title: Axonal transport defects in neurodegenerative diseases.
abstract: Adult-onset neurodegenerative diseases (AONDs) comprise a heterogeneous group of neurological disorders characterized by a progressive, age-dependent decline in neuronal function and loss of selected neuronal populations. Alterations in synaptic function and axonal connectivity represent early and critical pathogenic events in AONDs, but molecular mechanisms underlying these defects remain elusive. The large size and complex subcellular architecture of neurons render them uniquely vulnerable to alterations in axonal transport (AT). Accordingly, deficits in AT have been documented in most AONDs, suggesting a common defect acquired through different pathogenic pathways. These observations suggest that many AONDs can be categorized as dysferopathies, diseases in which alterations in AT represent a critical component in pathogenesis. Topics here address various molecular mechanisms underlying alterations in AT in several AONDs. Illumination of such mechanisms provides a framework for the development of novel therapeutic strategies aimed to prevent axonal and synaptic dysfunction in several major AONDs.
authors.affiliation: Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, Illinois 60612, USA. gmorfini@uic.edu
authors.forename: Gerardo A
authors.initials: GA
authors.lastname: Morfini
authors.forename: Matthew
authors.initials: M
authors.lastname: Burns
authors.forename: Lester I
authors.initials: LI
authors.lastname: Binder
authors.forename: Nicholas M
authors.initials: NM
authors.lastname: Kanaan
authors.forename: Nichole
authors.initials: N
authors.lastname: LaPointe
authors.forename: Daryl A
authors.initials: DA
authors.lastname: Bosco
authors.forename: Robert H
authors.initials: RH
authors.lastname: Brown
authors.forename: Hannah
authors.initials: H
authors.lastname: Brown
authors.forename: Ashutosh
authors.initials: A
authors.lastname: Tiwari
authors.forename: Lawrence
authors.initials: L
authors.lastname: Hayward
authors.forename: Julia
authors.initials: J
authors.lastname: Edgar
authors.forename: Klaus-Armin
authors.initials: KA
authors.lastname: Nave
authors.forename: James
authors.initials: J
authors.lastname: Garberrn
authors.forename: Yuka
authors.initials: Y
authors.lastname: Atagi
authors.forename: Yuyu
authors.initials: Y
authors.lastname: Song
authors.forename: Gustavo
authors.initials: G
authors.lastname: Pigino
authors.forename: Scott T
authors.initials: ST
authors.lastname: Brady
mesh_terms: D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D001370:Axonal Transport / Q000502:physiology*; D004195:Disease Models, Animal; D006801:Humans; D051379:Mice; D008869:Microtubule-Associated Proteins / Q000235:genetics / Q000378:metabolism; D008954:Models, Biological; D019636:Neurodegenerative Diseases / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology*; D009474:Neurons / Q000473:pathology*; D015398:Signal Transduction / Q000502:physiology; D013569:Synapses / Q000502:physiology; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D008869:Microtubule-Associated Proteins; D016875:tau Proteins