Amyloid Beta Proteins are fragments of protein cleaved from a larger protein known as Amyloid Precursor Protein (APP). They are naturally produced by metabolically active neurons and are critical in synaptic function and signaling when in their soluble, monomeric form. However, misfolding and aggregation into insoluble plaques are characteristic pathological hallmarks observed in neurodegenerative conditions. Maintaining a proper balance of production and clearance is essential for neuronal health and cognitive longevity.
Origin
The term combines “amyloid,” referring to a proteinaceous deposit, and “beta,” denoting the specific cleavage site on the parent APP molecule. This protein family is intrinsically linked to fundamental cellular processes within the central nervous system. Its discovery and subsequent research illuminated crucial pathways in brain aging and disease.
Mechanism
Amyloid beta peptides are generated through the sequential cleavage of APP by beta-secretase and gamma-secretase enzymes. During wakefulness, the production rate often exceeds the clearance rate, leading to a net accumulation. Effective clearance, primarily facilitated by the glymphatic system during sleep, is required to prevent the transition from soluble monomers to toxic oligomers and plaques that impair synaptic plasticity and neuronal communication.
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