Amyloid precursor protein (APP) was initially detected in cells of the central nervous system and is considered to be involved in the pathogenesis of Alzheimer's disease [1]. Since then, APP has been found in peripheral organs where it plays a variety of distinct biological roles. Mammalian amyloid proteins belongs to the family of integral membrane proteins, which are regulated on multiple levels.

ADAM9 cleaves APP to produce an 83-residue fragment (APP-C83 (CTF)) and alphaAPPs. Then Gamma-Secretase complex cleaves APP-C83 (CTF) to produce APP-C59 (AICD). These cleavage events do not produce Amyloid beta peptides, and represent non-amyloidogenic pathway. APP processing by BACE1 produces APP-C99 to initiate 'amyloidogenic pathway'. Gamma-Secretase complex cleaves APP-C99 at four different sites and produces a set of peptides including Amyloid beta 40, Amyloid beta 42 (which is hypothesized to initiate the cascade of events resulting in Alzheimer disease [2], [3]) and APP-C59 (AICD). APP-C59 (AICD) participates in intracellular signaling pathways to regulate neurogenesis [4], [5].

Parkinson protein 2, E3 ubiquitin protein ligase (Parkin) ubiqitinates APP and Amyloid beta 42 promoting their degradation [6], [7]. Also, Insulin-degrading enzyme (IDE) cleaves APP, APP-C59 (AICD) and Amyloid beta [8], [9], [10]. Additionally, Amyloid beta is cleaved by Transthyretin [11].

Serpin peptidase inhibitor, clade A (Alpha 1-antitrypsin) and Myelin basic protein associate with Amyloid beta and suppress its activity [12], [13].

Crystallin, alpha B (Alpha crystallin B) binds to the Amyloid beta fibrils inhibiting nucleation-dependent polymerization of amyloid fibrils [14].

Serum amyloid A1 (SAA1) was shown to be a chemotactic ligand for Formyl peptide receptor 2 (FPRL1) [15]. Amyloid beta complexed with FPRL1 can be phagocytosed by mononuclear phagocytes during process of inflammation [16].

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