Pranshul Sethi

@iimtu.edu.in

Assistant Professor in department of Pharmacy
IIMT University



                 

https://researchid.co/pranshulsethi

Hi! My name is Pranshul Sethi. I was originally born in Meerut, and now I’m an assistant professor at IIMT University, Meerut. I study the neurobiology of OCD and cellular and molecular pathways and their activators in the prevention of OCD. My interest in OCD developed during my master's From my teenage years, I was very fascinated by brain and its activity. I did my undergrad degree in pharmacy at Dr. KNMIPER, Modinagar and my master's at ISF College of Pharmacy, Moga.
Currently working on to develop the drug discovery screening procedures, establishment and validation of therapeutic moieties in, OCD, Bipolar Disease, Autism, Brain Hemorrhage, and Motor Neuron Diseases (Multiple sclerosis and Amyotrophic lateral sclerosis)
Current focusing Target: Calorie Restriction-Sirt-1, AMPK, Anti-oxidant defense mechanism, Nrf2, HO-1, Neurogenesis, Smoothened (Smo), sonic hedgehog (Shh), JAK-STAT, mTOR, PPAR-γ, IGF-1, GLP-1

EDUCATION

10th
CGPA: 9.2
Modern Senior Secondary School, Patiala (PB)

12th
Medical (Physics, Chemistry, Biology)
per: 82
Bhupindra International Public school, Patiala (PB)

B. Pharm
SGPA: 8.51
DR. KNMIPER, Modinagar (UP)

M. Pharm
Specialization: Pharmacology
SGPA: 8.53
ISF College of Pharmacy, Moga (PB)

RESEARCH INTERESTS

To understand and explore the molecular mechanisms and diagnostic markers involved in neurodegenerative and neuropsychiatric disorders (Alzheimer’s, Autism, Multiple Sclerosis, Amyotrophic lateral sclerosis, Parkinson’s, Huntington’s, Brain Hemorrhage, Obsessive Compulsive Disorder, BD)

9

Scopus Publications

226

Scholar Citations

9

Scholar h-index

9

Scholar i10-index

Scopus Publications


  • Activating SIRT-1 Signalling with the Mitochondrial-CoQ10 Activator Solanesol Improves Neurobehavioral and Neurochemical Defects in Ouabain-Induced Experimental Model of Bipolar Disorder
    Bidisha Rajkhowa, Sidharth Mehan, Pranshul Sethi, Aradhana Prajapati, Manisha Suri, Sumit Kumar, Sonalika Bhalla, Acharan S. Narula, Abdulrahman Alshammari, Metab Alharbi,et al.
    MDPI AG
    Bipolar disorder (BD) is a chronic mental illness characterized by mood fluctuations that range from depressive lows to manic highs. Several studies have linked the downregulation of SIRT-1 (silent mating type information regulation-2 homologs) signaling to the onset of BD and other neurological dysfunctions. This research aimed to look into the neuroprotective potential of Solanesol (SNL) in rats given ICV-Ouabain injections, focusing on its effect on SIRT-1 signaling activation in the brain. Ouabain, found in hypothalamic and medullary neurons, is an endogenous inhibitor of brain Na+/K+ ATPase. The inhibition of brain Na+/K+ ATPase by Ouabain may also result in changes in neurotransmission within the central nervous system. SNL is a Solanaceae family active phytoconstituent produced from the plant Nicotiana tabacum. SNL is used as a precursor for the production of CoQ10 (Coenzyme Q10), a powerful antioxidant and neuroprotective compound. In the current study, lithium (Li), an important mood stabilizer drug, was used as a control. This study looked at the neuroprotective potential of SNL at dosages of 40 and 80 mg/kg in ICV-OUA injections that caused BD-like neurobehavioral and neurochemical defects in Wistar rats. Wistar rats were placed into eight groups (n = 6) and administered 1 mM/0.5 µL ICV-OUA injections for three days. Neurochemical assessments were done in rat brain homogenates, CSF, and blood plasma samples at the end of the experiment protocol schedule. Long-term SNL and lithium administration have been shown to decrease the number of rearing and crossings and reduce time spent in the center, locomotor activities, and immobility time. Solansesol treatment gradually raises the amount of Na+/K+ ATPase, limiting the severity of behavioural symptoms. These findings also revealed that SNL increases the levels of SIRT-1 in CSF, blood plasma, and brain homogenate samples. Moreover, in rat brain homogenates and blood plasma samples, SNL modulates apoptotic markers such as Caspase-3, Bax (pro-apoptotic), and Bcl-2 (anti-apoptotic). Mitochondrial-ETC complex enzymes, including complex-I, II, IV, V, and CoQ10, were also restored following long-term SNL treatment. Furthermore, SNL lowered inflammatory cytokines (TNF-α, IL-1β) levels while restoring neurotransmitter levels (serotonin, dopamine, glutamate, and acetylcholine) and decreasing oxidative stress markers. Histological examinations also validated Solanesol’s protective effect. As a result, our findings suggest that SNL, as a SIRT-1 signalling activator, may be a promising therapeutic approach for BD-like neurological dysfunctions.

  • Nrf2/HO-1 Signaling Stimulation through Acetyl-11-keto-beta-boswellic Acid (AKBA) Provides Neuroprotection in Ethidium Bromide-Induced Experimental Model of Multiple Sclerosis
    Shubham Upadhayay, Sidharth Mehan, Aradhana Prajapati, Pranshul Sethi, Manisha Suri, Ayat Zawawi, Majed N. Almashjary, and Shams Tabrez
    MDPI AG
    Multiple sclerosis (MS) is a severe immune-mediated neurological disease characterized by neuroinflammation, demyelination, and axonal degeneration in the central nervous system (CNS). This is frequently linked to motor abnormalities and cognitive impairments. The pathophysiological hallmarks of MS include inflammatory demyelination, axonal injury, white matter degeneration, and the development of CNS lesions that result in severe neuronal degeneration. Several studies suggested downregulation of nuclear factor erythroid-2-related factor-2 (Nrf2)/Heme oxygenase-1 (HO-1) signaling is a causative factor for MS pathogenesis. Acetyl-11-keto-β-boswellic acid (AKBA) is an active pentacyclictriterpenoid obtained from Boswellia serrata, possessing antioxidant and anti-inflammatory properties. The present study explores the protective potential of AKBA on behavioral, molecular, neurochemical, and gross pathological abnormalitiesandhistopathological alterations by H&E and LFB staining techniques in an experimental model of multiple sclerosis, emphasizing the increase inNrf2/HO-1 levels in the brain. Moreover, we also examine the effect of AKBA on the intensity of myelin basic protein (MBP) in CSF and rat brain homogenate. Specific apoptotic markers (Bcl-2, Bax, andcaspase-3) were also estimated in rat brain homogenate. Neuro behavioralabnormalities in rats were examined using an actophotometer, rotarod test, beam crossing task (BCT),and Morris water maze (MWM). AKBA 50 mg/kg and 100 mg/kg were given orally from day 8 to 35 to alleviate MS symptoms in the EB-injected rats. Furthermore, cellular, molecular, neurotransmitter, neuroinflammatory cytokine, and oxidative stress markers in rat whole brain homogenate, blood plasma, and cerebral spinal fluid were investigated. This study shows that AKBA upregulates the level of antioxidant proteins such as Nrf2 and HO-1 in the rat brain. AKBA restores altered neurochemical levels, potentially preventing gross pathological abnormalities during MS progression.

  • Activation of IGF-1/GLP-1 Signalling via 4-Hydroxyisoleucine Prevents Motor Neuron Impairments in Experimental ALS-Rats Exposed to Methylmercury-Induced Neurotoxicity
    Ambika Shandilya, Sidharth Mehan, Sumit Kumar, Pranshul Sethi, Acharan S. Narula, Abdulrahman Alshammari, Metab Alharbi, and Abdullah F. Alasmari
    MDPI AG
    Amyotrophic lateral sclerosis (ALS) is a severe adult motor neuron disease that causes progressive neuromuscular atrophy, muscle wasting, weakness, and depressive-like symptoms. Our previous research suggests that mercury levels are directly associated with ALS progression. MeHg+-induced ALS is characterised by oligodendrocyte destruction, myelin basic protein (MBP) depletion, and white matter degeneration, leading to demyelination and motor neuron death. The selection of MeHg+ as a potential neurotoxicant is based on our evidence that it has been connected to the development of ALS-like characteristics. It causes glutamate-mediated excitotoxicity, calcium-dependent neurotoxicity, and an ALS-like phenotype. Dysregulation of IGF-1/GLP-1 signalling has been associated with ALS progression. The bioactive amino acid 4-hydroxyisoleucine (HI) from Trigonella foenum graecum acts as an insulin mimic in rodents and increases insulin sensitivity. This study examined the neuroprotective effects of 4-HI on MeHg+-treated adult Wistar rats with ALS-like symptoms, emphasising brain IGF1/GLP-1 activation. Furthermore, we investigated the effect of 4-HI on MBP levels in rat brain homogenate, cerebrospinal fluid (CSF), blood plasma, and cell death indicators such as caspase-3, Bax, and Bcl-2. Rats were assessed for muscular strength, locomotor deficits, depressed behaviour, and spatial learning in the Morris water maze (MWM) to measure neurobehavioral abnormalities. Doses of 4-HI were given orally for 42 days in the MeHg+ rat model at 50 mg/kg or 100 mg/kg to ameliorate ALS-like neurological dysfunctions. Additionally, neurotransmitters and oxidative stress markers were examined in rat brain homogenates. Our findings suggest that 4-HI has neuroprotective benefits in reducing MeHg+-induced behavioural, neurochemical, and histopathological abnormalities in ALS-like rats exposed to methylmercury.

  • Role of JAK-STAT and PPAR-Gamma Signalling Modulators in the Prevention of Autism and Neurological Dysfunctions
    Rishabh Khera, Sidharth Mehan, Sumit Kumar, Pranshul Sethi, Sonalika Bhalla, and Aradhana Prajapati
    Springer Science and Business Media LLC

  • Activation of SIRT-1 Signalling in the Prevention of Bipolar Disorder and Related Neurocomplications: Target Activators and Influences on Neurological Dysfunctions
    Bidisha Rajkhowa, Sidharth Mehan, Pranshul Sethi, and Aradhana Prajapati
    Springer Science and Business Media LLC

  • Smo-Shh Agonist Purmorphamine Prevents Neurobehavioral and Neurochemical Defects in 8-OH-DPAT-Induced Experimental Model of Obsessive-Compulsive Disorder
    Ria Gupta, Sidharth Mehan, Pranshul Sethi, Aradhana Prajapati, Abdulrahman Alshammari, Metab Alharbi, Haneen A. Al-Mazroua, and Acharan S. Narula
    MDPI AG
    Obsessive-compulsive disorder is a mental disorder characterized by repetitive, unwanted thoughts and behavior due to abnormal neuronal corticostriatal-thalamocortical pathway and other neurochemical changes. Purmorphamine is a smoothened-sonic-hedgehog agonist that has a protective effect against many neurological diseases due to its role in maintaining functional connectivity during CNS development and its anti-inflammatory and antioxidant properties. As part of our current research, we investigated the neuroprotective effects of PUR against behavioral and neurochemical changes in 8-hydroxy-2-(di-n-propylamino)-tetralin-induced obsessive-compulsive disorder in rats. Additionally, the effect of PUR was compared with the standard drug for OCD, i.e., fluvoxamine. The intra-dorsal raphe-nucleus injection of 8-OH-DPAT in rats for seven days significantly showed OCD-like repetitive and compulsive behavior along with increased oxidative stress, inflammation, apoptosis, as well as neurotransmitter imbalance. These alterations were dose-dependently attenuated by long-term purmorphamine treatment at 5 mg/kg and 10 mg/kg i.p. In this study, we assessed the level of various neurochemical parameters in different biological samples, including brain homogenate, blood plasma, and CSF, to check the drug’s effect centrally and peripherally. These effects were comparable to the standard oral treatment withfluvoxamine at 10 mg/kg. However, when fluvoxamine was given in combination with purmorphamine, there was a more significant restoration of these alterations than the individualtreatmentswithfluvoxamine and purmorphamine. All the above findings demonstrate that the neuroprotective effect of purmorphamine in OCD can be strong evidence for developing a new therapeutic target for treating and managing OCD.

  • Two-Year, randomized, controlled study of safinamide as add-on to levodopa in mid to late Parkinson's disease
    Rupam Borgohain, Jozsef Szasz, Paolo Stanzione, Chandrashekhar Meshram, Mohit H. Bhatt, Dana Chirilineau, Fabrizio Stocchi, Valentina Lucini, Rodolfo Giuliani, Emma Forrest,et al.
    Wiley
    In a 6‐month double‐blind, placebo‐controlled study of Parkinson's disease patients with motor fluctuations, safinamide 50 and 100 mg/d significantly increased ON‐time without increasing dyskinesia. Further long‐term safinamide use in these patients was evaluated over an additional 18 months. Patients continued on their randomized placebo, 50, or 100 mg/d safinamide. The primary endpoint was change in Dyskinesia Rating Scale total score during ON‐time over 24 months. Other efficacy endpoints included change in ON‐time without troublesome dyskinesia, changes in individual diary categories, depressive symptoms, and quality of life measures. Change in Dyskinesia Rating Scale was not significantly different in safinamide versus placebo groups, despite decreased mean total Dyskinesia Rating Scale with safinamide compared with an almost unchanged score in placebo. Ad hoc subgroup analysis of moderate to severe dyskinetic patients at baseline (36% of patients) showed a decrease with safinamide 100 mg/d compared with placebo (P = 0.0317). Improvements in motor function, activities of daily living, depressive symptoms, clinical status, and quality of life at 6 months remained significant at 24 months. Adverse events and discontinuation rates were similar with safinamide and placebo. This 2‐year, controlled study of add‐on safinamide in mid‐to‐late Parkinson's disease with motor fluctuations, although not demonstrating an overall difference in dyskinesias between patients and controls, showed improvement in dyskinesia in patients at least moderately dyskinetic at baseline. The study additionally demonstrated significant clinical benefits in ON‐time (without troublesome dyskinesia), OFF‐time, activities of daily living, motor symptoms, quality of life, and symptoms of depression. © 2014 International Parkinson and Movement Disorder Society

  • Randomized trial of safinamide add-on to levodopa in Parkinson's disease with motor fluctuations
    Rupam Borgohain, J. Szasz, P. Stanzione, C. Meshram, M. Bhatt, D. Chirilineau, F. Stocchi, V. Lucini, R. Giuliani, E. Forrest,et al.
    Wiley
    Levodopa is effective for the motor symptoms of Parkinson's disease (PD), but is associated with motor fluctuations and dyskinesia. Many patients require add‐on therapy to improve motor fluctuations without exacerbating dyskinesia. The objective of this Phase III, multicenter, double‐blind, placebo‐controlled, parallel‐group study was to evaluate the efficacy and safety of safinamide, an α‐aminoamide with dopaminergic and nondopaminergic mechanisms, as add‐on to l‐dopa in the treatment of patients with PD and motor fluctuations. Patients were randomized to oral safinamide 100 mg/day (n = 224), 50 mg/day (n = 223), or placebo (n = 222) for 24 weeks. The primary endpoint was total on time with no or nontroublesome dyskinesia (assessed using the Hauser patient diaries). Secondary endpoints included off time, Unified Parkinson's Disease Rating Scale (UPDRS) Part III (motor) scores, and Clinical Global Impression‐Change (CGI‐C). At week 24, mean ± SD increases in total on time with no or nontroublesome dyskinesia were 1.36 ± 2.625 hours for safinamide 100 mg/day, 1.37 ± 2.745 hours for safinamide 50 mg/day, and 0.97 ± 2.375 hours for placebo. Least squares means differences in both safinamide groups were significantly higher versus placebo. Improvements in off time, UPDRS Part III, and CGI‐C were significantly greater in both safinamide groups versus placebo. There were no significant between‐group differences for incidences of treatment‐emergent adverse events (TEAEs) or TEAEs leading to discontinuation. The addition of safinamide 50 mg/day or 100 mg/day to l‐dopa in patients with PD and motor fluctuations significantly increased total on time with no or nontroublesome dyskinesia, decreased off time, and improved parkinsonism, indicating that safinamide improves motor symptoms and parkinsonism without worsening dyskinesia. © 2013 International Parkinson and Movement Disorder Society

RECENT SCHOLAR PUBLICATIONS

  • Unravelling the epigenetic based mechanism in discovery of anticancer phytomedicine: Evidence based studies
    B Bashir, P Sethi, S Panda, HK Manikyam, S Vishwas, SK Singh, K Singh, ...
    Cellular Signalling, 111743 2025

  • Exploring the Dual Roles of Neural Stem Cells in Glioblastoma: Therapeutic Implications and Opportunities
    K Singh, P Sethi, JK Gupta, A Dubey, MC Sharma, D Jain, A Bhatt, ...
    Current Stem Cell Research & Therapy 2025

  • Inulin as Stabilizer
    BSR Desu, RM Biradar, MS Vijaykanth, P Sethi, K Krishnan, S Prema, ...
    Inulin for Pharmaceutical Applications: A Versatile Biopolymer, 73-90 2025

  • Inulin: a multifaceted ingredient in pharmaceutical sciences
    R Tiwari, P Sethi, SRS Rudrangi, PK Padarthi, V Kumar, S Rudrangi, ...
    Journal of Biomaterials Science, Polymer Edition 35 (16), 2570-2595 2024

  • The SIRT-1/nrf2/HO-1 Axis: guardians of neuronal health in neurological disorders
    P Sethi, S Mehan, Z Khan, PK Maurya, N Kumar, A Kumar, A Tiwari, ...
    Behavioural brain research, 115280 2024

  • Future Implications of Blockchain for Biomedical and Healthcare
    TK Vashishth, V Sharma, KK Sharma, P Sethi, T Chaudhary, A Bhardwaj
    Blockchain for Biomedical Research and Healthcare: Concept, Trends, and 2024

  • Neuroprotective action of hordenine against the aluminium chloride (AlCl3) induced Alzheimer's diseases & associated memory impairment in experimental rats
    M Agrawal, M Singhal, BC Semwal, S Arora, B Singh, V Sikarwar, P Sethi, ...
    Pharmacological Research-Modern Chinese Medicine 12, 100492 2024

  • Recent Advances in the Synthesis of Antioxidant Derivatives: Pharmacological Insights for Neurological Disorders
    K Singh, JK Gupta, P Sethi, S Mathew, A Bhatt, MC Sharma, S Saha, ...
    Current Topics in Medicinal Chemistry 24 (22), 1940-1959 2024

  • Design, optimization, and evaluation of methotrexate loaded and albumin coated polymeric nanoparticles
    G Tiwari, A Patil, P Sethi, A Agrawal, VA Ansari, MK Posa, VD Aher
    Journal of Biomaterials Science, Polymer Edition 35 (13), 2068-2089 2024

  • Recent review on biological barriers and host–material interfaces in precision drug delivery: advancement in biomaterial engineering for better treatment therapies
    R Deshmukh, P Sethi, B Singh, J Shiekmydeen, S Salave, RJ Patel, N Ali, ...
    Pharmaceutics 16 (8), 1076 2024

  • Emerging pharmacological approaches for Huntington's disease
    K Singh, D Jain, P Sethi, JK Gupta, AK Tripathi, S Kumar, SD Sarker, ...
    European Journal of Pharmacology, 176873 2024

  • Advances in gene therapy approaches targeting neuro-inflammation in neurodegenerative diseases
    K Singh, P Sethi, S Datta, JS Chaudhary, S Kumar, D Jain, JK Gupta, ...
    Ageing research reviews, 102321 2024

  • Mechanistic Insights into Tau Protein-Mediated Regulation of Oxidative Stress
    B Pavani, G Tiwari
    Chinese Journal of Applied Physiology, e20240028 2024

  • Formulation and Characterization of Docetaxel-Loaded Microsponge-Based Hydrogel for Basal Cell Carcinoma
    PDSRM Dr. Mohit Kotnala , Pranshul Sethi , Suraj Mandal , Aditi Chaudhary ...
    Journal of Cardiovascular Disease Research 14 (10) 2023

  • Parkinson's disease in experimental animals is improved by methanolic root extract of citrullus colocynthis
    BD Prasad, RS Chauhan, A Pandey, S Garg, P Kumar, SK Mishra, ...
    European Chemical Bulletin 2023

  • Acetyl-11-keto-beta boswellic acid (AKBA) modulates CSTC-pathway by activating SIRT-1/Nrf2-HO-1 signalling in experimental rat model of obsessive-compulsive disorder: Evidenced
    P Sethi, S Mehan, Z Khan, S Chhabra
    Neurotoxicology 98, 61-85 2023

  • DRUG DISCOVERY AND DESIGN: COMPUTATIONAL APPROACHES AND STRUCTURE-ACTIVITY RELATIONSHIP STUDIES
    NKU Brij Kishore Tiwari, Pranshul Sethi, Khushboo Shrimali, Vishnu Das, Tanu ...
    European Chemical Bulletin 2023

  • Nutrition and psychiatric disorders
    W Mohamed, F Kobeissy
    Springer 2022

  • Nutritional Deficiencies in Obsessive-Compulsive Disorder and Possible Treatment Interventions
    P Sethi, S Kumar, A Prajapati, Z Irfanullah, C Jatchavala, R Vadivel, ...
    Nutrition and Psychiatric Disorders, 171-200 2022

  • High-Fat Diet and Psychiatric Disorders: What Is the Interplay?
    P Sethi, T Chaudhary, T Mishra, A Prajapati, S Kumar
    Nutrition and Psychiatric Disorders, 369-383 2022

MOST CITED SCHOLAR PUBLICATIONS

  • Role of JAK-STAT and PPAR-gamma signalling modulators in the prevention of autism and neurological dysfunctions
    R Khera, S Mehan, S Kumar, P Sethi, S Bhalla, A Prajapati
    Molecular Neurobiology 59 (6), 3888-3912 2022
    Citations: 33

  • Smo-Shh agonist Purmorphamine prevents neurobehavioral and neurochemical defects in 8-OH-DPAT-induced experimental model of obsessive-compulsive disorder
    R Gupta, S Mehan, P Sethi, A Prajapati, A Alshammari, M Alharbi, ...
    Brain Sciences 12 (3), 342 2022
    Citations: 32

  • Nrf2/HO-1 signaling stimulation through acetyl-11-keto-beta-boswellic acid (AKBA) provides neuroprotection in ethidium bromide-induced experimental model of multiple sclerosis
    S Upadhayay, S Mehan, A Prajapati, P Sethi, M Suri, A Zawawi, ...
    Genes 13 (8), 1324 2022
    Citations: 29

  • Activating SIRT-1 signalling with the mitochondrial-CoQ10 activator solanesol improves neurobehavioral and neurochemical defects in ouabain-induced experimental model of
    B Rajkhowa, S Mehan, P Sethi, A Prajapati, M Suri, S Kumar, S Bhalla, ...
    Pharmaceuticals 15 (8), 959 2022
    Citations: 24

  • Activation of IGF-1/GLP-1 signalling via 4-hydroxyisoleucine prevents motor neuron impairments in experimental ALS-rats exposed to methylmercury-induced neurotoxicity
    A Shandilya, S Mehan, S Kumar, P Sethi, AS Narula, A Alshammari, ...
    Molecules 27 (12), 3878 2022
    Citations: 22

  • Advances in gene therapy approaches targeting neuro-inflammation in neurodegenerative diseases
    K Singh, P Sethi, S Datta, JS Chaudhary, S Kumar, D Jain, JK Gupta, ...
    Ageing research reviews, 102321 2024
    Citations: 15

  • Activation of SIRT-1 signalling in the prevention of bipolar disorder and related neurocomplications: target activators and influences on neurological dysfunctions
    B Rajkhowa, S Mehan, P Sethi, A Prajapati
    Neurotoxicity Research 40 (2), 670-686 2022
    Citations: 14

  • Acetyl-11-keto-beta boswellic acid (AKBA) modulates CSTC-pathway by activating SIRT-1/Nrf2-HO-1 signalling in experimental rat model of obsessive-compulsive disorder: Evidenced
    P Sethi, S Mehan, Z Khan, S Chhabra
    Neurotoxicology 98, 61-85 2023
    Citations: 12

  • Recent review on biological barriers and host–material interfaces in precision drug delivery: advancement in biomaterial engineering for better treatment therapies
    R Deshmukh, P Sethi, B Singh, J Shiekmydeen, S Salave, RJ Patel, N Ali, ...
    Pharmaceutics 16 (8), 1076 2024
    Citations: 11

  • Effects of malnutrition on brain development
    P Sethi, A Prajapati, T Mishra, T Chaudhary, S Kumar
    Nutrition and psychiatric disorders, 75-88 2022
    Citations: 8

  • Nutrition, Neurotransmitters, and Behavior
    S Kumar, T Mishra, A Prajapati, P Sethi
    Nutrition and Psychiatric Disorders, 89-108 2022
    Citations: 5

  • Neuroprotective action of hordenine against the aluminium chloride (AlCl3) induced Alzheimer's diseases & associated memory impairment in experimental rats
    M Agrawal, M Singhal, BC Semwal, S Arora, B Singh, V Sikarwar, P Sethi, ...
    Pharmacological Research-Modern Chinese Medicine 12, 100492 2024
    Citations: 4

  • Inulin: a multifaceted ingredient in pharmaceutical sciences
    R Tiwari, P Sethi, SRS Rudrangi, PK Padarthi, V Kumar, S Rudrangi, ...
    Journal of Biomaterials Science, Polymer Edition 35 (16), 2570-2595 2024
    Citations: 3

  • Nutrition and psychiatric disorders
    W Mohamed, F Kobeissy
    Springer 2022
    Citations: 3

  • The SIRT-1/nrf2/HO-1 Axis: guardians of neuronal health in neurological disorders
    P Sethi, S Mehan, Z Khan, PK Maurya, N Kumar, A Kumar, A Tiwari, ...
    Behavioural brain research, 115280 2024
    Citations: 2

  • Design, optimization, and evaluation of methotrexate loaded and albumin coated polymeric nanoparticles
    G Tiwari, A Patil, P Sethi, A Agrawal, VA Ansari, MK Posa, VD Aher
    Journal of Biomaterials Science, Polymer Edition 35 (13), 2068-2089 2024
    Citations: 2

  • Emerging pharmacological approaches for Huntington's disease
    K Singh, D Jain, P Sethi, JK Gupta, AK Tripathi, S Kumar, SD Sarker, ...
    European Journal of Pharmacology, 176873 2024
    Citations: 2

  • Mechanistic Insights into Tau Protein-Mediated Regulation of Oxidative Stress
    B Pavani, G Tiwari
    Chinese Journal of Applied Physiology, e20240028 2024
    Citations: 2

  • A study of effects of high altitude on H reflex
    PK Sethi, B Singh, N Singh, MS Boparai
    Transactions of the American Neurological Association 98, 304-306 1973
    Citations: 2

  • Solanesol Mediated SIRT-1 Activation Prevents Neurobehavioral and Neurochemical Defects in Ouabain-Induced Experimental Model of Bipolar Disorder in Rats
    B Rajkhowa, S Mehan, P Sethi, S Bhalla, A Prajapati, S Kumar, ...
     2021
    Citations: 1

RESEARCH OUTPUTS (PATENTS, SOFTWARE, PUBLICATIONS, PRODUCTS)

Developed an equipment for OCD.
Established a drug (AKBA) for the prevention of OCD.

INDUSTRY EXPERIENCE

Research Associate: 3 months (Research Developer)
Patient Advocate: 3 months (Navya Healthcare)
Medical Scribe: 6 months (Aquity Solutions)