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beta-Amyloid cores contain considerable amounts of D-Ser and D-Asp residues in Alzheimer's disease. We investigated the cytotoxic effects of various synthetic beta-amyloids, including D-Ser-substituted derivatives, on primary cultured neurons and nonneuronal HeLa cells. beta 25-35, its D-Ser26-substituted derivative, and beta 1-40 in 10-100 nM specifically(More)
It is unclear how and when insoluble beta-amyloid in senile plaques exerts degenerative effects on distant hippocampal neurons in Alzheimer's disease. Racemization of Ser and Asp residues of insoluble beta-amyloid is a typical age-dependent process. In this study, we investigated the fibril formation activity and cytotoxic activity of beta-amyloid 1-40(More)
The lag between beta-amyloid (A beta) deposition and neurodegeneration in Alzheimer's disease (AD) suggests that age-dependent factors are involved in the pathogenesis. Racemization of Ser and Asp in A beta is a typical age-dependent modification in AD. We have shown recently that A beta1-40 racemized at Ser(26) ([D-Ser(26)]A beta 1-40) is soluble and(More)
Senile plaques are a pathological hallmark of Alzheimer's disease. The major component of senile plaques is beta-amyloid which consists of approximately 4000 mol. wt of peptide. Accumulating evidence suggests that beta-amyloid may represent the underlying cause of Alzheimer's disease. In vitro, beta-amyloid has been shown either to be directly neurotoxic or(More)
Oligomeric and fibrillar beta-amyloid (Abeta) may be toxic in Alzheimer disease (AD), especially after post-translation modification cumulative over time. Racemization of Ser and Asp residues of Abeta in senile plaques (SPs) occurs as an age-dependent process in AD. We previously reported that Abeta1-40 racemized at Ser26 is soluble and susceptible to(More)
Amyloid beta peptide in the senile plaques of patients with Alzheimer's disease is considered to be responsible for the pathology of Alzheimer's disease. We have previously reported that 6-ethyl-N,N'-bis(3-hydroxyphenyl)[1,3,5]triazine-2,4-diamine, RS-0466, is capable of significantly inhibiting amyloid beta-induced cytotoxicity in HeLa cells. To determine(More)
We have previously shown that in vivo injection of beta-amyloid (beta 1-40, beta 25-35) with non-toxic amounts of ibotenic acid, an excitatory amino acid, causes synergistic and drastic neuronal degeneration in rat hippocampus. It was, however, yet not clear whether the neuronal degeneration in vivo was associated with their primary amino acid sequences,(More)
Recent observations on the neurotoxicity of beta-amyloid have been reviewed and possible roles of racemization of beta-amyloid are discussed. beta 1-40, beta 25-35 and D-Ser26 beta 25-35 (all HCl salt forms), but not commercially available beta 1-40 (TFA salt form), take the beta-structure within few hours in PBS, form fibrils, exert toxic effects on(More)
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