The article discusses the role of amyloid-β (Aβ) peptides in the pathogenesis of Alzheimer's disease, focusing on their effects on synaptic and neuronal network activity. Recent evidence suggests that Aβ may act as a positive regulator at low concentrations and a negative regulator at high concentrations, influencing synaptic transmission. Pathologically elevated Aβ levels can lead to synaptic depression, reduced glutamatergic transmission, and dendritic spine loss. Additionally, Aβ can cause GABAergic dysfunction, increasing synchrony among excitatory neurons and contributing to cognitive decline. The article also highlights the importance of understanding the specific types of neurons, synapses, and molecules affected by Aβ, as well as the relationship between Aβ-induced changes at the synaptic, circuit, and network levels. Finally, it addresses the multifactorial nature of Alzheimer's disease and the need for further research to elucidate the relative pathogenic impact of various factors.The article discusses the role of amyloid-β (Aβ) peptides in the pathogenesis of Alzheimer's disease, focusing on their effects on synaptic and neuronal network activity. Recent evidence suggests that Aβ may act as a positive regulator at low concentrations and a negative regulator at high concentrations, influencing synaptic transmission. Pathologically elevated Aβ levels can lead to synaptic depression, reduced glutamatergic transmission, and dendritic spine loss. Additionally, Aβ can cause GABAergic dysfunction, increasing synchrony among excitatory neurons and contributing to cognitive decline. The article also highlights the importance of understanding the specific types of neurons, synapses, and molecules affected by Aβ, as well as the relationship between Aβ-induced changes at the synaptic, circuit, and network levels. Finally, it addresses the multifactorial nature of Alzheimer's disease and the need for further research to elucidate the relative pathogenic impact of various factors.