About

Dr. Ashok K. Shetty is a University Distinguished Professor in the Department of Cell Biology and Genetics at Texas A&M University, where he also serves as Associate Director of the Institute for Regenerative Medicine. He earned his Ph.D. in Neuroscience from the All India Institute of Medical Sciences in New Delhi and completed postdoctoral research at Duke University. His research focuses on developing innovative therapies for neurodegenerative and brain injury conditions, including Alzheimer's Disease, Traumatic Brain Injury, and Gulf War Illness. His laboratory is dedicated to creating treatments such as nasal spray formulations of human neural stem cell-derived extracellular vesicles that contain anti-inflammatory and neuroprotective molecules, aiming to reduce neuroinflammation, amyloid plaques, and neurofibrillary tangles in Alzheimer's models, and to promote recovery in TBI and Gulf War Illness models. Dr. Shetty has received continuous extramural research funding for over 28 years from agencies like NIH, DOD, and VA, and has authored over 214 peer-reviewed publications. His work has significantly contributed to understanding brain dysfunction mechanisms and developing novel therapeutic strategies for these devastating conditions.

Research topics

• Neuroscience
• Biology
• Cell biology
• Medicine
• Biochemistry
• Pharmacology
• Internal medicine
• Chemistry
• Immunology
• Endocrinology

Selected publications

• Post-traumatic stress disorder: pathogenesis, epidemiological characteristics, animal models, and potential therapeutic strategies

  Military Medical Research · 2026-01-01

  articleOpen accessSenior author

  Post-traumatic stress disorder (PTSD) is a complex neurobehavioral disorder that disproportionately affects military service members. The clinical presentation of PTSD is heterogeneous and may overlap with other psychiatric conditions. According to the Fifth Edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5), common symptoms include memory loss, mood and personality changes, impulsiveness, aggression, anxiety, and depression. The pathophysiological mechanisms underlying PTSD remain incompletely understood, although research implicates pathways involving the hypothalamic-pituitary-adrenal (HPA) axis, dysfunctional neural circuitry, neurochemical imbalances, neuroinflammatory processes, and genetic and epigenetic factors. Approximately 7% of the U.S. adult population has met the diagnostic criteria for PTSD in their lifetime, with a substantially higher prevalence of 12%-30% among military personnel. Multiple animal models, including single-stressor, intermediate complexity, social interaction, predator stress, and blast exposure paradigms, have been employed to investigate PTSD mechanisms. Current treatment strategies typically integrate pharmacotherapy and psychotherapy. Military service members are at increased risk for blast injuries, which frequently result in traumatic brain injury (TBI). Although some symptoms of TBI may resolve, approximately 20% of affected individuals develop new symptoms, including PTSD. Evidence suggests that exposure to blast shock waves (BSWs) serves as a critical trigger for the clinical manifestations of both TBI and PTSD. Recent studies have identified several mechanisms contributing to BSW-induced brain dysfunction, including intraneuronal accumulation of phosphorylated Tau (p-Tau), activation of the dynorphin/kappa opioid receptor, and activation of metabotropic glutamate receptor 2/3 signaling pathways. This review provides an overview of the clinical features, treatments, pathophysiology, and epidemiology of PTSD, as well as animal models and their limitations in replicating PTSD-like symptoms. It further examines the relationship between BSW exposure, brain injury, and PTSD, discusses animal models that simulate blast trauma and PTSD-like symptoms, and evaluates potential therapies to mitigate BSW-induced PTSD. Finally, the review addresses the limitations of current models and proposes future directions for elucidating the mechanisms linking brain trauma to PTSD.

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• Host-membrane lipid composition controls Cryptococcus neoformans cellular targets

  Frontiers in Immunology · 2026-01-06

  articleOpen access

  Background Cryptococcus neoformans causes lethal meningoencephalitis and long-term neurological deficits, particularly in immunocompromised hosts of any age group. After penetrating the airway and crossing the blood-tissue barriers, C. neoformans rapidly enters the brain, where it extensively releases the capsular polysaccharide glucuronoxylomannan (GXM), a major virulence factor. Methods Cryptococcus neoformans ( ATCC 32045) was used to isolate and purify GXM. This study utilized human-induced pluripotent stem cell-derived 2D cultured neural stem cells, neurons, and microglia-deficient cerebral organoids to identify GXM-induced pathogenesis. Cryosectioning of frozen tissues, immunostaining, western blot analysis and untargeted lipidomics were employed to identify the GXM-induced impact on cellular proliferation and cell death, as well as possible cellular and molecular targets. The study utilized the first-ever atomistic models of neuronal and neural stem cells (NSC) membranes, built using a proportion of the original lipid compositions using the Materials Science Suite to identify subtle interactions between the membranes and GXM. Results GXM exposure induced subtle cell death, but progenitor cell proliferation was unaffected. Interestingly, GXM preferentially targeted neurons irrespective of the abundance of NSCs and astrocytes. Synaptophysin, an integral component of neuronal synaptic vesicles, was significantly reduced following GXM exposure. The untargeted lipidomics analysis revealed higher phosphatidylcholine levels and reduced phosphatidylethanolamine levels in human neurons compared to other cell types. The atomistic models revealed a significant attractive interaction energy between GXM and neuronal membranes, with phosphatidylcholine being primarily responsible. Conclusion This study provides novel evidence that lipid membranes containing higher phosphatidylcholine are a primary target of GXM of C. neoformans and could be the possible reason for the preferential targeting of GXM to neurons. Additionally, GXM induced synaptic deficits in neurons, which could be a significant factor contributing to the neurological dysfunctions observed in this fungal infection. This study opens the mechanism of pathogenesis and targeting opportunities for treating C. neoformans- induced meningoencephalitis.

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• Targeting autophagy in lateral habenula for alleviating depression

  Neural Regeneration Research · 2026-03-14

  articleOpen accessSenior authorCorresponding

  ABSTRACT: Depression affects over 300 million people worldwide and is a leading cause of disability. Current treatments have limited efficacy in achieving remission and require several weeks to months of therapy for lessening depressive symptoms. Reduced autophagy is commonly observed in the brain of individuals with major depressive disorder, impairing cellular homeostasis and synaptic plasticity, the processes vital for mood regulation. A recent study published in the journal Nature reported that a key driver for depression in a mouse model of acute and chronic stress is an impaired autophagy in the lateral habenula, a brain region known to regulate motivation, reward, and aversion. Notably, direct infusion of beclin-1 peptide into this region rapidly restored autophagy markers and reduced depressive symptoms, highlighting a fast-acting mechanism distinct from the way conventional antidepressants act. Such effects were attributed to reduced excitatory neurotransmitter receptors, which could ease neuronal hyperactivity without affecting inhibitory neurotransmission, demonstrating that the selective autophagic degradation of excitatory receptors in the lateral habenula can mediate antidepressant effects. However, several issues remain to be addressed, including the long-term efficacy and the feasibility of the approach for clinical translation. This review critically discusses the proficiency, limitations, and clinical translatability of the lateral habenula autophagy enhancement approach. The promise of other autophagy enhancers and the possibility of combinational therapy, where drugs or dietary supplements could enhance autophagy, diminish neuroinflammation, and regulate neurotransmitters, is also discussed.

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• Psilocybin Maintains Better Brain Function in an Alzheimer’s Disease Model with Reduced Neuroinflammation and Improved Hippocampal Neurogenesis

  Alzheimer s & Dementia · 2025-12-01

  articleOpen accessSenior authorCorresponding

  BACKGROUND: Chronic neuroinflammation plays a significant role in Alzheimer's disease (AD) pathogenesis associated with a decline in cognitive and mood function. Currently, there are no effective therapies to alleviate the progression of brain dysfunction in AD. Psilocybin, an FDA-approved drug for treating major depressive disorder, can restrain neuroinflammation and improve hippocampal neurogenesis. Therefore, the current study investigated the efficacy of psilocybin treatment in slowing down cognitive decline in 5x familial AD (5xFAD) mice. METHODS: Three-month-old male 5xFAD mice received monthly psilocybin (0.5mg/Kg) or vehicle treatment for 4 months (AD-Psilocybin and AD-Veh groups). A month after the last dose of psilocybin, the animals were interrogated with neurobehavioral tests to ascertain the extent of cognitive and mood function decline compared to age-matched naïve control mice. The animals were euthanized when they were 8 months old, and brain tissues were analyzed for the extent of neuroinflammation, hippocampal neurogenesis, synapse loss, and amyloid-beta plaques. The hippocampi from AD-Psilocybin and AD-Veh groups were also analyzed using proteomics. RESULTS: Mice in the AD-Psilocybin group displayed improved abilities to discern minor changes in the immediate environment, pattern separation, associative recognition memory, and no anhedonia compared to mice in the AD-Veh group. Analyses of brain tissues revealed a significant reduction of chronic neuroinflammatory markers in the AD-Psilocybin group vis-à-vis the AD-Veh group. These were apparent from reductions in astrocytic hypertrophy, microglial inflammasome complexes, concentrations of mediators and end products of NLRP3 inflammasome activation, proteins involved in p38/mitogen-activated protein kinase hyperactivation, and proteins linked to activation of cGAS-STING signaling. Additionally, AD-Psilocybin mice exhibited increased production of new neurons associated with improved maintenance of BDNF-ERK-CREB signaling and synaptic proteins. Proteomic analysis of the hippocampus revealed the upregulation of 16 proteins involved in regulating neuroinflammation, mTOR signaling, synaptic function, and axon extension in the AD-Psilocybin group. Notably, mice in the AD-Psilocybin group did not exhibit reduced amyloid-beta plaques or the formation of microglial clusters around plaques. CONCLUSIONS: Psilocybin treatment can maintain better brain function in an AD model without affecting amyloid-beta plaques. Improved brain function is likely due to psilocybin-induced reductions in neuroinflammatory signaling, enhanced hippocampal neurogenesis, and preservation of synapses.

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• AN INTERESTING CASE OF PEDIATRIC OPTIC NEURITIS

  INDIAN JOURNAL OF APPLIED RESEARCH · 2025-03-01

  article1st authorCorresponding

  Optic neuritis (ON) is a rare , uncommon condition in the paediatric population and usually underlies a viral cause. In comparison to adult population, paediatric optic neuritis (PON) occurs usually after acute febrile illness and has bilateral optic nerve involvement .Visual loss occurs as prominent symptom .Ocular pain is less common. It has relatively good visual prognosis with near 1 complete visual recovery. Mean age of occurrence is 10 years with female population more affected than male. It has reported incidence of 0.2 per 2 100,000 children .Children with ON are seropositive for either AQP-4(Aquaporin 4 or MOG Ab (anti-myelin-oligodendrocyte glycoprotein ) We hereby report a case of bilateral optic neuritis in 10 year old boy who presented to our institute with sudden onset of headache , retro orbital pain ,bilateral defective vision .

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• Umbilical Cord‐Mesenchymal Stromal Cell‐Derived Extracellular Vesicles Target the Liver to Improve Neurovascular Health in Type 2 Diabetes With Non‐Alcoholic Fatty Liver Disease

  Journal of Extracellular Vesicles · 2025-07-01 · 6 citations

  articleOpen access

  Type 2 diabetes mellitus (T2DM) combined with non-alcoholic fatty liver disease (NAFLD) exacerbates metabolic dysregulation and neurovascular complications, presenting significant therapeutic challenges. We demonstrate, using SPECT/CT imaging, that extracellular vesicles (EVs) from mesenchymal stromal cells (MSCs) predominantly accumulate in the liver, where they deliver miR-31-5p to suppress platelet-derived growth factor B (PDGFB) produced by hepatic macrophages. This intervention impedes NAFLD progression and establishes a mechanistic link between liver repair and neurovascular improvement. Specifically, single-nucleus RNA sequencing reveals that PDGFB suppression enhances hippocampal pericyte recovery via the PDGFB-PDGFRβ axis and orchestrates the activation of growth differentiation factor 11 (GDF11), thus promoting neuroplasticity. Furthermore, AAV injections indicate that hepatic PDGFB modulation recalibrates transthyretin (TTR) dynamics, thereby restoring its neuroprotective functions and preventing its pathological deposition in the brain. These findings position MSC-EVs as a transformative therapeutic platform that leverages the liver-brain axis to address the intertwined metabolic and neurovascular complications of T2DM, offering a promising avenue for clinical translation.

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• Editorial: Therapeutic potential of adult neurogenesis in neurodegenerative and neuropsychiatric disorders

  Frontiers in Neuroscience · 2025-11-11

  articleOpen access1st authorCorresponding

  Neurogenesis is the process by which new neurons are added to the brain from neural stem/progenitor cells (NSCs) [Bond et al., 2015;Elliott et al., 2025]. While such process is highly apparent during brain development [Villalba et al., 2021], investigations over the last three decades have shown that neurogenesis continues into adulthood in specific brain areas, such as the hippocampus and the olfactory bulb [Bond et al., 2015;Salta et al, 2023;Elliott et al., 2025].Moreover, while the issue remains controversial, there is sufficient evidence from multiple studies to support neurogenesis occurring in the adult human hippocampus [Zanirati et al, 2023;Márquez-Valadez et al., 2025;Dumitru et al., 2025]. Neurogenesis during brain development is a widespread process that builds the complex neural circuitry of the brain, occurring extensively across most regions [Villalba et al., 2021]. In contrast, adult neurogenesis is limited to specific areas, particularly the hippocampus, producing new neurons for specific functions rather than overall brain expansion approach is still in its early stages, and its effectiveness is being studied across various models of neurological and neurodegenerative diseases [Peterson, 2025]. If successful, it could revolutionize the replacement of specific types of neurons lost due to injury or disease. This research topic collection comprises five original research articles and one review article, all published in Frontiers in Neuroscience. These studies, conducted on animal models, have provided new insights into the mechanisms underlying postnatal neurogenesis, adult neurogenesis, lineage programming, and stem cell grafting. The significant novel findings from these studies are summarized in the following section.A study on neurogenesis during the development of the dentate gyrus (DG) reveals discrete transcriptional programs coordinating the differentiation and neurogenic progression of granule neuronal progenitors (GNPs) at embryonic versus postnatal stages of DG neurogenesis (Ohyama et al., 2024). Specifically, the study identified that during development, a sequential expression of the transcription factor Zeb1 is observed in neural stem progenitor pools, characterized by cells positive for GFAP and Sox2, followed by Scratch2 (Scrt2) expression in intermediate progenitors that are positive for Tbr2, Prox1, and NeuroD. Additionally, the study suggested that postnatal GNPs utilize the transcription factor Nkx6-2 to facilitate neuronal differentiation through epithelial-to-mesenchymal transition (EMT)-associated mechanisms (Ohyama et al., 2024). A study by Miyamoto and colleagues provided insights into the gene expression profiles of neuroblasts migrating in the peri-injured cortex (Miyamoto et al., 2025). They demonstrate that in neuroblasts migrating in the peri-injured cortex, the expression of genes involved in regulating migration direction and preventing cell death is upregulated, while the expression of genes involved in cell proliferation and maintenance of the immature state is downregulated. Additional analysis implied that in the injured brain, the proliferative activity of neuroblasts migrating toward lesions is suppressed by TGF-β secreted from microglia and macrophages surrounding the lesion (Miyamoto et al., 2025). The results highlighted that migrating neuroblasts can exhibit slightly but distinctly different properties depending on the microenvironment along their journey.In another study, Otsubo and associates employed an adeno-associated virus knockdown system in mice, providing evidence that Desmoplakin (Dsp), a component of desmosomal cell-cell junctions, has a role in maintaining DG function, including neuronal activity and adult neurogenesis, and anxiolytic-like effects [Otsubo et al., 2024]. Dsp expression was observed primarily in mature dentate granule cells, and its knockdown resulted in reduced expression of the activity-dependent transcription factor FosB, as well as increased expression of calbindin, a mature neuronal marker.Additionally, knockdown of Dsp in DG diminished the serotonin responsiveness of synapses formed by dentate granule cell axons, adversely affecting adult neurogenic processes in the DG and altering behavioral outcomes in a test for anxiety-like behavior. Overall, the study uncovered a previously unknown function of Dsp in the DG. However, it remains to be determined how Dsp binds to dentate granule cells and how it regulates neuronal activity, neurogenesis, and emotional behaviors.Two additional articles in this special issue focus on the altered development of DG neurogenesis and its impact on epileptic susceptibility, as well as the role of seizure-induced neurogenesis in cognitive impairments. The study by Ruiz-Reig and collaborators investigated the functional consequences of p53 deletion in the cortex and hippocampus by generating a conditional mutant mouse (p53-cKO) in which p53 is deleted from pallial progenitors and their derivatives [Ruiz-Reig et al., 2025]. Interestingly, such deletion did not alter the number of neurons in the cortex or the hippocampal cornu ammonis but led to increased proliferative cells in the subgranular zone of the DG and more granule cells in the granule cell layer of the DG. Additionally, p53-cKO mice exhibited a higher density of glutamatergic synapses in the CA3 region, resulting in hyperexcitability and increased epileptic susceptibility [Ruiz-Reig et al., 2025]. The authors suggest that, considering the role of p53 in the proliferation and self-renewal of neural stem cells in the subventricular zone, its potential role in glioblastoma genesis warrants further investigation. The study by Francis and colleagues investigated whether reducing the aberrant increase in neurogenesis could prevent cognitive impairments that emerge in the chronic epilepsy phase [Francis et al., 2025]. In a long-term amygdala kindling model (consisting of 99 electrical stimulations), they showed that treatment with temozolomide, a DNA-alkylating agent, during a period of heightened neurogenesis can reduce aberrant neurogenesis in the hippocampus and prevent impairments in contextual fear discrimination and object recognition memory tasks [Francis et al., 2025]. Overall, the study implied that strategies that can selectively reduce aberrant adult neurogenesis could prevent cognitive deficits associated with chronic epilepsy.In addition to the original research articles discussed above, the research topic collection includes a mini-review article that critically discusses the promise of recruiting resident nonneuronal cells by lineage programming, vis-à-vis replacing lost neurons via grafting of stem cellderived neurons [Peterson, 2025]. The review highlighted that the therapeutic recruitment strategy enables the more precise control of the location, connectivity, and extent of replacement neurons, thereby providing a wider range of therapeutic options than those offered by the engraftment of stem cell-derived neurons alone. However, the review noted that although progress has been made in recruiting resident non-neuronal cells using a direct in vivo reprogramming strategy, further refinements in efficiency and subtype specification are needed to advance this strategy. The review also highlighted the current limitations of the approach of direct reprogramming of non-neuronal cells, including the low conversion yield, preciseness in targeting only non-neuronal cells, the use of viral vectors for reprogramming, potential loss of cells because of unsuccessful reprogramming, yet to be proven long-term survival and integration of reprogrammed neurons and the need to test the efficacy of reprogramming strategies to convert human non-neuronal cells implanted into the brain in animal models into Bonafide mature neurons [Peterson, 2025].In summary, the article collection in this Research Topic, representing the second volume of the RT "Advances in Adult Neurogenesis," provides several novel insights into neurogenesis in the developing and adult DG, injured cortex, and aberrant neurogenesis in pathological conditions such as chronic epilepsy. In addition, the mini-review article weighs the pros and cons of in vivo reprogramming versus stem cell-derived neuronal grafting for replacing lost neurons in the brain affected by neurological and neurodegenerative conditions.

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• Intranasal delivery of metformin using metal–organic framework (MOF)-74-Mg nanocarriers

  Advanced Composites and Hybrid Materials · 2025-01-18 · 7 citations

  articleOpen access

  Dosage tolerance is one of the translational challenges of using metformin (Met) in brain therapeutics. This paper presents metal-organic framework (MOF)-74-Mg nanocarriers (NCs) for intranasal (IN) delivery of brain-specific agents with a prolonged release time. We confirmed their excellent biocompatibility (5 mg/mL) and intrinsic fluorescence properties (370/500 nm excitation/emission peak) in Neuro-2A cells. This NC exhibited a high Met loading rate (10% wt/wt) and a sustained and prolonged release pattern of Met (90% release in 16 h) in Dulbecco's Modified Eagle Medium. We observed an optimal brain accumulation of Met-MOF (9% of the injected dosage) 8 h after IN injection. This percentage is at least 82 times higher than oral administration. Confocal imaging demonstrated significantly higher uptake of Met-MOF, 45 min after IN injection, by 79-85% neurons and 93-97% microglia than astrocytes and oligodendrocytes across 5xFAD mouse brain regions, including hippocampus and striatum. These results suggest MOF-74-Mg is a potential NC for high brain Met accumulation, real-time imaging, and prolonged and sustained release of Met and other neurotherapeutic agents that are challenging to deliver using traditional carriers and administration routes.

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• Long-Term Exposure to Bitters (A&Y) Exacerbates Inflammation in Wistar Rats: A Study on Male Renal Function

  Journal of Health Science and Medical Research · 2025-05-13

  articleOpen accessSenior author

  Objective: This study aims to evaluate the effects of long-term exposure to bitters (A&Y) on inflammation and renal functions in male Wistar rats. Specifically, the research focuses on assessing weight changes, lipid profiles, pro-inflammatory and anti-inflammatory markers, oxidative and anti-oxidative markers, renal function markers, electrolytes, and kidney histology.Material and Methods: Forty-nine male Wistar rats weighing between 160-180g were used for this study and were evenly divided into 7 groups (n=7): control (normal saline, 1ml), Y bitter low dose [YBL, 0.22 ml/kg], Y bitter average dose [YBA, 0.43 ml/kg], Y bitter high dose [YBH, 0.65 ml/kg], A bitter low dose [ABL, 0.22 ml/kg], A bitter average dose [ABA, 0.43 ml/kg] and A bitter high dose [ABH, 0.65 ml/kg] administered for 8 weeks. Biochemicals were assayed using enzyme-linked immunosorbent assays kits. Hematoxylin and eosin stains were used for kidney histology. Statistically significant values (p-value<0.05) were accepted. Results: The results of malondialdehyde, glutathione transferase, superoxide dismutase, catalase, creatinine, urea, and gamma glutamyl transferase significantly increased. The inflammatory cytokines like tumor necrotic factor, C-reactive protein, and interleukin-6 significantly increased, whereas the anti-inflammatory cytokine interleukin-1 significantly decreased in the bitters-treated groups. The histology results showed a progressive decrease in the glomerular count of the bitters treated groups. Conclusion: The findings of this study suggest that the arbitrary use of bitters has a significant negative impact on kidney health, leading to the development of glomerular nephritis and architectural changes in the renal tissue at a dose differential severity.

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• Corrigendum: Brain-specific increase in leukotriene signaling accompanies chronic neuroinflammation and cognitive impairment in a model of Gulf War Illness

  Frontiers in Immunology · 2025-01-31 · 1 citations

  erratumOpen accessSenior authorCorresponding

  Corrigendum on: Attaluri S, Upadhya R, Kodali M, Madhu LN, Upadhya D, Shuai B and Shetty AK (2022) Brain-Specific Increase in Leukotriene Signaling Accompanies Chronic Neuroinflammation and Cognitive Impairment in a Model of Gulf War Illness. Front. Immunol. 13:853000. doi: 10.3389/fimmu.2022.853000 In the published article, there was an error in Figure 5 (B,C,D,E,F,G) as published. In Figure 5 bar charts B, C, D, E, F, G, y-axis labels were inadvertently misspelled as "ng/mg protein", instead of "pg/mg protein.". The corrected Figure 5 and its caption appear below. The authors apologize for this error, and this does not change the scienGfic conclusions of the arGcle in any way. The original arGcle has been updated.

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Recent grants

• Memory and Mood Enhancing Therapies for Gulf War Illness

  NIH · 2011–2015

• NIH Grant R21AT006256

  NIH · $352k · 2014

• NIH Grant R01NS043507

  NIH · $1.3M · 2008

• NIH Grant R01NS054780

  NIH · $1.2M · 2012

• BLR&D Research Career Scientist Award

  NIH · 2016–2018

Frequent coauthors

• Bharathi Hattiangady

  Texas A&M Health Science Center

  464 shared

• Bing Shuai

  Texas A&M University

  265 shared

• Maheedhar Kodali

  248 shared

• Dennis A. Turner

  Duke University

  170 shared

• Dinesh Upadhya

  Manipal Academy of Higher Education

  154 shared

• Sahithi Attaluri

  121 shared

• Raghavendra Upadhya

  Manipal Academy of Higher Education

  103 shared

• Olagide Wagner de Castro

  Universidade Federal de Alagoas

  85 shared

Awards & honors

• Texas A&M University Distinguished Professor Award- 2024
• AAAS Fellow conferred by American Association For The Advanc…
• Research Career Scientist Award conferred by United States D…
• Honoree of Fast Company's World Changing Ideas- 2025