The Role of Neuroinflammation in Cellular Damage in Neurodegenerative Diseases

Muthuraju, Sangu; Zakaria, Rahimah; Karuppan, Mohan Kumar Muthu; Al-Rahbi, Badriya

doi:10.1155/2020/9231452

Cited by 12 publications

(11 citation statements)

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“…Neuroinflammation damages the brain and causes glial activation, proinflammatory production, and abnormal neural signaling [ 37 , 38 ]. MHY2699 was administered to the mice, which were treated with MPTP to induce PD pathologies to evaluate the neuroprotective effects of MHY2699, which has both antioxidative and anti-inflammatory effects.…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effects of the Novel Barbiturate Derivative MHY2699 in an MPTP-Induced Mouse Model of Parkinson’s Disease

et al. 2021

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Parkinson’s disease (PD) is one of the most common neurodegenerative disorders, and is caused by the death of dopamine neurons and neuroinflammation in the striatum and substantia nigra. Furthermore, the inflammatory response in PD is closely related to glial cell activation. This study examined the neuroprotective effects of the barbiturate derivative, MHY2699 [5-(4-hydroxy 3,5-dimethoxybenzyl)-2 thioxodihydropyrimidine-4,6(1H,5H)-dione] in a mouse model of PD. MHY2699 ameliorated MPP⁺-induced astrocyte activation and ROS production in primary astrocytes and inhibited the MPP⁺-induced phosphorylation of MAPK and NF-κB. The anti-inflammatory effects of MHY2699 in protecting neurons were examined in an MPTP-induced mouse model of PD. MHY2699 inhibited MPTP-induced motor dysfunction and prevented dopaminergic neuronal death, suggesting that it attenuated neuroinflammation. Overall, MHY2699 has potential as a neuroprotective treatment for PD.

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Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effects of the Novel Barbiturate Derivative MHY2699 in an MPTP-Induced Mouse Model of Parkinson’s Disease

et al. 2021

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“…RGMa can induce neuropathological and behavioral changes similar to Parkinson's disease [ 11 ]. If RGMa in substantia nigra dopaminergic (DA) neurons of Parkinson's disease mouse is significantly increased, it can lead to progressive dyskinesia, including motor coordination and imbalance, which is a typical manifestation of DA reduction in striatum [ 11 , 54 – 56 ]. The mechanism may be the selective degeneration of DA neurons and the activation of microglia and astrocytes in substantia nigra induced by elevated RGMa ( Table 1 ) [ 11 , 57 ].…”

Section: Rgma As a Therapeutic Target In Cns Disordersmentioning

confidence: 99%

Repulsive Guidance Molecule-a and Central Nervous System Diseases

Tang

Zeng

et al. 2021

BioMed Research International

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Repulsive guidance molecule-a (RGMa) is a member of glycosylphosphatidylinositol- (GPI-) anchored protein family, which has axon guidance function and is widely involved in the development and pathological processes of the central nervous system (CNS). On the one hand, the binding of RGMa and its receptor Neogenin can regulate axonal guidance, differentiation of neural stem cells into neurons, and the survival of these cells; on the other hand, RGMa can inhibit functional recovery of CNS by inhibiting axonal growth. A number of studies have shown that RGMa may be involved in the pathogenesis of CNS diseases, such as multiple sclerosis, neuromyelitis optica spectrum diseases, cerebral infarction, spinal cord injury, Parkinson’s disease, and epilepsy. Targeting RGMa can enhance the functional recovery of CNS, so it may become a promising target for the treatment of CNS diseases. This article will comprehensively review the research progression of RGMa in various CNS diseases up to date.

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“…Nonetheless, when neuroinflammation is prolonged, it overcomes the limits of physiological control and induces harmful effects, including pro-inflammatory signalling pathways, increased oxidative stress, and the death of neurons linked to chronic pathogenesis of neuropathic pain [24,25]. For these reasons, neuroinflammation in both the CNS and PNS plays a central role in the pathogenesis of neuropathic pain [26], as well as chronic neurodegenerative diseases [27][28][29], psychiatric illness [30], and even autism spectrum disorder [31].…”

Section: Neuroinflammationmentioning

confidence: 99%

ALIAmides Update: Palmitoylethanolamide and Its Formulations on Management of Peripheral Neuropathic Pain

D’Amico

Impellizzeri

Cuzzocrea

et al. 2020

IJMS

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Neuropathic pain results from lesions or diseases of the somatosensory nervous system and it remains largely difficult to treat. Peripheral neuropathic pain originates from injury to the peripheral nervous system (PNS) and manifests as a series of symptoms and complications, including allodynia and hyperalgesia. The aim of this review is to discuss a novel approach on neuropathic pain management, which is based on the knowledge of processes that underlie the development of peripheral neuropathic pain; in particular highlights the role of glia and mast cells in pain and neuroinflammation. ALIAmides (autacoid local injury antagonist amides) represent a group of endogenous bioactive lipids, including palmitoylethanolamide (PEA), which play a central role in numerous biological processes, including pain, inflammation, and lipid metabolism. These compounds are emerging thanks to their anti-inflammatory and anti-hyperalgesic effects, due to the down-regulation of activation of mast cells. Collectively, preclinical and clinical studies support the idea that ALIAmides merit further consideration as therapeutic approach for controlling inflammatory responses, pain, and related peripheral neuropathic pain.

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The Role of Neuroinflammation in Cellular Damage in Neurodegenerative Diseases

Cited by 12 publications

References 0 publications

Anti-Inflammatory Effects of the Novel Barbiturate Derivative MHY2699 in an MPTP-Induced Mouse Model of Parkinson’s Disease

Anti-Inflammatory Effects of the Novel Barbiturate Derivative MHY2699 in an MPTP-Induced Mouse Model of Parkinson’s Disease

Repulsive Guidance Molecule-a and Central Nervous System Diseases

ALIAmides Update: Palmitoylethanolamide and Its Formulations on Management of Peripheral Neuropathic Pain

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