title: Physical damage to rat cortical axons mimics early Alzheimer's neuronal pathology.
abstract: We investigated the reactive cytoskeletal changes following physical damage to axons in the rodent neocortex and compared these with the earliest neuronal alterations seen in Alzheimer's disease (AD). Insertion of a 25 gauge needle into the rodent somatosensory cortex resulted in ring- and club-like axonal changes characterized by an accumulation of neurofilaments. Morphologically and neurochemically identical abnormal axons were present within neocortical beta-amyloid deposits of individuals in the early stages of AD. Physically damaged rat cortical axons may therefore serve as a model for the early neuronal pathology of AD. Furthermore, these results suggest that insoluble beta-amyloid deposition may physically damage local axons, with further neurofibrillary changes due to the reactive neuronal response to this type of injury.
authors.affiliation: Division of Pathology, Clinical School, University of Tasmania, Hobart, Australia.
authors.forename: C E
authors.initials: CE
authors.lastname: King
authors.forename: I
authors.initials: I
authors.lastname: Jacobs
authors.forename: T C
authors.initials: TC
authors.lastname: Dickson
authors.forename: J C
authors.initials: JC
authors.lastname: Vickers
mesh_terms: D000368:Aged; D000544:Alzheimer Disease / Q000473:pathology*; D000818:Animals; D001369:Axons / Q000473:pathology*; D002540:Cerebral Cortex / Q000473:pathology*; D004195:Disease Models, Animal; D006801:Humans; D007150:Immunohistochemistry; D009454:Neurofibrils / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar