Are antibodies directed against amyloid-β (Aβ) oligomers the last call for the Aβ hypothesis of Alzheimer’s disease?

Written by Francesco Panza, Madia Lozupone, Vittorio Dibello, Antonio Greco, Antonio Daniele, Davide Seripa, Giancarlo Logroscino & Bruno P Imbimbo

Alzheimer’s disease (AD) is a devastating and incurable age-related neurodegenerative disorder with a long presymptomatic period. The accumulation of the amyloid-β (Aβ) peptide in the brain is believed to be the initial event of the AD process and starts 15–20 years before clinical symptoms occur. During the last 20 years, several compounds were designed to decrease the levels of monomeric, oligomeric, aggregates and Aβ plaques. Drugs have been developed and shown to decrease the Aβ production, antagonize Aβ aggregation or increase Aβ brain clearance. Unfortunately, all these drugs, including Aβ aggregation inhibitors (tramiprosate, scyllo-inositol, PBT2), Aβ antigens (AN-1792, vanutide, AD02, CAD-106), anti-Aβ...

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