دورية أكاديمية
أعرض في EDS

Regulation of motor proteins, axonal transport deficits and adult-onset neurodegenerative diseases.

التفاصيل البيبلوغرافية
العنوان: Regulation of motor proteins, axonal transport deficits and adult-onset neurodegenerative diseases.
المؤلفون: Brady ST; Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, USA; Marine Biological Laboratory, Woods Hole, MA 02543, USA. Electronic address: stbrady@uic.edu., Morfini GA; Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, USA; Marine Biological Laboratory, Woods Hole, MA 02543, USA. Electronic address: gmorfini@uic.edu.
المصدر: Neurobiology of disease [Neurobiol Dis] 2017 Sep; Vol. 105, pp. 273-282. Date of Electronic Publication: 2017 Apr 11.
نوع المنشور: Journal Article; Review
اللغة: English
بيانات الدورية: Publisher: Academic Press Country of Publication: United States NLM ID: 9500169 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1095-953X (Electronic) Linking ISSN: 09699961 NLM ISO Abbreviation: Neurobiol Dis Subsets: MEDLINE
أسماء مطبوعة: Publication: San Diego, CA : Academic Press
Original Publication: Oxford : Blackwell Science, c1994-
مواضيع طبية MeSH: Neurodegenerative Diseases*/metabolism , Neurodegenerative Diseases*/pathology , Neurodegenerative Diseases*/physiopathology, Axonal Transport/*physiology , Microtubule-Associated Proteins/*metabolism , Molecular Motor Proteins/*metabolism, Animals ; Humans ; Signal Transduction/physiology
مستخلص: Neurons affected in a wide variety of unrelated adult-onset neurodegenerative diseases (AONDs) typically exhibit a "dying back" pattern of degeneration, which is characterized by early deficits in synaptic function and neuritic pathology long before neuronal cell death. Consistent with this observation, multiple unrelated AONDs including Alzheimer's disease, Parkinson's disease, Huntington's disease, and several motor neuron diseases feature early alterations in kinase-based signaling pathways associated with deficits in axonal transport (AT), a complex cellular process involving multiple intracellular trafficking events powered by microtubule-based motor proteins. These pathogenic events have important therapeutic implications, suggesting that a focus on preservation of neuronal connections may be more effective to treat AONDs than addressing neuronal cell death. While the molecular mechanisms underlying AT abnormalities in AONDs are still being analyzed, evidence has accumulated linking those to a well-established pathological hallmark of multiple AONDs: altered patterns of neuronal protein phosphorylation. Here, we present a short overview on the biochemical heterogeneity of major motor proteins for AT, their regulation by protein kinases, and evidence revealing cell type-specific AT specializations. When considered together, these findings may help explain how independent pathogenic pathways can affect AT differentially in the context of each AOND.
(Copyright © 2017 Elsevier Inc. All rights reserved.)
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معلومات مُعتمدة: R01 NS023320 United States NS NINDS NIH HHS; R01 NS082730 United States NS NINDS NIH HHS; R01 NS041170 United States NS NINDS NIH HHS; R21 NS096642 United States NS NINDS NIH HHS; R01 NS023868 United States NS NINDS NIH HHS; R01 NS066942 United States NS NINDS NIH HHS
فهرسة مساهمة: Keywords: Alzheimer's disease; Amyotrophic lateral sclerosis; Axonal transport; Dynen; Huntington's disease; Kinases; Kinesin; Neurodegeneration; Parkinson's disease; Signaling
المشرفين على المادة: 0 (Microtubule-Associated Proteins)
0 (Molecular Motor Proteins)
تواريخ الأحداث: Date Created: 20170416 Date Completed: 20180418 Latest Revision: 20181113
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC5522763
DOI: 10.1016/j.nbd.2017.04.010
PMID: 28411118
قاعدة البيانات: MEDLINE
الوصف
تدمد:1095-953X
DOI:10.1016/j.nbd.2017.04.010