Calcium and cell death signaling in neurodegeneration and aging

Smaili, Soraya Soubhi; Hirata, Hanako; Ureshino, Rodrigo Portes; Monteforte, Priscila Totarelli; Morales, Ana Paula; Muler, Mari Luminosa; Terashima, Juliana Yoshie; Oseki, Karen Tubono; Rosenstock, Tatiana R.; Lopes, Guiomar Silva; Bincoletto, Cláudia

doi:10.1590/s0001-37652009000300011

Cited by 72 publications

(53 citation statements)

References 44 publications

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“…Aging is the single most important risk factor for the onset of aggregation-associated degenerative diseases, such as Alzheimer's disease, Huntington's disease, and Parkinson's disease (Morley et al 2002;Chaney et al 2003;Morley and Morimoto 2004;Cohen et al 2006Cohen et al , 2009Cohen et al , 2010Weissman et al 2007;Tatsuta and Langer 2008;Ben-Zvi et al 2009;Morimoto and Cuervo 2009;Schue 2009;Smaili et al 2009;Douglas and Dillin 2010). Aggregate accumulation largely targets the degeneration of tissues that cannot regenerate ( postmitotic tissues).…”

Section: Adaptation Of the Proteostasis Network To Ameliorate Misfoldmentioning

confidence: 99%

Chemical and Biological Approaches for Adapting Proteostasis to Ameliorate Protein Misfolding and Aggregation Diseases-Progress and Prognosis

Lindquist

Kelly²

2011

Cold Spring Harbor Perspectives in Biology

169

139

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Maintaining the proteome to preserve the health of an organism in the face of developmental changes, environmental insults, infectious diseases, and rigors of aging is a formidable task. The challenge is magnified by the inheritance of mutations that render individual proteins subject to misfolding and/or aggregation. Maintenance of the proteome requires the orchestration of protein synthesis, folding, degradation, and trafficking by highly conserved/deeply integrated cellular networks. In humans, no less than 2000 genes are involved. Stress sensors detect the misfolding and aggregation of proteins in specific organelles and respond by activating stress-responsive signaling pathways. These culminate in transcriptional and posttranscriptional programs that up-regulate the homeostatic mechanisms unique to that organelle. Proteostasis is also strongly influenced by the general properties of protein folding that are intrinsic to every proteome. These include the kinetics and thermodynamics of the folding, misfolding, and aggregation of individual proteins. We examine a growing body of evidence establishing that when cellular proteostasis goes awry, it can be reestablished by deliberate chemical and biological interventions. We start with approaches that employ chemicals or biological agents to enhance the general capacity of the proteostasis network. We then introduce chemical approaches to prevent the misfolding or aggregation of specific proteins through direct binding interactions. We finish with evidence that synergy is achieved with the combination of mechanistically distinct approaches to reestablish organismal proteostasis.

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Section: Adaptation Of the Proteostasis Network To Ameliorate Misfoldmentioning

confidence: 99%

Chemical and Biological Approaches for Adapting Proteostasis to Ameliorate Protein Misfolding and Aggregation Diseases-Progress and Prognosis

Lindquist

Kelly²

2011

Cold Spring Harbor Perspectives in Biology

169

139

View full text Add to dashboard Cite

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“…Excessive Ca 2ϩ influx into cells is thought to be a major contributor to cell death in ischemic and excitotoxic models of neuronal injury (Smaili et al 2009). Therefore mechanisms of Ca 2ϩ entry are prime candidates as targets for potential neuroprotective effects.…”

Section: Introductionmentioning

confidence: 99%

Modulation of Voltage-Gated Ion Channels in Rat Retinal Ganglion Cells Mediated by Somatostatin Receptor Subtype 4

Farrell

Raymond

Foote³

et al. 2010

Journal of Neurophysiology

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“…Activation of such resident caspase led to internucleosomal cleavage of DNA [39] . The endoplasmic reticulum, which is mainly responsible for the calcium homeostasis in cell acts in connection to mitochondria to modulate the mitochondrial pore formation and release of cytochrome-c from mitochondria [40][41][42] . Bcl-2 family proteins could regulate the apoptosis by modulating the release of cytochrome-c from mitochondria into the cytosol [43] .…”

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

confidence: 99%

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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Calcium and cell death signaling in neurodegeneration and aging

Cited by 72 publications

References 44 publications

Chemical and Biological Approaches for Adapting Proteostasis to Ameliorate Protein Misfolding and Aggregation Diseases-Progress and Prognosis

Chemical and Biological Approaches for Adapting Proteostasis to Ameliorate Protein Misfolding and Aggregation Diseases-Progress and Prognosis

Modulation of Voltage-Gated Ion Channels in Rat Retinal Ganglion Cells Mediated by Somatostatin Receptor Subtype 4

Antioxidants as a preventive therapeutic option for age related neurodegenerative diseases

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