Amyloid-beta (Aβ) accumulation is a defining pathological feature of Alzheimer’s disease and a critical target in both research and therapy. Aβ is a peptide fragment derived from the amyloid precursor protein (APP) through sequential cleavage by β- and γ-secretases. In Alzheimer’s disease, the aggregation of Aβ into insoluble extracellular plaques disrupts neuronal communication, induces oxidative stress, and activates inflammatory responses. Soluble Aβ oligomers, rather than plaques, are now considered the most neurotoxic species, impairing synaptic function and plasticity even before plaque deposition is evident. Genetic mutations in APP, PSEN1, and PSEN2 enhance Aβ production and are linked to familial Alzheimer’s. Diagnostic techniques such as PET imaging with Aβ tracers and cerebrospinal fluid (CSF) assays measuring Aβ42 are now widely used in clinical and research settings.

Therapeutically, monoclonal antibodies targeting Aβ (e.g., aducanumab, lecanemab) have shown promise in reducing plaque burden, though their clinical efficacy remains under evaluation. The journal encourages contributions investigating the molecular biology of Aβ metabolism, its interactions with tau and other cellular pathways, biomarker development, and the efficacy and safety of Aβ-targeting therapies.