title: The origin and development of plaques and phosphorylated tau are associated with axonopathy in Alzheimer's disease.
abstract: OBJECTIVE
  The production of neurotoxic β-amyloid and the formation of hyperphosphorylated tau are thought to be critical steps contributing to the neuropathological mechanisms in Alzheimer's disease (AD). However, there remains an argument as to their importance in the onset of AD. Recent studies have shown that axonopathy is considered as an early stage of AD. However, the exact relationship between axonopathy and the origin and development of classic neuropathological changes such as senile plaques (SPs) and neurofibrillary tangles (NFTs) is unclear. The present study aimed to investigate this relationship.
  
  
  METHODS
  Postmortem tracing, combined with the immunohistochemical or immunofluorescence staining, was used to detect axonopathy and the formation of SPs and NFTs.
  
  
  RESULTS
  Axonal leakage-a novel type of axonopathy, was usually accompanied with the extensive swollen axons and varicosities, and was associated with the origin and development of Aβ plaques and hyperphosphorylated tau in the brains of AD patients.
  
  
  CONCLUSIONS
  Axonopathy, particularly axonal leakage, might be a key event in the initiation of the neuropathological processes in AD.
authors.affiliation: Wuhan Institute for Neuroscience and Neuroengineering, South-Central University for Nationalities, Wuhan 430074, China.
authors.forename: Ai-Wu
authors.initials: AW
authors.lastname: Xiao
authors.forename: Jing
authors.initials: J
authors.lastname: He
authors.forename: Qian
authors.initials: Q
authors.lastname: Wang
authors.forename: Yi
authors.initials: Y
authors.lastname: Luo
authors.forename: Yan
authors.initials: Y
authors.lastname: Sun
authors.forename: Yan-Ping
authors.initials: YP
authors.lastname: Zhou
authors.forename: Yang
authors.initials: Y
authors.lastname: Guan
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Lucassen
authors.forename: Jia-Pei
authors.initials: JP
authors.lastname: Dai
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology*; D001370:Axonal Transport; D001369:Axons / Q000378:metabolism / Q000473:pathology*; D001921:Brain / Q000378:metabolism / Q000473:pathology* / Q000648:ultrastructure; D016022:Case-Control Studies; D005260:Female; D005625:Frontal Lobe / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D006801:Humans; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008297:Male; D008875:Middle Aged; D056347:Neuroanatomical Tract-Tracing Techniques / Q000379:methods; D016874:Neurofibrillary Tangles / Q000378:metabolism / Q000473:pathology; D058225:Plaque, Amyloid / Q000473:pathology*; D011180:Postmortem Changes; D012016:Reference Values; D013702:Temporal Lobe / Q000378:metabolism / Q000473:pathology / Q000648:ultrastructure; D014015:Tissue Banks; D016875:tau Proteins / Q000378:metabolism*
chemical_list: D016875:tau Proteins