Alzheimer’s disease (AD) is characterized by neuronal loss
and extracellular senile plaque, whose major constituent is b -
amyloid protein (Ab ), a 39—43 amino acid peptide derived
from amyloid precursor protein.1) Both in vitro and in vivo
studies have reported the toxic effects of Ab or Ab peptide
fragments suggesting an important role for Ab in the pathogenesis
of AD.2,3) In cultures, Ab can directly induce neuronal
cell death and render neurons vulnerable to excitotoxicity
and oxidative insults.4—6) The mechanisms underlying
Ab -neurotoxicity are complex but may involve N-methyl-Daspartate
(NMDA) receptor, a glutamate receptor subtype,
modulation induced by glutamate release, sustained elevations
of intracellular Ca2 concentration ([Ca2]i), and oxidative
stresses.7—10)
Alzheimer’s disease (AD) is characterized by neuronal lossand extracellular senile plaque, whose major constituent is b -amyloid protein (Ab ), a 39—43 amino acid peptide derivedfrom amyloid precursor protein.1) Both in vitro and in vivostudies have reported the toxic effects of Ab or Ab peptidefragments suggesting an important role for Ab in the pathogenesisof AD.2,3) In cultures, Ab can directly induce neuronalcell death and render neurons vulnerable to excitotoxicityand oxidative insults.4—6) The mechanisms underlyingAb -neurotoxicity are complex but may involve N-methyl-Daspartate(NMDA) receptor, a glutamate receptor subtype,modulation induced by glutamate release, sustained elevationsof intracellular Ca2 concentration ([Ca2]i), and oxidativestresses.7—10)
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