Amyloid-beta protein fragment 25-35 (Aβ25-35)

Amyloid-beta protein fragment 25-35 (Aβ25-35) is an 11-amino acid undecapeptide that constitutes the biologically active and highly neurotoxic core of the full-length Amyloid-beta protein (Aβ1-40/42) [1, 10, 15]. It is distinguished by its rapid rate of aggregation and its ability to form insoluble beta-sheet fibrils more aggressively than longer fragments, leading to the disruption of neuronal membranes and the induction of significant oxidative stress [4, 5, 8]. In Alzheimer's disease pathology, Aβ25-35 acts as a potent mediator of synaptic dysfunction and neuronal apoptosis by interfering with mitochondrial potential and activating pro-apoptotic pathways [5, 12, 14]. Therapeutic interest in this fragment focuses on the development of small molecule inhibitors, such as polyphenols, and monoclonal antibodies that can specifically target the 25-35 sequence to prevent aggregation or neutralize its cytotoxic effects [4, 10, 16]. While research primarily utilizes Aβ25-35 as a model for amyloid toxicity, clinical interventions targeting Amyloid-beta peptides must navigate serious safety challenges, including amyloid-related imaging abnormalities (ARIA) characterized by cerebral edema and microhemorrhages [2, 6, 7].

Other names

Aβ(25-35)Beta-amyloid(25-35)Amyloid-beta 25-35Abeta25-35Amyloid beta-peptide (25-35)

Inhibition of peptide self-assembly and aggregation, destabilization of beta-sheet fibrils, neutralization of fragment-induced neurotoxicity, and promotion of antibody-mediated clearance.