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  • 1
    Online Resource
    Online Resource
    Energy Metabolism and Lifespan Determination. (2003)
    San Diego :Elsevier Science & Technology,
    Details
    Keywords: Energy metabolism. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (227 pages)
    Edition: 1st ed.
    ISBN: 9780080494760
    Series Statement: Issn Series ; v.Volume 14
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=296995
    Language: English
    Note: Cover -- Energy Metabolism and Lifespan Determination -- Copyright Page -- Table of Content -- Preface -- Chapter 1. The Search for Energy: A Driving Force in Evolution and Aging -- Chapter 2. Insulin Signaling, Glucose Metabolism Oxidative Stress, and Aging -- Chapter 3. Oxidative Phosphorylation, Mitochondrial Proton Cycling, Free-radical Production and Aging -- Chapter 4. Protein Turnover, Energy Metabolism, Aging, and Caloric Restriction -- Chapter 5. Cellular and Molecular Mechanisms Whereby Dietary Restriction Extends Healthspan: A Beneficial Type of Stress -- Chapter 6. Mitochondrial Oxidative Stress and Caloric Restriction -- Chapter 7. Understanding the Aging Fly Through Physiological Genetics -- Chapter 8. Metabolism and Life span Determination in C. elegans -- Chapter 9. Electron Transport and Life span in C. elegans -- Chapter 10. Cellular Glucose Sensing, Energy Metabolism, and Aging in Saccharomyces cerevisiae -- List of Contributors.
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  • 2
    Online Resource
    Online Resource
    Genetic Aberrancies and Neurodegenerative Disorders. (2000)
    San Diego :Elsevier Science & Technology,
    Details
    Keywords: Nervous system -- Degeneration -- Genetic aspects. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (443 pages)
    Edition: 1st ed.
    ISBN: 9780080876733
    Series Statement: Issn Series ; v.Volume 3
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=402891
    Language: English
    Note: Front Cover -- Genetic Aberrancies and Neurodegenerative Disorders, Volume 3 -- Copyright Page -- CONTENTS -- LIST OF CONTRIBUTORS -- PREFACE -- Chapter 1. Genetic Contributions to The Pathogenesis of Alzheimer's Disease -- Chapter 2. The Biology of Trinucleotide Repeat Disorders -- Chapter 3. The Genetic Basis and Molecular Pathogenesis of Huntington's Disease -- Chapter 4. Genetic Abnormalities in Amyotrophic Lateral Sclerosis -- Chapter 5. Human Prion Diseases -- Chapter 6. Progress in Understanding the Genetics of Epilepsy -- Chapter 7. Cerebrovascular Disease -- Chapter 8. Genetic Susceptibility in Multiple Sclerosis -- Chapter 9. The Role of Mitochondrial Genome Mutations in Neurodegeneratwe Disease -- Chapter 10. Hereditary Disorders of Copper Metabolism -- Chapter 11. The Neuronal Ceroid-Lipofuscinoses (Batten Disease) -- INDEX.
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  • 3
    Online Resource
    Online Resource
    Membrane Lipid Signaling in Aging and Age-Related Disease. (2003)
    San Diego :Elsevier Science & Technology,
    Details
    Keywords: Membrane lipids. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (237 pages)
    Edition: 1st ed.
    ISBN: 9780080522500
    Series Statement: Issn Series ; v.Volume 12
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=298320
    Language: English
    Note: Cover -- TABLE OF CONTENTS -- Preface -- Chapter 1. Overview: Spatial Control of Signal Transduction by Caveolae and Lipid Rafts -- Chapter 2. Overview: Membrane Lipid Peroxidation -- Chapter 3. Regulation of Invertebrate Longevity by Inositol Phosphate Signaling -- Chapter 4. Ceramide-Driven Stress Signals in Cancer and Aging -- Chapter 5. Sphingolipid Metabolism and Signaling in Atherosclerosis -- Chapter 6. Sphingomyelin and Ceramide in Brain Aging, Neuronal Plasticity and Neurodegenerative Disorders -- Chapter 7. The Eicosanoid Pathway and Brain Aging -- Chapter 8. Cellular Cholesterol, Membrane Signaling, and Disease -- Chapter 9. Cholesterol, β-amyloid, and Alzheimer's Disease -- Chapter 10. Phospholipase A2 in the Pathogenesis of Cardiovascular Disease -- Chapter 11. Retinal Docosahexaenoic Acid, Age-Related Diseases, and Glaucoma -- List of Contributors.
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  • 4
    Electronic Resource
    Electronic Resource
    PKC is involved in arachidonic acid-induced choline acetyltransferase activity in spinal cord neurons (2003)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 85 (2003), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Arachidonic acid (AA) may affect cholinergic neuronal circuits in spinal cord. To test this hypothesis, activity of choline acetyltransferase (ChAT) was studied in cultured spinal cord neurons treated with AA (0.1–10 mm). AA increased ChAT activity in dose- and time-dependent manners. These effects were mimicked by exposure to PMA but inhibited by a coexposure to PKC inhibitors. AA-mediated increase in ChAT activity also was prevented by treatments with EGTA, indicating the role of calcium. In contrast, cotreatments with 7-nitroindazole, sodium vanadate, and N-acetyl-cysteine had no influence on AA-induced changes in ChAT activity. These results indicate that the AA-evoked increase in ChAT activity in spinal cord neurons is mediated by PKC, most likely, at the post-transcriptional level.Acknowledgements: Supported by grants from KSCHIRT and Philip Morris Research Program.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.85.s2.15_1.x
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  • 5
    Electronic Resource
    Electronic Resource
    HIV-1 Tat through phosphorylation of NMDA receptors potentiates glutamate excitotoxicity (2001)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 78 (2001), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Toxic effects of HIV-1 proteins contribute to altered function and decreased survival of select populations of neurons in HIV-1-infected brain. One such HIV-1 protein, Tat, can activate calcium release from IP3-sensitive intracellular pools, induce calcium influx in neural cells, and, as a result, can increase neuronal cell death. Here, we provide evidence that Tat potentiates excitatory amino acid (glutamate and NMDA) triggered calcium flux, as well as glutamate- and staurosporine-mediated neurotoxicity. Calcium flux in cultured rat hippocampal neurons triggered by the transient application of glutamate or NMDA was facilitated by pre-exposure to Tat. Facilitation of glutamate-triggered calcium flux by Tat was prevented by inhibitors of ADP-ribosylation of Gi/Go proteins (pertussis toxin), protein kinase C (H7 and bisindolymide), and IP3-mediated calcium release (xestospongin C), but was not prevented by an activator of Gs (cholera toxin) or an inhibitor of protein kinase A (H89). Facilitation of NMDA-triggered calcium flux by Tat was reversed by inhibitors of tyrosine kinase (genestein and herbimycin A) and by an inhibitor of NMDA receptor function (zinc). Tat increased 32P incorporation into NMDA receptor subunits NR2A and NR2B and this effect was blocked by genestein. Subtoxic concentrations of Tat combined with subtoxic concentrations of glutamate or staurosporine increased neuronal cell death significantly. Together, these findings suggest that NMDA receptors play an important role in Tat neurotoxicity and the mechanisms identified may provide additional therapeutic targets for the treatment of HIV-1 associated dementia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.2001.00396.x
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  • 6
    Electronic Resource
    Electronic Resource
    Elevated hepatic and depressed renal cytochrome P450 activity in the Tg2576 transgenic mouse model of Alzheimer's disease (2002)
    Oxford, UK : Blackwell Science, Ltd
    Journal of neurochemistry 80 (2002), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Recent studies indicate that the Tg2576 transgenic mouse model of Alzheimer's disease [tg(hAPP)] demonstrates disturbances in plasma glucose and neuroendocrine function reminiscent of Alzheimer's disease (AD). Alterations in any one of these systems can have a profound effect on hepatic cytochrome P450 (CYP) expression. Additionally, the recent discovery that amyloid beta 1–42 can induce the expression of CYP reductase in neuronal cultures further suggests that hepatic CYP-related metabolism may be affected by the expression of mutant human amyloid precursor protein in these tg(hAPP) mice. Therefore, the current study was conducted to investigate the activity and protein content of several CYP isoforms in the livers and kidneys of aged (20-month-old) tg(hAPP) mice. tg(hAPP) mice exhibit significant elevations in hepatic CYP2B, CYP2E1-, CYP3A- and CYP4A-associated activities and CYP4A immunoreactive protein compared with wild-type. In contrast to the liver, a significant depression in renal CYP2E1- and CYP4A-associated activities were demonstrated in tg(hAPP) mice. The presence of the mutant hAPP protein was detected in the brain, kidney and livers of tg(hAPP) mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.0022-3042.2001.00724.x
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  • 7
    Electronic Resource
    Electronic Resource
    Participation of Gene Expression in the Protection against Amyloid β-Peptide Toxicity by the β-Amyloid Precursor Protein (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 777 (1996), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: The amyloid β-peptide (Aβ) is a toxic derivative of the β-amyloid precursor protein. Alternative processing of this precursor also yields large soluble forms (APPSs) which are secreted from many cell types. These APPSs have neuritogenic and neuroprotective activities; indeed, APPSs can protect primary neurons from the toxicity of Aβ itself. To begin to explore the regulation of gene expression by APPS, we have focused on the NF-κB transcription factor family. NF-κB is induced by conditions of stress, including cellular oxidation. We report that NF-κB can also be induced by APPS. Furthermore, we effected direct activation of NF-κB through disinhibition using antisense oligonucleotide technology. This means of activating NF-κB resulted in protection of neuroblastoma cells from the toxicity of a calcium ionophore and protection of primary hippocampal neurons from the toxicity of Aβ. Together, these data suggest that NF-κB may exist as a common agent inducing a neuroprotective pattern of gene expression in response to either trophic cytokines or stress itself.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1996.tb34437.x
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  • 8
    Electronic Resource
    Electronic Resource
    β-Amyloid Precursor Protein Mismetabolism and Loss of Calcium Homeostasis in Alzheimer's Disease (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 695 (1993), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: The suspected involvement of the β-amyloid precursor protein (βAPP) in the etiology of Alzheimer's disease (AD) has been strengthened by recent genetic evidence, but pursuit of the mechanisms involved will initially require basic cell biology approaches. Several studies have concentrated on toxic activities of β-amyloid peptide (βAP) itself, illuminating its contributions to excitotoxicity and calcium-mediated degeneration in general. We now know that generation of βAP from βAPP also compromises the production of an important set of trophic factors: the secreted forms of βAPP (APPS), which may act—ironically—by conferring protection from calcium-mediated insults. Therefore, conditions which contribute to the formation of βAP (possibly including ischemia) not only produce an agent which exacerbates calcium-mediated cell death, but also reduce the levels of one of the few factors able to rescue calcium homeostasis. The implications of these postulates and their relationship to the process of aging are discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1993.tb23045.x
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  • 9
    Electronic Resource
    Electronic Resource
    Calcium-Induced Neuronal Degeneration: A Normal Growth Cone Regulating Signal Gone Awry (?) (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 568 (1989), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1989.tb12514.x
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  • 10
    Electronic Resource
    Electronic Resource
    Reactive Oxygen Species as Causal Agents in the Neurotoxicity of the Alzheimer's Disease-Associated Amyloid Beta Peptide (1996)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 786 (1996), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1996.tb39057.x
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