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A\u03b2 protein aggregates disrupt synaptic architecture, calcium homeostasis, and mitochondrial function, leading to excitotoxicity and synaptic plasticity deficits. Animal models and human studies reveal that A\u03b2-induced alterations in synaptic activity and neuronal circuit function appear before irreversible damage and the onset of cognitive impairment. This review examines the multifaceted effects of A\u03b2 on synaptic and neuronal circuits across its distinct aggregation states, including monomeric, oligomeric, protofibrillar, and fibrillar forms. Its novelty lies in providing a comprehensive map of A\u03b2-induced mechanisms that disrupt neuronal electrical function, based on electrophysiological evidence from neuronal cultures, animal models, and patient studies, with a particular focus on preclinical stages of cognitive decline. 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