Apoptotic neuronal death in Parkinson's disease: Involvement of nitric oxide

Singh, Sarika; Dikshit, Madhu

doi:10.1016/j.brainresrev.2007.02.001

Cited by 119 publications

(72 citation statements)

References 209 publications

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“…1) Even though the risk factors and pathogenic mechanisms of PD are various, the most common mechanism of dopaminergic cell death in PD is a vicious cycle of oxidative stress, mitochondrial dysfunction, and the activation of an apoptotic cascade. [2][3][4] 6-Hydroxydopamine (6-OHDA) is an oxidative metabolite of dopamine that induces selective death of catecholaminergic neurons, including dopaminergic neurons. It is used extensively to create in vivo and in vitro models of PD, because it generates reactive oxygen species (ROS) and reactive nitrogen species (RNS).…”

mentioning

confidence: 99%

Isoliquiritigenin Isolated from LicoriceGlycyrrhiza uralensisPrevents 6-Hydroxydopamine-Induced Apoptosis in Dopaminergic Neurons

Hwang

Chun

2012

Bioscience, Biotechnology, and Biochemistry

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mentioning

confidence: 99%

Isoliquiritigenin Isolated from LicoriceGlycyrrhiza uralensisPrevents 6-Hydroxydopamine-Induced Apoptosis in Dopaminergic Neurons

Hwang

Chun

2012

Bioscience, Biotechnology, and Biochemistry

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“…6,9 Though we acknowledge that in vitro models may not be clinically relevant, our findings suggest that ICP10PK has the distinct advantage over other previously considered gene therapy strategies in that it targets those components of the death regulatory network which seem to be important in the demise of dopaminergic neurons. In this context, it may be significant to point out that the physiopathology of PD was also associated with death programs that were not studied in the present series of experiments, including growth factor depletion (viz nerve growth factor, NGF), 46 activation of the JNK pathway, 35 and glial cell activation and production of proinflammatory cytokines (viz tumor-necrosis factor-a, and interleukin-1b), 46 all of which are also inhibited by ICP10PK. 11,12,14,27 ICP10PK also upregulates XIAP, 12 which was also implicated in PD therapy.…”

Section: Discussionmentioning

confidence: 91%

ICP10PK inhibits calpain-dependent release of apoptosis-inducing factor and programmed cell death in response to the toxin MPP+

et al. 2008

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Apoptosis is a widely accepted component of the pathogenesis of Parkinson's disease (PD), a debilitating neurodegenerative disorder characterized by loss of dopaminergic neurons in the substantia nigra. However, additional death programs were implicated, and current understanding of the cycle of intracellular events that leads to the demise of these neurons is limited. Gene therapy strategies were proposed to inhibit apoptosis, but they have met with relatively limited success. Here we report that the antiapoptotic herpes simplex virus type 2 gene ICP10PK protects neuronally differentiated PC12 cells from death caused by 1-methyl-4-phenylpyridinium (in vitro PD model) through inhibition of calpain I activation and the resulting inhibition of Bax translocation to the mitochondria, apoptosis-inducing factor release and caspase-3 activation. Neuroprotection is through ICP10PK-mediated activation of the PI3-K/Akt survival pathway and upregulation/stabilization of the antiapoptotic protein Bcl-2 and the cytoprotective chaperone heat-shock protein 70.

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“…Exhaustive research is undergoing in this field but still the enigma behind such progressive neuronal death is not well understood. Over the last several decades the studies have showed that the progression of neurodegenerative diseases involve the decreased antioxidant levels, impaired mitochondrial activity, increased oxidative damage protein, lipid peroxidation, protein modification, DNA damage and apoptosis [4][5][6][7][8][9] . Oxidative protein modifications occur at a low and persistent level in diverse cells and tissues and accumulate in aging and neurodegenerative diseases [10][11][12][13][14][15][16][17][18][19] .…”

Section: Reviewmentioning

confidence: 99%

“…The apoptosome binds to procaspase-9 to activate it which in turn cleaves the procaspase-3 to form the caspase-3. The cytochrome-c, Apaf-1 and caspase-9 mediated apoptotic pathway is mitochondria mediated and termed as intrinsic apoptotic pathway [4] . The intrinsic mitochondria-mediated pathway is controlled by Bcl-2 family proteins [51] .…”

Section: (A) Oxidative Stress and Mitochondrial Dysfunction In Neurodmentioning

confidence: 99%

“…In normal cells this apoptotic mechanism could be antagonized with protein family of apoptosis inhibitory proteins (IAPs). Caspase-3 and 9 are the major target of the IAPs by their reversible direct interaction with caspases to block the substrate cleavage [4] . Mitochondrial protein Smac and DIABLO could inactivate the antiapoptotic action of IAPs and termed as proapoptotic proteins.…”

Section: (A) Oxidative Stress and Mitochondrial Dysfunction In Neurodmentioning

confidence: 99%

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Antioxidants as a preventive therapeutic option for age related neurodegenerative diseases

Singh

2015

Ther Targets Neurol Dis

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Neurodegenerative diseases: an overview -Neurodegenerative disease term illustrate a range of conditions in which primarily neurons get affected or die. Neurons are the building blocks of the central and peripheral nervous system. Neurons could not reproduce or replace themselves with age therefore, when they get damaged or die they cannot be replaced and lead to specific neurodegenerative disease. Few evidences for the presence of stem cells are reported [1] but still it is not understood whether damaged neuron could regenerate or not. The Parkinson's, Alzheimer's, and Huntington's diseases are the most prevalent age related neurodegenerative diseases of central nervous system involving death of specific neuronal population. The treatment of these neurodegenerative diseases might involve the re-supplementation of specific neuronal population with the help of stem cells but researchers and clinicians did not get noticeable success in this approach yet. Millions of people each year are getting affected by these neurodegenerative diseases and the incidences are increasing further significantly with the extended life expectancy. It has been reported by World Health Organisation (2006) that the number of older people of more than 65 years age are expected to increase to approximately 1 billion in 2030 worldwide. Developing countries like India and China will see the largest increase in numbers of aged persons. Therefore the percentage of aged population in developing countries would increase from 59% to 71% worldwide [2] . Since occurrence of most of the neurodegenerative Advances in our understanding for neurodegenerative mechanisms have increased significantly in last few decades. But still no novel disease modifying therapy has been developed which could prevent the disease progression and drawn our attention towards the development of new alternative therapy. The major obstacle for the development of disease therapy is incomplete knowledge about neurodegenerative mechanisms. Due to the insufficient information about neurodegenerative mechanisms no standard diagnostic tests for the detection of neurodegenerative disease could be develop to date, causes delayed diagnosis and disease worsening. So far the exploratory reports and clinical data have suggested the involvement of oxidative stress, mitochondrial impairment and apoptosis as major neurodegenerative mechanisms. Investigations have elicited that once initiated the degeneration of neurons could not be arrested therefore in the scarcity of curative therapy we should approach for the preventive neurodegenerative therapy. Since oxidative stress has noteworthy involvement in neuronal death solely, and in connection to other death pathways therefore, antioxidants as preventive therapeutics might provide beneficial effects in age related neurodegenerative diseases. With this hypothesis in this review we are discussing about the use of antioxidants as a preventive treatment of neurodegenerative diseases. Such therapies may work in the preventive phase or in curati...

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Apoptotic neuronal death in Parkinson's disease: Involvement of nitric oxide

Cited by 119 publications

References 209 publications

Isoliquiritigenin Isolated from LicoriceGlycyrrhiza uralensisPrevents 6-Hydroxydopamine-Induced Apoptosis in Dopaminergic Neurons

Isoliquiritigenin Isolated from LicoriceGlycyrrhiza uralensisPrevents 6-Hydroxydopamine-Induced Apoptosis in Dopaminergic Neurons

ICP10PK inhibits calpain-dependent release of apoptosis-inducing factor and programmed cell death in response to the toxin MPP+

Antioxidants as a preventive therapeutic option for age related neurodegenerative diseases

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