Neuronal Cell Death Mechanisms in Major Neurodegenerative Diseases

Ran, Hao; Chang, Hui-Yun; Sang, Tzu-Kang

doi:10.3390/ijms19103082

Cited by 277 publications

(198 citation statements)

References 155 publications

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“…Necroptosis has been implicated in the development of some neurodegenerative diseases [74]. Alzheimer's disease (AD) is a degenerative brain disease and is characterized by the damage and loss of neurons.…”

Section: Necroptosis In Neurodegenerative Diseasesmentioning

confidence: 99%

Molecular Insights into the Mechanism of Necroptosis: The Necrosome as a Potential Therapeutic Target

Chen

Garssen

et al. 2019

Cells

129

115

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Necroptosis, or regulated necrosis, is an important type of programmed cell death in addition to apoptosis. Necroptosis induction leads to cell membrane disruption, inflammation and vascularization. It plays important roles in various pathological processes, including neurodegeneration, inflammatory diseases, multiple cancers, and kidney injury. The molecular regulation of necroptotic pathway has been intensively studied in recent years. Necroptosis can be triggered by multiple stimuli and this pathway is regulated through activation of receptor-interacting protein kinase 1 (RIPK1), RIPK3 and pseudokinase mixed lineage kinase domain-like (MLKL). A better understanding of the mechanism of regulation of necroptosis will further aid to the development of novel drugs for necroptosis-associated human diseases. In this review, we focus on new insights in the regulatory machinery of necroptosis. We further discuss the role of necroptosis in different pathologies, its potential as a therapeutic target and the current status of clinical development of drugs interfering in the necroptotic pathway.

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Section: Necroptosis In Neurodegenerative Diseasesmentioning

confidence: 99%

Molecular Insights into the Mechanism of Necroptosis: The Necrosome as a Potential Therapeutic Target

Chen

Garssen

et al. 2019

Cells

129

115

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“…They are typically characterized by abnormal proteostasis, where the cell is unable to maintain regulation of protein folding, translation, and degradation pathways. These defects in proteostasis lead to processes of cell death such as apoptosis and disrupted signaling mechanisms within the cell from oxidative stress, glutamate-mediated cytotoxicity, neuroinflammation, mitochondrial dysfunction, and increased endoplasmic reticulum (ER) stress [2][3][4][5][6][7]. However, the early factors involved in neuronal cell death are still not understood.…”

Section: Introductionmentioning

confidence: 99%

Metabolite therapy guided by liquid biopsy proteomics delays retinal neurodegeneration

Wert

Vélez

Vijayalakshmi

et al. 2019

Preprint

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One Sentence Summary: The study shows protein and metabolite pathways affected during neurodegeneration and that replenishing metabolites provides a neuroprotective effect on the retina. Abstract: 244Main Text: 9,039References: 83 AbstractNeurodegenerative diseases are debilitating, incurable disorders caused by progressive neuronal cell death.Retinitis pigmentosa (RP) is a blinding neurodegenerative disease that results in retinal photoreceptor cell death and progresses to the loss of the entire neural retinal network. We previously found that proteomic analysis of the adjacent vitreous serves as way to indirectly biopsy the neural retina and identify changes in the retinal proteome. We therefore analyzed protein expression in liquid vitreous biopsies from autosomal recessive retinitis pigmentosa (arRP) patients with PDE6A mutations and arRP mice with Pde6ɑ mutations. Proteomic analysis of retina and vitreous samples identified molecular pathways affected at the onset of photoreceptor cell death. Based on affected molecular pathways, arRP mice were treated with a ketogenic diet or metabolites involved in fatty-acid synthesis, oxidative phosphorylation, and the tricarboxylic acid (TCA) cycle. Dietary supplementation of a single metabolite, ɑ-ketoglutarate, increased docosahexaeonic acid (DHA) levels, provided neuroprotection, and enhanced visual function in arRP mice. A ketogenic diet delayed photoreceptor cell loss, while vitamin B supplementation had a limited effect. Finally, desorption electrospray ionization mass spectrometry imaging (DESI-MSI) revealed restoration of key metabolites that correlated with our proteomic findings: pyrimidine and purine metabolism (uridine, dihydrouridine, and thymidine), glutamine and glutamate (glutamine/glutamate conversion), and succinic and aconitic acid (TCA cycle). This study demonstrates that replenishing TCA cycle metabolites via oral supplementation prolongs vision and provides a neuroprotective effect on the photoreceptor cells and inner retinal network.

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“…Neuronal cell death is considered as a major hallmark of NDs. Neurotoxic molecules such as reactive oxygen species (ROS) and protein aggregates induce neuroin lammation or neuronal cell death, which eventually lead to neurodegeneration (Chi et al, 2018). Number of preclinical studies demonstrated the neuroprotective effects of crude extract or puri ied compounds of M. charantia by attenuating oxidative stress, neu-roin lammation and cell death.…”

Section: Neuroprotective Propertiesmentioning

confidence: 99%

Neuroprotective effects of Momordica charantia: A review from preclinical studies

Valarmathi¹,

Sree

Rajan

2020

ijrps

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Momordica charantia L. (M. charantia), also referred as bitter gourd or bitter melon, is a cucurbit plant commonly found in tropical and subtropical regions of the world. As an important ingredient in traditional medicine, it has been consumed to treat a wide range of diseases including diabetics and cancer in India, Indian subcontinent and China. This plant contains a rich source of flavonoids, saponins, triterpenes, polysaccharides, proteins, and other phytochemicals. Earlier studies have demonstrated the medicinal properties such as anti-diabetic, anti-cancer, anti-oxidant, anti-inflammatory and anthelmintic properties present in M. charantia. Neurodegenerative diseases are the devastating diseases which affect millions of people worldwide. Alzheimer’s disease, Parkinson’s disease, multiple sclerosis and amyotrophic lateral sclerosis are some of the common neurodegenerative diseases. These diseases are described by degeneration and /or loss of selective neuron populations in a progressive manner. Oxidative stress and inflammation are the hallmarks of neurodegenerative diseases. Many medicinal herbs and their derivatives have been investigated to treat neurodegenerative diseases. However, very few studies have reported the protective effects of M. charantia against neurodegenerative diseases. In this short review, we discuss the preclinical studies with the focus on the neuroprotective effects of M. charantia. Based on the anti-oxidant and anti-inflammatory properties, in this review we emphasize to further explore the protective effects of M. charantia in neurodegenerative and neuroinflammatory diseases.

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Neuronal Cell Death Mechanisms in Major Neurodegenerative Diseases

Cited by 277 publications

References 155 publications

Molecular Insights into the Mechanism of Necroptosis: The Necrosome as a Potential Therapeutic Target

Molecular Insights into the Mechanism of Necroptosis: The Necrosome as a Potential Therapeutic Target

Metabolite therapy guided by liquid biopsy proteomics delays retinal neurodegeneration

Neuroprotective effects of Momordica charantia: A review from preclinical studies

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