Non-Aβ Component of Alzheimer's Disease Amyloid refers to the diverse array of non-amyloid β (Aβ) molecules and proteins that coexist with Aβ peptides in the amyloid plaques of Alzheimer’s disease (AD) brains. These components include tau protein (forming neurofibrillary tangles), apolipoprotein E (APOE), α-synuclein, complement factors, prion proteins, and various cellular and vascular elements. Unlike Aβ, which is the primary structural component of plaques, non-Aβ constituents modulate plaque formation, stability, and neurotoxicity, often interacting with Aβ to enhance aggregation, inflammation, or synaptic dysfunction. For example, tau pathology synergizes with Aβ to drive neurodegeneration, while APOE influences Aβ clearance and deposition. Studying these components is critical for understanding the complex interplay of molecular pathways in AD, as they contribute to disease progression, therapeutic resistance, and phenotypic variability. By characterizing their roles in plaque biology and cross-talk with Aβ, researchers aim to develop more comprehensive strategies targeting the multifaceted nature of Alzheimer’s pathology, beyond single-component interventions.

Chemical Formula: C141H235N39O49

Molecular Weight: 3260.68

Sequence: Glu-Gln-Val-Thr-Asn-Val-Gly-Gly-Ala-Val-Val-Thr-Gly-Val-Thr-Ala-Val-Ala-Gln-Lys-Thr-Val-Glu-Gly-Ala-Gly-Ser-Ile-Ala-Ala-Ala-Thr-Gly-Phe-Val

Purity: From crude to 98%

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