PMID- 1716043
OWN - NLM
STAT- MEDLINE
DCOM- 19911010
LR  - 20181113
IS  - 0002-9440 (Print)
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 139
IP  - 3
DP  - 1991 Sep
TI  - Amyloid precursor protein and ubiquitin immunoreactivity in dystrophic axons is 
      not unique to Alzheimer's disease.
PG  - 485-9
AB  - A distinctive feature of Alzheimer's disease (AD) is the presence of dystrophic 
      neurites that immunoreact with antibodies to amyloid precursor protein (APP) and 
      ubiquitin (Ub). The authors examined dystrophic axons (DA) present in other 
      chronic conditions such as familial infantile neuroaxonal dystrophy (INAD), 
      aging, cystic fibrosis, and biliary obstruction as well as in conditions of 
      shorter duration such as human immunodeficiency virus (HIV) leucoencephalopathy, 
      infarction and radiation therapy to determine whether APP and Ub immunoreactivity 
      was unique to the DA of AD. A large number of DA immunoreacted with antibodies to 
      the A4, C- and N-terminal regions of APP as well as to Ub. Ub and APP 
      immunoreactivities often, but not always, colocalized. "Acute" DA generally 
      reacted more intensely and in larger number with antibodies to APP than to Ub, 
      whereas the reverse was true for "chronic" DA. Structureless DA immunostained 
      diffusely. In DA with cores or granules, the Ub immunoreaction was occasionally 
      limited to these structures, whereas reaction with antibodies to APP was more 
      diffuse. In view of the contention that impairment of proteolysis is the common 
      pathogenetic step in the formation of DA, Ub immunoreactivity in all DA may 
      indicate a vicarious attempt to degrade accumulated components through an 
      activation of the Ub system. The role of APP in the formation of DA remains to be 
      determined.
FAU - Cochran, E
AU  - Cochran E
AD  - Division of Neuropathology, Case Western Reserve University, Cleveland, Ohio 
      44106.
FAU - Bacci, B
AU  - Bacci B
FAU - Chen, Y
AU  - Chen Y
FAU - Patton, A
AU  - Patton A
FAU - Gambetti, P
AU  - Gambetti P
FAU - Autilio-Gambetti, L
AU  - Autilio-Gambetti L
LA  - eng
GR  - AG08155/AG/NIA NIH HHS/United States
GR  - NS14509/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (Amyloid)
RN  - 0 (Protein Precursors)
RN  - 0 (Ubiquitins)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Aged
MH  - Aged, 80 and over
MH  - Alzheimer Disease/*metabolism
MH  - Amyloid/*metabolism
MH  - Axons/*metabolism
MH  - Child
MH  - Humans
MH  - Immunohistochemistry/methods
MH  - Protein Precursors/*metabolism
MH  - Staining and Labeling
MH  - Ubiquitins/*metabolism
PMC - PMC1886228
EDAT- 1991/09/01 00:00
MHDA- 1991/09/01 00:01
PMCR- 1992/03/01
CRDT- 1991/09/01 00:00
PHST- 1991/09/01 00:00 [pubmed]
PHST- 1991/09/01 00:01 [medline]
PHST- 1991/09/01 00:00 [entrez]
PHST- 1992/03/01 00:00 [pmc-release]
PST - ppublish
SO  - Am J Pathol. 1991 Sep;139(3):485-9.