Physical damage to rat cortical axons mimics early Alzheimer's neuronal pathology.
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.
King
C E
CE
Division of Pathology, Clinical School, University of Tasmania, Hobart, Australia.
Jacobs
I
I
Dickson
T C
TC
Vickers
J C
JC
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