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Alzheimer’s disease (AD) is a neurodegenerative disease and the most common form of dementia, characterized by the overproduction and accumulation of different amyloidβ peptide peptides (Aβ) within different areas in the brain conducting to memory loss and dementia. The Aβ cascade hypothesis of AD was originally proposed by Selkoe in 1991 by the theory that accumulation of Aβ42 is the initial trigger for neurodegenera‐ tion. The Aβ cascade hypothesis assumes that changes in the production or accumula‐ tion of Aβ are responsible for AD pathology. Different Aβ clearance mechanisms are also affected by AD pathology. Studies from the past years have revealed that the blocking of Aβ production is not effective for reducing the brain Aβ levels. However, the relevance of Aβ clearance in AD, especially in late-onset sporadic AD (LOAD), has been height‐ ened, and the study of the Aβ clearance mechanisms has elucidated new possible therapeutic targets. This chapter summarizes recent data underlying the idea of the reduced Aβ clearance and subsequent Aβ spread in AD. We discuss the Aβ clearance mechanisms altered in AD, and the Aβ clearance through autophagy in more detail, a more recent mechanism proposed, and the new strategies to eliminate Aβ42 inducing autophagy.

Beta Amyloid Peptides: Extracellular and Intracellular Mechanisms of Clearance in Alzheimer’s Disease