School Of Health Sciences
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Item Involvement of the G-Protein-Coupled Estrogen Receptor-1 (GPER) Signaling Pathway in Neurodegenerative Disorders: A Review(Springer, 2022-10-28T00:00:00) Upadhayay, Shubham; Gupta, Rishav; Singh, Surbhi; Mundkar, Maroti; Singh, Gursewak; Kumar, PuneetThe G-protein-coupled estrogen receptor-1 (GPER) is an extranuclear estrogen receptor that regulates the expression of several downstream signaling pathways with a variety of biological actions including cell migration, proliferation, and apoptosis in different parts of the brain area. It is endogenously activated by estrogen, a steroidal hormone that binds to GPER receptors which help in maintaining cellular homeostasis and neuronal integrity as well as influences neurogenesis. In contrast, neurodegenerative disorders are a big problem for society, and still many people suffer from motor and cognitive impairments. Research to date reported that GPER has the potential to whittle down motor abnormalities and cognitive dysfunction by limiting the progression of neurodegenerative disorders. Although several findings suggest that GPER activation accelerated transcription of the PI3K/Akt/Gsk-3? and ERK1/2 signaling pathway that halt disease progression by decreasing oxidative stress, neuroinflammation, and apoptosis. Accordingly, the goal of this review is to highlight the basic mechanism of GPER signaling pathway-mediated neuroprotection in various neurodegenerative disorders including Parkinson�s disease (PD), Huntington�s disease (HD), Tardive dyskinesia (TD), and Epilepsy. This review also discusses the role of the GPER activators which might be a promising therapeutic target option to treat neurodegenerative disorders. All the data were obtained from published articles in PubMed (353), Web of Science (788), and Scopus (770) databases using the search terms: GPER, PD, HD, TD, epilepsy, and neurodegenerative disorders. � 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.Item Neuroprotective role of apocynin against pentylenetetrazole kindling epilepsy and associated comorbidities in mice by suppression of ROS/RNS(Elsevier B.V., 2021-11-30T00:00:00) Jaiswal, Gagandeep; Kumar, PuneetEpilepsy is a neurological disease that transpires due to the unusual synchronized neuronal discharge within the central nervous system, which drives repetitious unprovoked seizures. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is a complex enzyme accountable for reactive oxygen species (ROS) production, neurodegeneration, neurotoxicity, memory impairment, vitiates normal cellular processes, long term potentiation, and thus, implicated in the pathogenesis of epilepsy. Therefore, the present study was sketched to examine the neuroprotective effect of apocynin, NADPH oxidase inhibitor in pentylenetetrazole kindling epilepsy, and induced comorbidities in mice. Mice (either sex) were given pentylenetetrazole (35 mg/kg, i.p.) every other day up to 29 days, and a challenge test was executed on the 33rd day. Pretreatment with apocynin (25, 50, and 100 mg/kg, i.p.) was carried out from 1st to 33rd day. Rotarod and open field test were performed on the 1st, 10th, 20th, and 30th days of the study. Animals were tutored on the morris water maze from 30th to 33rd day, and the retention was registered on the 34th day. Tail suspension test and elevated plus maze were sequentially performed on the 32nd and 33rd day of the study. On the 34th day, animals were sacrificed, and their brains were isolated to conduct biochemical estimation. NADPH oxidase activation due to chronic pentylenetetrazole treatment resulted in generalized tonic-clonic seizures, enhanced oxidative stress, remodeled neurotransmitters' level, and resulted in comorbidities (anxiety, depression, and memory impairment). Pretreatment with apocynin significantly restricted the pentylenetetrazole induced seizure severity, ROS production, neurotransmitter alteration, and comorbid conditions by inhibiting the NADPH oxidase enzyme. � 2021Item Celiac disease poses significant risk in developing depression, anxiety, headache, epilepsy, panic disorder, dysthymia: A�meta-analysis(Springer, 2021-11-28T00:00:00) Sharma, Nidhi; Singh, Kavita; Senapati, SabyasachiCeliac disease (CD) primarily affects the small intestine. Previous studies have identified higher incidences of neuropsychiatric diseases among CD patients compared to non-CD controls. Genome-wide association studies have identified >60 non-human leukocyte antigen (HLA) genes associated with CD, where estimated 15% genes have role in neurological health. We carried out a systematic review and meta-analysis to estimate the potential risk conferred by CD in developing neuropsychiatric diseases. Literature search was performed till June 2019. Incidences of neuropsychiatric diseases were compared among CD and non-CD controls. Funnel plots and Egger�s tests were used to evaluate publication bias and estimate study effects. Qualities of the included studies were estimated using Newcastle-Ottawa Scale. Quality of evidence was graded using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach. Odds of developing neuropsychiatric diseases among CD were evaluated by computing meta-odds ratio (Manten-Haenszel method) and Z test p-value using random and fixed effect�models based on the degree of study heterogeneity. Thirteen non-randomized case-control studies were found eligible. Subjects suffering from CD were found to have significantly more risk to develop depression (p<1.00E-05; OR=1.60 [1.37�1.86]), anxiety (p=0.05; OR=1.41 [1.00�1.97]), headache (p<0.1.00E-05; OR=3.27 [2.46�4.34]), epilepsy (p<1.00E-04; OR=11.90 [3.78�37.43]), panic disorder (p<1.00E-04; OR=4.64 [2.22�9.70]), and dysthymia (p=2.00E-03; OR=5.27 [1.83�15.22]). CD is a major predisposing factor in developing array of common neuropsychiatric diseases. Shared biological processes and molecular networks could play a crucial role in disease co-occurrence. Detailed molecular evidences are needed to establish the cause-effect relationship between these diseases. � 2021, Indian Society of Gastroenterology.Item Epilepsy and Migraine Shared Genetic and Molecular Mechanisms: Focus on Therapeutic Strategies(Springer, 2021-04-15T00:00:00) Gotra, Palvi; Bhardwaj, Nidhi; Ludhiadch, Abhilash; Singh, Gagandeep; Munshi, AnjanaEpilepsy and migraine are both episodic disorders and share clinical as well as pathophysiological mechanisms. The prevalence of epilepsy in migraine patients is generally higher than normal as compared to general population and vice versa. Various environmental risk factors and genetic factors have been reported to be associated with susceptibility of these comorbid diseases. Specific genes have been implicated in the pathogenesis of the two diseases. However, the shared genetic susceptibility has not been explored extensively. Previous studies have reported that the alterations in the genes encoding ion channel proteins are common risk factors for both the diseases. The alterations in ion channel-encoding genes CACNAIA (T666M) and SCNIA (Q1489K and L1649Q) have been found to be involved in the development of familial hemiplegic migraine (FHM) as well as generalized epilepsy and some cases of focal epilepsy as well. The fact that both these disorders are treated with anti-epileptic drugs (AEDs) strongly supports common underlying mechanisms. This review has been compiled with an aim to explore the alterations in common genes involved in various pathways regulating neuronal hyperexcitability, a common risk factor for both these conditions. The avenue for future treatment strategies targeting common genes and molecular mechanisms has also been discussed. � 2021, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.