The N-terminally truncated pyroglutamate Aβ (Aβ) and Aβ peptides are known to be highly abundant in the brain of Alzheimer's disease (AD) patients. Both peptides show enhanced aggregation and neurotoxicity in comparison to full-length Aβ, suggesting that these amyloid peptides may play an important role in the pathogenesis of AD. The aim of the present work was to study the direct effect of the combination of Aβ and Aβ on ongoing AD-related neuron loss, pathology, and neurological deficits in transgenic mice.
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