Cellular and Molecular Neuroscience, Aging, Immunology, Behavioral Neuroscience
35
Scopus Publications
2840
Scholar Citations
22
Scholar h-index
28
Scholar i10-index
Scopus Publications
Characterization of spinal cord tissue-derived extracellular vesicles in neuroinflammation Larissa Jank, Ajay Kesharwani, Taekyung Ryu, Deepika Joshi, Dimitrios C. Ladakis, Matthew D. Smith, Saumitra Singh, Tanina Arab, Kenneth W. Witwer, Peter A. Calabresi, Chan-Hyun Na, Pavan Bhargava Journal of Neuroinflammation, 2024 Extracellular vesicles (EVs) are released by all cells, can cross the blood–brain barrier, and have been shown to play an important role in cellular communication, substance shuttling, and immune modulation. In recent years EVs have shifted into focus in multiple sclerosis (MS) research as potential plasma biomarkers and therapeutic vehicles. Yet little is known about the disease-associated changes in EVs in the central nervous system (CNS). To address this gap, we characterized the physical and proteomic changes of mouse spinal cord-derived EVs before and at 16 and 25 days after the induction of experimental autoimmune encephalomyelitis (EAE), a neuroinflammatory model of MS. Using various bioinformatic tools, we found changes in inflammatory, glial, and synaptic proteins and pathways, as well as a shift in the predicted contribution of immune and glial cell types over time. These results show that EVs provide snapshots of crucial disease processes such as CNS-compartmentalized inflammation, re/de-myelination, and synaptic pathology, and might also mediate these processes. Additionally, inflammatory plasma EV biomarkers previously identified in people with MS were also altered in EAE spinal cord EVs, suggesting commonalities of EV-related pathological processes during EAE and MS and overlap of EV proteomic changes between CNS and circulating EVs.
Oleuropein confers neuroprotection against rotenone-induced model of Parkinson’s disease via BDNF/CREB/Akt pathway Richa Singh, Walia Zahra, Saumitra Sen Singh, Hareram Birla, Aaina Singh Rathore, Priyanka Kumari Keshri, Hagera Dilnashin, Shekhar Singh, Surya Pratap Singh Scientific Reports, 2023 Major pathological features of Parkinson’s disease (PD) include increase in oxidative stress leading to the aggregation of α-synuclein, mitochondrial dysfunction and apoptosis of dopaminergic neurons. In addition, downregulation of the expression of neurotrophic factors like-Brain Derived Neurotrophic Factor (BDNF) is also involved in PD progression. There has been a lot of interest in trophic factor-based neuroprotective medicines over the past few decades to treat PD symptoms. Rotenone, an insecticide, inhibits the mitochondrial complex I causing overproduction of ROS, oxidative stress, and aggregation of α-synuclein. It has been shown that BDNF and Tropomyosin receptor kinase B (TrkB) interaction initiates the regulation of neuronal cell development and differentiation by the serine/threonine protein kinases like Akt and GSK-3β. Additionally, Transcription factor CREB (cAMP Response Element-binding protein) also determines the gene expression of BDNF. The homeostasis of these signalling cascades is compromised with the progression of PD. Therefore, maintaining the equilibrium of these signalling cascades will delay the onset of PD. Oleuropein (OLE), a polyphenolic compound present in olive leaves has been documented to cross blood brain barrier and shows potent antioxidative property. In the present study, the dose of 8, 16 and 32 mg/kg body weight (bwt) OLE was taken for dose standardisation. The optimised doses of 16 and 32 mg/kg bwt was found to be neuroprotective in Rotenone induced PD mouse model. OLE improves motor impairment and upregulate CREB regulation along with phosphorylation of Akt and GSK-3β in PD mouse. In addition, OLE also reduces the mitochondrial dysfunction by activation of enzyme complexes and downregulates the proapoptotic markers in Rotenone intoxicated mouse model. Overall, our study suggests that OLE may be used as a therapeutic agent for treatment of PD by regulating BDNF/CREB/Akt signalling pathway.
BAFF blockade in experimental autoimmune encephalomyelitis reduces inflammation in the meninges and synaptic and neuronal loss in adjacent brain regions Kanak Gupta, Ajay Kesharwani, Steven Rua, Saumitra Sen Singh, Catherine Siu, Larissa Jank, Matthew D. Smith, Peter A. Calabresi, Pavan Bhargava Journal of Neuroinflammation, 2023 Multiple sclerosis (MS) has traditionally been viewed as a chronic inflammatory disease affecting the white matter of the central nervous system. However, over the past two decades, increasing evidence has highlighted the role of gray matter pathology in MS-related disability. Numerous studies have linked the presence of leptomeningeal inflammation to a more severe disease course, underscoring its potential importance as a driver of gray matter pathology in MS. The major components of leptomeningeal inflammation include T cells, B cells, macrophages, follicular dendritic cells, and plasma cells. Since BAFF [B cell-activating factor of the tumor necrosis factor (TNF) family] promotes B cell survival and maturation and is a co-stimulator of T cells, we used anti-BAFF antibody 10F4 as a BAFF antagonist to study its effect on meningeal inflammation and adjacent brain regions in a relapsing–remitting PLP-EAE (rr-EAE) model of multiple sclerosis in SJL/J mice. rr-EAE mice were treated either with anti-BAFF antibody 10F4 or with IgG control antibody. We performed ultra-high field (11.7 T) MRI to identify areas of meningeal inflammation and track them over time in both treatment groups. We also performed histopathological analysis in brain sections of these mice to study the effects of the BAFF antagonist on leptomeningeal inflammation, and hippocampal and cortical neurons and synapses. We observed that BAFF antagonist treatment reduced B cells, T cells, and myeloid cells in regions of meningeal inflammation. Additionally, we noted that BAFF treatment protected against EAE-induced synaptic and neuronal loss in the adjacent cortex and in the CA1, CA3, and dentate gyrus regions of the hippocampus likely due to its effects on meningeal inflammation.
Neuroprotective Effects of Tinospora cordifolia via Reducing the Oxidative Stress and Mitochondrial Dysfunction against Rotenone-Induced PD Mice Hagera Dilnashin, Hareram Birla, Chetan Keswani, Saumitra Sen Singh, Walia Zahra, Aaina Singh Rathore, Richa Singh, Priyanka Kumari Keshri, Surya Pratap Singh ACS Chemical Neuroscience, 2023 Oxidative stress and mitochondrial dysfunction are leading mechanisms that play a crucial role in the progression of Parkinson's disease (PD). Tinospora cordifolia shows a wide range of biological activities including immunomodulatory, antimicrobial, antioxidant, and anti-inflammatory properties. This study explored the neuroprotective activities of T. cordifolia ethanolic extract (TCE) against Rotenone (ROT)-intoxicated Parkinsonian mice. Four experimental groups of mice were formed: control, ROT (2 mg/kg body wt, subcutaneously), TCE (200 mg/kg body wt, oral) + ROT, and TCE only. Mice were pretreated with TCE for a week and then simultaneously injected with ROT for 35 days. Following ROT-intoxication, motor activities, antioxidative potential, and mitochondrial dysfunction were analyzed. Decrease in the activity of the mitochondrial electron transport chain (mETC) complex, loss of mitochondrial membrane potential (Ψm), increase in Bax/Bcl-2 (B-cell lymphoma 2) ratio, and caspase-3 expression are observed in the ROT-intoxicated mice group. Our results further showed ROT-induced reactive oxygen species (ROS)-mediated alpha-synuclein (α-syn) accumulation and mitochondrial dysfunction. However, pre- and cotreatment with TCE along with ROT-intoxication significantly reduced α-syn aggregation and improved mitochondrial functioning in cells by altering mitochondrial potential and increasing mETC activity. TCE also decreases the Bax/Bcl-2 ratio and also the expression of caspase-3, thus reducing apoptosis of the cell. Altogether, TCE is effective in protecting neurons from rotenone-induced cytotoxicity in the Parkinsonian mouse model by modulating oxidative stress, ultimately reducing mitochondrial dysfunction and cell death.
Anti-Parkinsonian effect of Mucuna pruriens and Ursolic acid on GSK3β/Calcium signaling in neuroprotection against Rotenone-induced Parkinsonism Walia Zahra, Hareram Birla, Saumitra Sen Singh, Aaina Singh Rathore, Hagera Dilnashin, Richa Singh, Priyanka Kumari Keshri, Shekhar Singh, Surya Pratap Singh Phytomedicine Plus, 2022 Exposure of environmental toxin is linked to the onset of Parkinson's disease (PD), especially in majority of sporadic cases. One of such toxins, namely Rotenone has been widely investigated to produce the Parkinsonian model in laboratories. The toxin causes the death of the dopaminergic neurons, aggregation of α-Synuclein, oxidative stress, neuroinflammation and initiate other pathways leading to PD pathogenesis. Glycogen synthase kinase-3 (GSK-3) is a pleiotropic serine/threonine protein kinase found in eukaryotes. One of the two isoforms of the enzyme; GSK-3β plays an important role in regulating the pathogenesis of neurodegenerative diseases, including PD. Whereas, Calcium (Ca2+) is found to regulate important cellular activities in all eukaryotic cells. However, an increased Ca2+ concentration is seen during ageing and the progression of neurodegenerative diseases. Thus, maintaining the Ca2+ homoeostasis is very crucial for proper cell function. Hence, behavioural tests were performed to assess the motor abnormalities; immunohistochemical and western blot analyses to identify the alteration in the protein expression; and mitochondrial complexes and antioxidants assay to detect the extent of mitochondrial dysfunction in Rotenone-induced Parkinsonian mouse model. Alternatively, the effect of Mucuna pruriens (Mp) and Ursolic acid (UA) in the PD mouse model was also observed. Increased Ca2+level, and activation of GSK-3β was observed in the Rotenone-intoxicated mouse model of PD. The extract of Mp and UA, on the other hand shows neuroprotection through their anti-oxidative and anti-inflammatory properties. However, their role in maintaining the Ca2+ level and GSK-3β signaling is not yet observed in PD. So, our study deals with the downregulated activity of GSK-3β and Ca2+ level upon the administration of Mp extract and UA, thereby providing neuroprotection to the PD mouse model. Thus, this study deals to explore further the neuroprotective activity of Mp and UA through GSK-3β/Calcium signaling by ameliorating mitochondrial dysfunction mediated apoptosis and inhibiting the overexpression of α-Synuclein in Rotenone-induced PD mouse model.
Medicinal Plants and Natural Compounds as Antiparkinsonian Agents Walia Zahra, Hareram Birla, Saumitra Sen Singh, Aaina Singh Rathore, Hagera Dilnashin, Richa Singh, Priyanka Kumari Keshri, Surya Pratap Singh Neurodegenerative Diseases Multifactorial Degenerative Processes Biomarkers and Therapeutic Approaches First Edition, 2022 Medicinal plants have been used since ages for the treatment of human diseases in the Indian medicinal system of Ayurveda. Parkinson's diseases (PD) on the other hand is a kind of neurodegenerative disorder that shows debilitating symptoms; and the treatment of the disease rely on the symptomatic management. The drugs available for the treatment of the disease show severe side effects on prolonged usage. Thus, many medicinal plants and their derivative natural compounds have been tested for their anti-Parkinsonian activity with minimal side effects. Mucuna pruriens, Withania somnifera, Tinospora cordifolia are the example of medicinal plants that have shown anti-Parkinsonian activity while the natural compounds found in medicinal plants like Baicalein, curcumin, Ginseng, Resveratol have also maintained the nerve cell function and prevented the neuronal death. Thus, the polyphenols and other bioactive constituent of medicinal plants should be further studied for their therapeutic intervention against PD.
Curcumin Modulates p62-Keap1-Nrf2-Mediated Autophagy in Rotenone-Induced Parkinson’s Disease Mouse Models Aaina Singh Rathore, Saumitra Sen Singh, Hareram Birla, Walia Zahra, Priyanka Kumari Keshri, Hagera Dilnashin, Richa Singh, Shekhar Singh, Surya Pratap Singh ACS Chemical Neuroscience, 2022 Autophagy mediates self-digestion of abnormally aggregated proteins and organelles present in the cytoplasm. This mechanism may prove to be neuroprotective against Parkinson's disease (PD) by clearing misfolded α-synuclein (α-syn) aggregates from dopaminergic neurons. p62, an adaptor protein acts as a selective substrate for autophagy and regulates the formation as well as the degradation of protein aggregates. p62 sequesters keap1 freeing Nrf2 and consequently activating the transcription of its target genes. In the present study, we aimed to investigate the anti-parkinsonian activity of curcumin targeting primarily activation of autophagy via the Nrf2-Keap1 pathway. The mice were subcutaneously injected with rotenone (2.5 mg/kg bodyweight) and co-treated with oral administration of curcumin (80 mg/kg bodyweight) for 35 days. Following completion of dosing, motor activities, anti-oxidative potential, mitochondrial dysfunction, and various protein expressions, including Nrf2, Keap1, p62, LC3, Bcl2, Bax, and caspase 3, were assessed. The results revealed that curcumin restored the motor coordination and anti-oxidative activity while improving the mitochondrial functioning in PD mice. Autophagy was evaluated by the change in the expression of autophagic markers, p62 and LC3-II. Reduced p62 and LC3-II expressions in the rotenone mouse model of PD confirmed the compromised autophagy pathway, consequently increasing the aggregation of misfolded protein α-syn. Whereas, curcumin treatment-enhanced autophagy-mediated clearance of misfolded α-syn proteins by increasing the LC3-II expression and blocked apoptotic cascade. Curcumin administration upregulated the Nrf2 expression and normalized the Nrf2-Keap1 pathway, which justifies the improved anti-oxidative activity. Therefore, the findings reveal that curcumin is a Nrf2-inducer and is endowed with neuroprotective potential, which may prove to be a potential candidate for the anti-Parkinson's disease treatment therapy.
Unraveling the Neuroprotective Effect of Tinospora cordifolia in a Parkinsonian Mouse Model through the Proteomics Approach Hareram Birla, Chetan Keswani, Saumitra Sen Singh, Walia Zahra, Hagera Dilnashin, Aaina Singh Rathore, Richa Singh, Monika Rajput, Priyanka Keshri, Surya Pratap Singh ACS Chemical Neuroscience, 2021 Stress-induced dopaminergic (DAergic) neuronal death in the midbrain region is the primary cause of Parkinson's disease (PD). Following the discovery of l-dopa, multiple drugs have been developed to improve the lifestyle of PD patients; however, none have been suitable for clinical use due to their multiple side effects. Tinospora cordifolia has been used in traditional medicines to treat neurodegenerative diseases. Previously, we reported the neuroprotective role of Tc via inhibition of NF-κB-associated proinflammatory cytokines against MPTP-intoxicated Parkinsonian mice. In the present study, we investigated the neuroprotective molecular mechanism of Tc in a rotenone (ROT)-intoxicated mouse model, using a proteomics approach. Mice were pretreated with Tc extract by oral administration, followed by ROT intoxication. Behavioral tests were performed to check motor functions of mice. Protein was isolated, and label-free quantification (LFQ) was carried out to identify differentially expressed protein (DEP) in control vs PD and PD vs treatment groups. Results were validated by qRT-PCR with the expression of target genes correlating with the proteomics data. In this study, we report 800 DEPs in control vs PD and 133 in PD vs treatment groups. In silico tools demonstrate significant enrichment of biochemical and molecular pathways with DEPs, which are known to be important for PD progression including mitochondrial gene expression, PD pathways, TGF-β signaling, and Alzheimer's disease. This study provides novel insights into the PD progression as well as new therapeutic targets. More importantly, it demonstrates that Tc can exert therapeutic effects by regulating multiple pathways, resulting in neuroprotection.
Unraveling the Variable Penetrance of Inflammatory Gene Signatures into Adjacent Brain Parenchyma in Meningeal Inflammation SS Singh S, Gadani S, Kim S, Smith M, Calabresi P, Bhargava P Journal of Neurochemistry 169 (https://doi.org/10.1111/jnc.70097) , 2025 2025
Restoring the Multiple Sclerosis Associated Imbalance of Gut Indole Metabolites Promotes Remyelination and Suppresses Neuroinflammation L Jank, SS Singh, J Lee, A Dhukhwa, F Siavoshi, D Joshi, V Minney, ... bioRxiv, 2024.10. 27.620437 , 2025 2025 Citations: 6
Spatial transcriptomics of meningeal inflammation reveals inflammatory gene signatures in adjacent brain parenchyma SP Gadani, S Singh, S Kim, J Hu, MD Smith, PA Calabresi, P Bhargava Elife 12, RP88414 , 2024 2024 Citations: 4
Characterization of spinal cord tissue-derived extracellular vesicles in neuroinflammation L Jank, A Kesharwani, T Ryu, D Joshi, DC Ladakis, MD Smith, S Singh, ... Journal of Neuroinflammation 21 , 2024 2024 Citations: 8
BAFF blockade in experimental autoimmune encephalomyelitis reduces inflammation in the meninges and synaptic and neuronal loss in adjacent brain regions K Gupta, A Kesharwani, S Rua, SS Singh, C Siu, L Jank, MD Smith, ... Journal of Neuroinflammation 20 (1), 229 , 2023 2023 Citations: 11
Neuroprotective Effects of Tinospora cordifolia via Reducing the Oxidative Stress and Mitochondrial Dysfunction against Rotenone-Induced PD Mice H Dilnashin, H Birla, C Keswani, SS Singh, W Zahra, AS Rathore, R Singh, ... ACS Chemical Neuroscience 14 (17), 3077-3087 , 2023 2023 Citations: 15
Curcumin Modulates p62–Keap1–Nrf2-Mediated Autophagy in Rotenone-Induced Parkinson’s Disease Mouse Models AS Rathore, SS Singh, H Birla, W Zahra, PK Keshri, H Dilnashin, R Singh, ... ACS Chemical Neuroscience 14 (8), 1412-1423 , 2023 2023 Citations: 49
Oleuropein confers neuroprotection against rotenone-induced model of Parkinson’s disease via BDNF/CREB/Akt pathway R Singh, W Zahra, SS Singh, H Birla, AS Rathore, PK Keshri, H Dilnashin, ... Scientific Reports 13 (1), 2452 , 2023 2023 Citations: 46
Anti-Parkinsonian effect of Mucuna pruriens and Ursolic acid on GSK3β/Calcium signaling in neuroprotection against Rotenone-induced Parkinsonism W Zahra, H Birla, SS Singh, AS Rathore, H Dilnashin, R Singh, PK Keshri, ... Phytomedicine Plus 2 (4), 100343 , 2022 2022 Citations: 18
Medicinal Plants and Natural Compounds as Antiparkinsonian Agents W Zahra, H Birla, SS Singh, AS Rathore, H Dilnashin, R Singh, PK Keshri, ... Neurodegenerative Diseases: Multifactorial Degenerative Processes … , 2022 2022 Citations: 1
Neuroprotection by Mucuna pruriens in Neurodegenerative Diseases W Zahra, H Birla, SS Singh, AS Rathore, H Dilnashin, R Singh, PK Keshri, ... Neurochemical Research 47 (7), 1816-1829 , 2022 2022 Citations: 38
Unraveling the Neuroprotective Effect of Tinospora cordifolia in a Parkinsonian Mouse Model through the Proteomics Approach H Birla, C Keswani, SS Singh, W Zahra, H Dilnashin, AS Rathore, R Singh, ... ACS Chemical Neuroscience 12 (22), 4319-4335 , 2021 2021 Citations: 29
Lipid-Coated MCM-41 Mesoporous Silica Nanoparticles Loaded with Berberine Improved Inhibition of Acetylcholine Esterase and Amyloid Formation AK Singh, SS Singh, AS Rathore, SP Singh, G Mishra, R Awasthi, ... ACS Biomaterials Science & Engineering 7 (8), 3737-3753 , 2021 2021 Citations: 104
Evaluation of Triclosan-induced reproductive impairments in the accessory reproductive organs and sperm indices in the mice S Raj, SS Singh, SP Singh, P Singh Acta Histochemica 123 (5), 151744 , 2021 2021 Citations: 21
Epigenetic modulation in Parkinson’s disease and potential treatment therapies AS Rathore, H Birla, SS Singh, W Zahra, H Dilnashin, R Singh, PK Keshri, ... Neurochemical Research 46 (7), 1618-1626 , 2021 2021 Citations: 58
Neuroprotection of rotenone-induced Parkinsonism by ursolic acid in PD mouse model W Zahra, SN Rai, H Birla, SS Singh, AS Rathore, H Dilnashin, R Singh, ... CNS & Neurological Disorders-Drug Targets (Formerly Current Drug Targets-CNS … , 2020 2020 Citations: 91
Correction to “Novel Molecular Hybrids of N -Benzylpiperidine and 1,3,4-Oxadiazole as Multitargeted Therapeutics to Treat Alzheimer’s Disease” P Sharma, A Tripathi, PN Tripathi, SS Singh, SP Singh, SK Shrivastava ACS Chemical Neuroscience 11 (17), 2782-2782 , 2020 2020 Citations: 3
NF-κB-mediated neuroinflammation in Parkinson’s disease and potential therapeutic effect of polyphenols SS Singh, SN Rai, H Birla, W Zahra, AS Rathore, SP Singh Neurotoxicity Research 37, 491-507 , 2020 2020 Citations: 232
Immunohistochemistry as an Important Technique in Experimental and Clinical Practices H Birla, SN Rai, SS Singh, W Zahra, N Tiwari, AA Naik, A Misra, S Bharati, ... Protocols used in Molecular Biology, 44-59 , 2020 2020
A Modified Western Blot Protocol for Enhanced Sensitivity in the Detection of a Tissue Protein SN Rai, MR Gedda, W Zahra, H Birla, SS Singh, P Singh, N Tiwari, ... Protocols used in Molecular Biology, 35-43 , 2020 2020 Citations: 1
MOST CITED SCHOLAR PUBLICATIONS
The role of PI3K/Akt and ERK in neurodegenerative disorders SN Rai, H Dilnashin, H Birla, SS Singh, W Zahra, AS Rathore, BK Singh, ... Neurotoxicity research 35, 775-795 , 2019 2019 Citations: 520
NF-κB-mediated neuroinflammation in Parkinson’s disease and potential therapeutic effect of polyphenols SS Singh, SN Rai, H Birla, W Zahra, AS Rathore, SP Singh Neurotoxicity Research 37, 491-507 , 2020 2020 Citations: 232
Anti-inflammatory activity of ursolic acid in MPTP-induced parkinsonian mouse model SN Rai, W Zahra, SS Singh, H Birla, C Keswani, H Dilnashin, AS Rathore, ... Neurotoxicity research 36, 452-462 , 2019 2019 Citations: 193
Mucuna pruriens protects against MPTP intoxicated neuroinflammation in Parkinson’s disease through NF-κB/pAKT signaling pathways SN Rai, H Birla, SS Singh, W Zahra, RR Patil, JP Jadhav, MR Gedda, ... Frontiers in Aging Neuroscience 9, 421 , 2017 2017 Citations: 186
Neuroprotective effect of chlorogenic acid on mitochondrial dysfunction‐mediated apoptotic death of DA neurons in a parkinsonian mouse model SS Singh, SN Rai, H Birla, W Zahra, AS Rathore, H Dilnashin, R Singh, ... Oxidative medicine and cellular longevity 2020 (1), 6571484 , 2020 2020 Citations: 174
Tinospora cordifolia Suppresses Neuroinflammation in Parkinsonian Mouse Model H Birla, SN Rai, SS Singh, W Zahra, A Rawat, N Tiwari, RK Singh, ... Neuromolecular medicine 21, 42-53 , 2019 2019 Citations: 136
Effect of chlorogenic acid supplementation in MPTP-intoxicated mouse SS Singh, SN Rai, H Birla, W Zahra, G Kumar, MR Gedda, N Tiwari, ... Frontiers in pharmacology 9, 757 , 2018 2018 Citations: 136
Neuroprotective effects of Withania somnifera in BPA induced-cognitive dysfunction and oxidative stress in mice H Birla, C Keswani, SN Rai, SS Singh, W Zahra, H Dilnashin, AS Rathore, ... Behavioral and Brain Functions 15, 1-9 , 2019 2019 Citations: 132
The global economic impact of neurodegenerative diseases: Opportunities and challenges W Zahra, SN Rai, H Birla, SS Singh, H Dilnashin, AS Rathore, SP Singh Bioeconomy for sustainable development, 333-345 , 2020 2020 Citations: 122
Economic Importance of Medicinal Plants in Asian Countries W Zahra, SN Rai, H Birla, SS Singh, AS Rathore, H Dilnashin, C Keswani, ... Bioeconomy for Sustainable Development, 359-377 , 2020 2020 Citations: 119
Lipid-Coated MCM-41 Mesoporous Silica Nanoparticles Loaded with Berberine Improved Inhibition of Acetylcholine Esterase and Amyloid Formation AK Singh, SS Singh, AS Rathore, SP Singh, G Mishra, R Awasthi, ... ACS Biomaterials Science & Engineering 7 (8), 3737-3753 , 2021 2021 Citations: 104
Immunomodulation of Parkinson’s disease using Mucuna pruriens (Mp) SN Rai, H Birla, W Zahra, SS Singh, SP Singh Journal of Chemical Neuroanatomy 85, 27-35 , 2017 2017 Citations: 103
Neuroprotection of rotenone-induced Parkinsonism by ursolic acid in PD mouse model W Zahra, SN Rai, H Birla, SS Singh, AS Rathore, H Dilnashin, R Singh, ... CNS & Neurological Disorders-Drug Targets (Formerly Current Drug Targets-CNS … , 2020 2020 Citations: 91
Neuroprotective effect of chlorogenic acid in global cerebral ischemia-reperfusion rat model G Kumar, S Mukherjee, P Paliwal, SS Singh, H Birla, SP Singh, ... Naunyn-Schmiedeberg's Archives of Pharmacology 392, 1293-1309 , 2019 2019 Citations: 81
Novel Molecular Hybrids of N -Benzylpiperidine and 1,3,4-Oxadiazole as Multitargeted Therapeutics to Treat Alzheimer’s Disease P Sharma, A Tripathi, PN Tripathi, SS Singh, SP Singh, SK Shrivastava ACS chemical neuroscience 10 (10), 4361-4384 , 2019 2019 Citations: 68
Epigenetic modulation in Parkinson’s disease and potential treatment therapies AS Rathore, H Birla, SS Singh, W Zahra, H Dilnashin, R Singh, PK Keshri, ... Neurochemical Research 46 (7), 1618-1626 , 2021 2021 Citations: 58
Curcumin Modulates p62–Keap1–Nrf2-Mediated Autophagy in Rotenone-Induced Parkinson’s Disease Mouse Models AS Rathore, SS Singh, H Birla, W Zahra, PK Keshri, H Dilnashin, R Singh, ... ACS Chemical Neuroscience 14 (8), 1412-1423 , 2023 2023 Citations: 49
Quality control in Huntington’s disease: A therapeutic target SN Rai, BK Singh, AS Rathore, W Zahra, C Keswani, H Birla, SS Singh, ... Neurotoxicity Research 36, 612-626 , 2019 2019 Citations: 48
Oleuropein confers neuroprotection against rotenone-induced model of Parkinson’s disease via BDNF/CREB/Akt pathway R Singh, W Zahra, SS Singh, H Birla, AS Rathore, PK Keshri, H Dilnashin, ... Scientific Reports 13 (1), 2452 , 2023 2023 Citations: 46
Neuroprotection by Mucuna pruriens in Neurodegenerative Diseases W Zahra, H Birla, SS Singh, AS Rathore, H Dilnashin, R Singh, PK Keshri, ... Neurochemical Research 47 (7), 1816-1829 , 2022 2022 Citations: 38