S. Hoshino et al., EMERGENCE OF IMMUNOREACTIVITIES FOR PHOSPHORYLATED-TAU AND AMYLOID-BETA PROTEIN IN CHRONIC STAGE OF FLUID PERCUSSION INJURY IN RAT-BRAIN, NeuroReport, 9(8), 1998, pp. 1879-1883
HEAD injury is one of the potential environmental factors in Alzheimer
's disease (AD). To study the chronic stage of concussive brain injury
, histological analyses were performed 2-6 months after right lateral
fluid percussion (FP) brain injury (3.6-4.8 atm) in rats. Six months a
fter injury, numerous normal-looking neurons in the telencephalon and
brain stem were immunoreactive with either antibody to phosphorylated
tau or with four antibodies to beta-amyloid protein. Neuronal counts i
n the cortices were gradually decreased after injury, up to 42% loss a
t 6 months after injury. These neuropathological changes suggest that
this animal model could serve as a good animal model of neurodegenerat
ive diseases such as AD. (C) 1998 Rapid Science Ltd.