scholarly journals TLR-Mediated Signal Transduction and Neurodegenerative Disorders

2021 ◽  
Vol 11 (11) ◽  
pp. 1373
Author(s):  
Shashank Vishwanath Adhikarla ◽  
Niraj Kumar Jha ◽  
Vineet Kumar Goswami ◽  
Ankur Sharma ◽  
Anuradha Bhardwaj ◽  
...  

A special class of proteins called Toll-like receptors (TLRs) are an essential part of the innate immune system, connecting it to the adaptive immune system. There are 10 different Toll-Like Receptors that have been identified in human beings. TLRs are part of the central nervous system (CNS), showing that the CNS is capable of the immune response, breaking the long-held belief of the brain’s “immune privilege” owing to the blood–brain barrier (BBB). These Toll-Like Receptors are present not just on the resident macrophages of the central nervous system but are also expressed by the neurons to allow them for the production of proinflammatory agents such as interferons, cytokines, and chemokines; the activation and recruitment of glial cells; and their participation in neuronal cell death by apoptosis. This study is focused on the potential roles of various TLRs in various neurodegenerative diseases such as Parkinson’s disease (PD) and Alzheimer’s disease (AD), namely TLR2, TLR3, TLR4, TLR7, and TLR9 in AD and PD in human beings and a mouse model.

2020 ◽  
Vol 18 (9) ◽  
pp. 861-867
Author(s):  
Kai Chen ◽  
Liu Nan Yang ◽  
Chuan Lai ◽  
Dan Liu ◽  
Ling-Qiang Zhu

Glutamate receptor, ionotropic, N-methyl-D-aspartate associated protein 1 (GRINA) is a member of the NMDA receptors (NMDARs) and is involved in several neurological diseases, which governs the key processes of neuronal cell death or the release of neurotransmitters. Upregulation of GRINA has been reported in multiple diseases in human beings, such as major depressive disorder (MDD) and schizophrenia (SCZ), with which the underlying mechanisms remain elusive. In this review, we provide a general overview of the expression and physiological function of GRINA in the central nervous system (CNS) diseases, including stroke, depression ,epilepsy, SCZ, and Alzheimer’s disease (AD).


2000 ◽  
Vol 28 (4) ◽  
pp. 452-455 ◽  
Author(s):  
D. E. Brenneman ◽  
C. Y. Spong ◽  
I. Gozes

In studying the mediators of VIP neurotrophism in the central nervous system, two glial proteins have been discovered. Both of these proteins contain short peptides that exhibit femtomolar potency in preventing neuronal cell death from a wide variety of neurotoxic substances. Extension of these peptides to models of oxidative stress or neurodegeneration in vivo have indicated significant efficacy in protection. These peptides, both as individual agents and in combination, have promise as possible protective agents in the treatment of human neurodegenerative disease and in pathologies involving oxidative stress.


Physiology ◽  
2008 ◽  
Vol 23 (5) ◽  
pp. 263-274 ◽  
Author(s):  
Tamer Rabie ◽  
Hugo H. Marti

Many hematopoietic growth factors are produced locally in the brain. Among these, erythropoietin (Epo), has a dominant role for neuroprotection, neurogenesis, and acting as a neurotrophic factor in the central nervous system. These functions make erythropoietin a good candidate for treating diseases associated with neuronal cell death.


2004 ◽  
Vol 13 (3) ◽  
pp. 205-207 ◽  
Author(s):  
Rosaria Alba Merendino ◽  
Giuseppe Di Pasquale ◽  
Filippo De Luca ◽  
Laura Di Pasquale ◽  
Edoardo Ferlazzo ◽  
...  

MODERATE-severe depression (MSD) is linked to overexpression of proinflammatory cytokines and chemokines. Fractalkine (FKN) and macrophage inflammatory protein-1 alpha (MIP-1α) are, respectively, members of CX3C and C-C chemokines, and both are involved in recruiting and activating mononuclear phagocytes in the central nervous system. We analysed the presence of FKN and MIP-1α in sera of untreated MSD patients and healthy donors. High FKN levels were observed in all MSD patients as compared with values only detectable in 26% of healthy donors. MIP-1α was measurable in 20% of patients, while no healthy donors showed detectable chemokine levels. In conclusion, we describe a previously unknown involvement of FKN in the pathogenesis of MSD, suggesting that FKN may represent a target for a specific immune therapy of this disease.


Author(s):  
Marleen H. van Coevorden-Hameete ◽  
Maarten J. Titulaer ◽  
Marco W. J. Schreurs ◽  
Esther de Graaff ◽  
Peter A. E. Sillevis Smitt ◽  
...  

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