Protection against β‐amyloid neurotoxicity by a non‐toxic endogenous N‐terminal β‐amyloid fragment and its active hexapeptide core sequence

High levels of beta amyloid oligomers are associated with neurotoxic effects, while low levels may act as neuromodulators.

• The hydrophobic C-terminal domain of beta amyloid is essential for its neurotoxic effects.
• Conversely, the hydrophilic N-terminal domain of beta amyloid could function as a positive neuromodulator.
• An N-terminal beta amyloid fragment (1-15/16) may reverse impairments caused by beta amyloid on long-term potentiation.
• The N-terminal fragment and a shorter hexapeptide core sequence (Aβcore: 10-15) could protect against Aβ-induced neuronal toxicity and fear memory deficits.
• Neuroprotective effects were demonstrated through assessments of mitochondrial function, oxidative stress, and apoptotic neuronal death.
• Stabilized derivatives of the N-terminal Aβcore may provide full protection against Aβ-triggered oxidative stress.

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