Journal ArticleDOI
Axon pathology in neurological disease: a neglected therapeutic target.
Michael P. Coleman,V. Hugh Perry +1 more
TLDR
In the C57BL/Wld(S) mouse, a dominant mutation dramatically delays Wallerian degeneration in injury and disease, possibly by influencing multi-ubiquitination.About:
This article is published in Trends in Neurosciences.The article was published on 2002-10-01. It has received 403 citations till now. The article focuses on the topics: Wallerian degeneration & Axon.read more
Citations
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Journal ArticleDOI
Principles of Neural Science
TL;DR: The editors have done a masterful job of weaving together the biologic, the behavioral, and the clinical sciences into a single tapestry in which everyone from the molecular biologist to the practicing psychiatrist can find and appreciate his or her own research.
Journal ArticleDOI
Neuropathological Alterations in Alzheimer Disease
TL;DR: Postmortem studies have enabled the staging of the progression of both amyloid and tangle pathologies, and the development of diagnostic criteria that are now used worldwide, and these cross-sectional neuropathological data have been largely validated by longitudinal in vivo studies using modern imaging biomarkers such as amyloids PET and volumetric MRI.
Journal ArticleDOI
Mammalian sirtuins: biological insights and disease relevance.
TL;DR: There have been major advances in the understanding of the enzymology of sirtuins, their regulation, and their ability to broadly improve mammalian physiology and health span, and the challenges that will confront the field in the coming years are discussed.
Journal ArticleDOI
Amyotrophic lateral sclerosis is a distal axonopathy: evidence in mice and man.
Lindsey R. Fischer,Deborah G. Culver,Philip Tennant,Albert A. Davis,Minsheng Wang,Amilcar A. Castellano-Sanchez,Jaffar M. Khan,Meraida Polak,Jonathan D. Glass +8 more
TL;DR: It is concluded that in this widely studied animal model of human ALS, and in this single human case, motor neuron pathology begins at the distal axon and proceeds in a "dying back" pattern.
Journal ArticleDOI
Increased nuclear NAD biosynthesis and SIRT1 activation prevent axonal degeneration.
TL;DR: It is demonstrated that increased Nmnat activity is responsible for the axon-sparing activity of the Wlds protein and that SIRT1, a mammalian ortholog of Sir2, is the downstream effector of increased NMNat activity that leads to axonal protection.
References
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Principles of Neural Science
TL;DR: The principles of neural science as mentioned in this paper have been used in neural networks for the purpose of neural network engineering and neural networks have been applied in the field of neural networks, such as:
Journal ArticleDOI
Principles of Neural Science
TL;DR: The editors have done a masterful job of weaving together the biologic, the behavioral, and the clinical sciences into a single tapestry in which everyone from the molecular biologist to the practicing psychiatrist can find and appreciate his or her own research.
Journal ArticleDOI
Motor neuron degeneration in mice that express a human Cu,Zn superoxide dismutase mutation.
Mark E. Gurney,Haifeng Pu,Arlene Y. Chiu,Mauro C. Dal Canto,Cynthia Y. Polchow,Denise D. Alexander,Jan Caliendo,Afif Hentati,Young W. Kwon,Han Xiang Deng,W. Chen,Ping Zhai,Robert L. Sufit,Teepu Siddique +13 more
TL;DR: In this article, the authors found that mutations of human Cu,Zn superoxide dismutase (SOD) contribute to the pathogenesis of familial amyotrophic lateral sclerosis (ALS).
Journal ArticleDOI
Axonal transection in the lesions of multiple sclerosis.
TL;DR: Transected axons are common in the lesions of multiple sclerosis, and axonal transection may be the pathologic correlate of the irreversible neurologic impairment in this disease.
Journal ArticleDOI
Identification of Ubiquitin Ligases Required for Skeletal Muscle Atrophy
Sue C. Bodine,Esther Latres,Susanne Baumhueter,Venus Lai,Lorna Nunez,Brian A. Clarke,William Poueymirou,Frank J. Panaro,Erqian Na,Kumar Dharmarajan,Zhen-Qiang Pan,David M. Valenzuela,Thomas M. DeChiara,Trevor Stitt,George D. Yancopoulos,David J. Glass +15 more
TL;DR: Two genes encode ubiquitin ligases that are potential drug targets for the treatment of muscle atrophy, and mice deficient in either MAFbx orMuRF1 were found to be resistant to atrophy.