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  1. Article ; Online: An opinion on the debatable function of brain resident immune protein, T-cell receptor beta subunit in the central nervous system

    Komal, Pragya / Manjari, S.K.V. / Nashmi, Raad

    IBRO Neuroscience Reports. 2022 Dec., v. 13 p.235-242

    2022  

    Abstract: In recent years scientific research has established that the nervous and immune systems have shared molecular signaling components. Proteins native to immune cells, which are also found in the brain, have neuronal functions in the nervous system where ... ...

    Abstract In recent years scientific research has established that the nervous and immune systems have shared molecular signaling components. Proteins native to immune cells, which are also found in the brain, have neuronal functions in the nervous system where they affect synaptic plasticity, axonal regeneration, neurogenesis, and neurotransmission. Certain native immune molecules like major histocompatibility complex I (MHC-I), paired immunoglobulin receptor B (PirB), toll-like receptor (TLR), cluster of differentiation-3 zeta (CD3ζ), CD4 co-receptor, and T-cell receptor beta (TCR-β) expression in neurons have been extensively documented. In this review, we provide our opinion and discussed the possible roles of T-cell receptor beta subunits in modulating the function of neurons in the central nervous system. Based on the previous findings of Syken and Shatz., 2003; Nishiyori et al., 2004; Rodriguez et., 1993 and Komal et., 2014; we discuss whether restrictive expression of TCR-β subunits in selected brain regions could be involved in the pathology of neurological disorders and whether their aberrant enhancement in expression may be considered as a suitable biomarker for aging or neurodegenerative diseases like Huntington's disease (HD).
    Keywords T-lymphocytes ; Toll-like receptors ; biomarkers ; brain ; immunoglobulins ; major histocompatibility complex ; neurogenesis ; neurons ; neuroplasticity ; synaptic transmission ; T-cell receptors (TCRs) ; Major histocompatibility complex I (MHC-I) ; Central nervous system (CNS) ; Immune receptors ; Neurodegeneration ; HD ; PD ; AD ; TAP-1 ; NMDA ; CP-AMPA ; α7 nAChRs ; LTP
    Language English
    Dates of publication 2022-12
    Size p. 235-242.
    Publishing place Elsevier Ltd
    Document type Article ; Online
    Note Use and reproduction
    ISSN 2667-2421
    DOI 10.1016/j.ibneur.2022.09.003
    Database NAL-Catalogue (AGRICOLA)

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  2. Article ; Online: Unprecedented effect of vitamin D3 on T-cell receptor beta subunit and alpha7 nicotinic acetylcholine receptor expression in a 3-nitropropionic acid induced mouse model of Huntington's disease.

    Manjari, Skv / Abraham, Sharon Mariam / Poornima, R / Chaturvedi, Rajneesh Kumar / Maity, Shuvadeep / Komal, Pragya

    IBRO neuroscience reports

    2023  Volume 15, Page(s) 116–125

    Abstract: Introduction: 3-NP induction in rodent models has been shown to induce selective neurodegeneration in the striatum followed by the cortex (Brouillet, 2014). However, it remains unclear whether, under such a neurotoxic condition, characterized by ... ...

    Abstract Introduction: 3-NP induction in rodent models has been shown to induce selective neurodegeneration in the striatum followed by the cortex (Brouillet, 2014). However, it remains unclear whether, under such a neurotoxic condition, characterized by neuroinflammation and oxidative stress, the gene expression of the immune resident protein, T-cell receptor beta subunit (TCR-β), α7 nicotinic acetylcholine receptor (α7 nAChRs), the nuclear factor kappa B (NF-κB), inflammatory cytokines (TNF-α and IL-6), and antioxidants (Cat and GpX4) get modulated on Vitamin D3 (VD) supplementation in the central nervous system.
    Methods: In the present study, real-time polymerase chain reaction (RT-PCR) was performed to study the expression of respective genes. Male C57BL/6 mice (8-12 weeks) were divided into four groups namely,
    Results: On administration of 500IU/kg/day of VD, HD mice showed a significant reduction in the gene expression of the immune receptor, TCR-β subunit, nuclear factor kappa B (NF-κB), inflammatory cytokines, and key antioxidants, followed by a decrease in the acetylcholinesterase activity.
    Conclusion: A novel neuroprotective effect of VD in HD is demonstrated by combating the immune receptor, TCR-β gene expression, antioxidant markers, and inflammatory cytokines. In addition, HD mice on VD administration for 0-15 days showed an enhancement in cholinergic signaling with restoration in α7 nAChRs mRNA and protein expression in the striatum and cortex.
    Language English
    Publishing date 2023-07-14
    Publishing country Netherlands
    Document type Journal Article
    ISSN 2667-2421
    ISSN (online) 2667-2421
    DOI 10.1016/j.ibneur.2023.07.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Restorative Action of Vitamin D3 on Motor Dysfunction Through Enhancement of Neurotrophins and Antioxidant Expression in the Striatum.

    Manjari, S K V / Maity, Shuvadeep / Poornima, R / Yau, Suk-Yu / Vaishali, K / Stellwagen, David / Komal, Pragya

    Neuroscience

    2022  Volume 492, Page(s) 67–81

    Abstract: A number of studies has explored a positive correlation between low levels of serum Vitamin ... ...

    Abstract A number of studies has explored a positive correlation between low levels of serum Vitamin D
    MeSH term(s) Animals ; Antioxidants/metabolism ; Cholecalciferol/adverse effects ; Huntington Disease/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Nerve Growth Factors ; Nitro Compounds ; Propionates ; Rats ; Rats, Wistar
    Chemical Substances Antioxidants ; Nerve Growth Factors ; Nitro Compounds ; Propionates ; Cholecalciferol (1C6V77QF41)
    Language English
    Publishing date 2022-04-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 196739-3
    ISSN 1873-7544 ; 0306-4522
    ISSN (online) 1873-7544
    ISSN 0306-4522
    DOI 10.1016/j.neuroscience.2022.03.039
    Database MEDical Literature Analysis and Retrieval System OnLINE

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