writing workshops and creative practice.
Antibiotics are the pivotal pillar of contemporary healthcare and have contributed towards its advancement over the decades. Antibiotic resistance emerged as a critical warning to public wellbeing because of unsuccessful management efforts. Resistance is a natural adaptive tool that offers selection pressure to bacteria, and hence cannot be stopped entirely but rather be slowed down. Antibiotic resistance mutations mostly diminish bacterial reproductive fitness in an environment without antibiotics; however, a fraction of resistant populations ‘accidentally’ emerge as the fittest and thrive in a specific environmental condition, thus favouring the origin of a successful resistant clone. Therefore, despite the time-to-time amendment of treatment regimens, antibiotic resistance has evolved relentlessly. According to the World Health Organization (WHO), we are rapidly approaching a ‘post-antibiotic’ era. The knowledge gap about antibiotic resistance and room for progress is evident and unified combating strategies to mitigate the inadvertent trends of resistance seem to be lacking. Hence, a comprehensive understanding of the genetic and evolutionary foundations of antibiotic resistance will be efficacious to implement policies to force-stop the emergence of resistant bacteria and treat already emerged ones. Prediction of possible evolutionary lineages of resistant bacteria could offer an unswerving impact in precision medicine. In this review, we will discuss the key molecular mechanisms of resistance development in clinical settings and their spontaneous evolution.
Abstract Guillain‐Barré syndrome (GBS) is the commonest post‐infectious inflammatory peripheral neuropathy with undiscerned aetiology. The commonly reported antecedent infections implicated in India include Campylobacter jejuni , chikungunya, dengue, and Japanese encephalitis (JE). In this study from south India, we investigated the role of these four agents in triggering GBS. This case‐control study was performed on 150 treatment‐naive patients with GBS and 150 age and sex‐matched controls from the same community. IgM immunoreactivity for C. jejuni , chikungunya, and dengue was detected by enzyme‐linked immunosorbent assay (ELISA) in serum of patients with GBS and control subjects. Immunoreactivity against JE was detected in serum as well as cerebrospinal fluid (CSF) from patients (n = 150) and orthopaedic control (n = 45) subjects. The immunoreactivity against infections was compared between demyelinating and axonal subtypes of GBS. Overall, 119/150 patients with GBS had serological evidence of antecedent infection. Amongst those with evidence of antecedent infection, 24 (16%), 8 (5%), and 9 (6%) patients were exclusively immunoreactive to chikungunya, JE, and C. jejuni , respectively. In the remaining patients (78/119), immunoreactivity to multiple pathogens was noted. Immunoreactivity to C. jejuni infection was found in 32% of GBS patients compared to 2.7% controls ( P < .001), whereas to chikungunya virus was reported in 66.7% of patients with GBS compared to 44.7% controls ( P = .006). Anti‐dengue immunoreactivity was significantly associated with the demyelinating subtype of GBS. Patients positive for JE IgM (CSF) manifested demyelinating electrophysiology. In this large case‐control study, immunoreactivity against multiple infectious agents was observed in a subset of patients. Chikungunya was the commonest antecedent infection, followed by C. jejuni .
Abstract Guillain‐Barré syndrome (GBS) is the commonest post‐infectious polyradiculopathy. Although genetic background of the host seems to play an important role in the susceptibility to GBS, genes conferring major risk are not yet known. Dysregulation of Toll‐like receptor (TLR) molecules exacerbates immune‐inflammatory responses and the genetic variations within TLR pathway‐related genes contribute to differential risk to infection. The aim of this study was to delineate the impact of genetic variations within TLR2 , TLR3 , and TLR4 genes as well as TLR signaling pathway‐related genes such as MyD88 , TRIF , TRAF3 , TRAF6 , IRF3 , NFκβ1 , and IκBα on risk of developing GBS. Fourteen polymorphisms located within TLR2 (rs3804099, rs111200466), TLR3 (rs3775290, rs3775291), TLR4 (rs1927911, rs11536891), MyD88 (rs7744, rs4988453), TRIF (rs8120), TRAF3 (rs12147254), TRAF6 (rs4755453), IRF3 (rs2304204), NFκβ1 (rs28362491), and IκBα (rs696) genes were genotyped in 150 GBS patients and 150 healthy subjects either by PCR‐RFLP or TaqMan Allelic Discrimination Assay. Genotypes of two polymorphic variants, Del/Del of rs111200466 insertion and deletion (INDEL) polymorphism of TLR2 gene and TT of rs3775290 single nucleotide polymorphism (SNP) of TLR3 gene had significantly higher frequencies among GBS patients, while the frequencies of TT genotype of rs3804099 SNP of TLR2 gene and TT genotype of rs11536891 SNP of TLR4 gene were significantly higher in controls. Gene‐gene interaction study by Multifactor Dimensionality Reduction analysis also suggested a significant combined effect of TLR2 , and NFκβ1 genes on the risk of GBS. The SNPs in the IκBα and IRF3 genes correlated with severity of GBS. The genes encoding TLRs and TLR signaling pathway‐related molecules could serve as crucial genetic markers of susceptibility and severity of GBS.
Abstract Background Antibodies against ganglioside complexes (GSCs) are associated with various clinical features and subtypes of Guillain‐Barré syndrome (GBS). Methods One‐hundred patients were evaluated for antibodies to GSCs formed by combination of GM1, GM2, GD1a, GD1b, GT1b, and GQ1b using manual enzyme linked immuno‐sorbent assay (ELISA). Results Twenty‐six patients were GSC antibody‐positive, most frequent being against GM1‐containing GSC (76.9%). Gender distribution, mean age, symptom‐duration, antecedent events, electrophysiological subtypes, requirement for mechanical ventilation, and median duration of hospital stay were comparable between the GSC antibody‐positive and negative groups. There was no association between specific GSC antibody and electrophysiological subtypes or clinical variants. After controlling for false discovery rate (FDR) using the Benjamini‐Hochberg method, the number of subjects who improved in overall disability sum score, modified Erasmus GBS outcome score, and neuropathy symptom score at discharge was significantly higher in the GSC antibody‐positive group. Improvements in Medical Research Council sum scores and Hughes Disability Scale during the hospital stay between the GSC antibody‐positive and negative groups were not significantly different after controlling for FDR. Conclusions The GSC antibody‐positive group had better outcome at hospital discharge in some of the disability scores. Pathophysiological pathways among patients without GSC antibodies may be different and this requires further evaluation.
Background and Aims: Guillain-Barré Syndrome (GBS), an immune-mediated neuropathy, is characterized by antibodies against gangliosides/ganglioside complexes (GSCs) of peripheral nerves. Antecedent infections have been reported to induce antibodies that cross-react with the host gangliosides and thereby have a pivotal role in conferring an increased risk for developing GBS. Data pertaining to the impact of various antecedent infections, particularly those prevalent in tropical countries like India on the ganglioside/GSC antibodies is sparse. We aimed at exploring the association between six antecedent infections and the profile of ganglioside/GSC antibodies in GBS. Methods: Patients with GBS ( n = 150) and healthy controls ( n = 50) were examined for the serum profile of antibodies against GM1, GM2, GD1a, GD1b, GT1b, and GQ1b and their GSCs by ELISA. These antibodies were correlated with immunoreactivities against Campylobacter jejuni , Japanese encephalitis (JE), dengue, influenza, zika, and chikungunya infections. Results: The frequencies of antibodies against six single gangliosides ( P < 0.001) and their GSCs ( P = 0.039) were significantly higher in patients as compared to controls. Except for GT1b-antibody which was more frequent in axonal GBS, none of the other ganglioside/GSC antibodies correlated with the electrophysiological subtypes of GBS. Antecedent JE infection was significantly associated with increased frequency of antibodies against GD1a, GD1b, GT1b, and GQ1b. Antibodies against GSCs were not influenced by the antecedent infections. Interpretation: This study for the first time shows an association between antecedent JE infection and ganglioside antibodies in GBS. This finding reinforces the determining role of antecedent infections on ganglioside antibody responses and the subsequent immunological processes in GBS.
Coronavirus disease COVID-19 caused by SARSCoV-2 infection leading the current precarious pandemic which is affecting most of the countries in the world. Clinical portrait of COVID-19 might vary from trivial to debilitating febrile illness. Recent hospital-based studies have recorded the possible neurological symptomatology of SARS-CoV-2 infection. Neurological complications might be of Central Nervous System (CNS) such as dizziness,headache, consciousness impairment, cerebrovascular illness, epilepsy, ataxia and encephalopathy. PeripheralNervous System (PNS) illnesses include Guillain-Barré syndrome, hyposmia, hypogeusia, neuralgia. Positive results of Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and serological assays in patients before and during neurological symptoms infer the possibility of both para and post-infectious association of neurological disorders with SARS-CoV-2.Elements of SARS-CoV-2 have been spotted in cerebrospinal fluid (CSF) too.
Cognitive connectomics is a field of study that focuses on mapping and annotating the neural connections underlying cognitive processes. Recent progress in neuroimaging techniques has enabled researchers to investigate the neural basis of cognitive functions with greater precision. Sociomics, on the other hand, is the study of social cognition, including social perception, interaction, and decision-making. Integrating cognitive connectomics and sociomics approaches can lead to a better comprehension of the neural network of sociocognitive phenotypes. However, unifying both approaches can be challenging due to differences in theoretical frameworks and methodologies. Future trends in cognitive connectomics and sociomics research include exploring machinery for higher-order functionalities in the brain and investigating the causal relationships between brain regions. Understanding the synergies and squabbles between two notions is important for advancing translational research on clinical and subclinical pathologies of social cognition.
Abstract Four principal types of authorised COVID-19 vaccines include inactivated whole-virus vaccines, protein subunit vaccines, viral-vector vaccines and nucleic acid (mRNA and DNA) vaccines. Despite numerous Randomised Controlled Trials (RCTs), comprehensive systematic review and comparative meta-analysis have not been performed to validate the immunogenicity, safety and efficacy of COVID-19 vaccines in the healthy adult population. We aim to fulfil this unmet void. We searched for peer-reviewed articles about RCTs of the COVID-19 vaccines on healthy adults (18-64 years) available in eight major bibliographic databases (PubMed, EMBASE, Web of Science, Cochrane Library, Scopus, ScienceDirect, POPLINE, HINARI) till August 28, 2022. The Risk of Bias (RoB) was assessed using the Cochrane RoB-2. Random effects meta-analysis was conducted by pooling dichotomous outcomes using risk ratios (safety outcomes) and continuous outcomes using standardised mean differences (immunogenicity outcomes). Efficacy outcomes were summarised narratively. Moderate to high-quality evidence suggests that those receiving COVID-19 vaccines had significantly higher immune responses compared to placebo. Serious adverse events were rare, confirming that COVID-19 vaccines were safe and immunogenic for the healthy adult population. Remarkably, adverse events were the least common in inactivated vaccines, and nucleic acid vaccines were the most immunogenic. The efficacies of COVID-19 vaccines ranged from 21.9% to 95.9% in preventing COVID-19. We endorse all four types of COVID-19 vaccines for public health policy implementing taskforces. Yet, meta-analyses based on individual patient data are warranted for more extensive measurement of differential impacts of COVID-19 vaccines on different genders, ethnicities, comorbidities and types of vaccine jabbed.
Guillain-Barré syndrome (GBS) is the commonest postinfectious autoimmune peripheral neuropathy of undiscerned etiology. Campylobacter jejuni (C. jejuni) is the most widely reported antecedent infection in GBS is. In this case-control investigation, we assessed the contribution of C. jejuni in GBS and ganglioside autoantibody response in a tertiary care hospital in India. This case-control study was performed on 150 treatment-naive patients with GBS and 150 age and sex matched controls from the same community. IgM immunoreactivity for C. jejuni was detected by enzyme-linked immunosorbent assay (ELISA) in sera of patients and control subjects. Autoantibody response was evaluated for single ganglioside targets GM1, GM2, GD1a, GD1b, GT1b, GQ1b as well as all possible heterodimeric complexes in patients’ sera. The immunoreactivity against C. jejuni was compared between demyelinating and axonal subtypes of GBS. C. jejuni infection was found in 48/150 (32%) of GBS patients compared to 4/150 (2.7%) of controls. This garners evidence of significantly higher immunoreactivity against C. jejuni (p<0.001, OR=17.170 CI=6.005-49.128) in the patient group compared to controls. However, the anti-C. jejuni immunoreactivity was not found to significantly differ between demyelinating and axonal subtypes of GBS (P=0.585, OR=0.79, CI=0.342-1.832). Further, C. jejuni-preceded patients demonstrated no association with any specific single ganglioside or ganglioside complex (GSC) autoantibodies. In this large case-control study, C. jejuni was observed to be an antecedent trigger of GBS and ascertaining a significantly higher prevalence among patients than controls.
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