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Failure of anti-amyloid-β peptide (Aβ) therapies against Alzheimer's disease (AD), a neurodegenerative disorder characterized by high amounts of the peptide in the brain, raised the question of the physiological role of Aβ released at low concentrations in the healthy brain. To address this question, we studied the presynaptic and postsynaptic mechanisms underlying the neuromodulatory action of picomolar amounts of oligomeric Aβ₄₂ (oAβ₄₂) on synaptic glutamatergic function in male and female mice. We found that 200 pm oAβ₄₂ induces an increase of frequency of miniature EPSCs and a decrease of paired pulse facilitation, associated with an increase in docked vesicle number, indicating that it augments neurotransmitter release at presynaptic level. oAβ₄₂ also produced postsynaptic changes as shown by an increased length of postsynaptic density, accompanied by an increased expression of plasticity …