Since its discovery in 1984, the beta amyloid peptide has treaded the boards of
neurosciences as the star molecule in Alzheimer’s disease pathogenesis. In the last decade, however,
this vision has been challenged by evidence-based medicine showing the almost complete failure of
clinical trials that experimented anti-amyloid therapies with great hopes. Moreover, data have
accumulated which clearly indicate that this small peptide plays a key role in the physiological
processes of memory formation. In the present review, we will discuss the different aspects of the
amyloid cascade hypothesis, highlighting its pros and cons, and we will analyse the results of the
therapeutic approaches attempted to date that should change the direction of Alzheimer’s disease
research in the future.
Keywords: Alzheimer's disease, beta amyloid, clinical trials, LTP, memory, anti-amyloid therapy.
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