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Differential dynamics of Aβ and tau oligomer synaptic binding may suggest diverse therapeutic targets for early vs. late Alzheimer's disease

At the basis of the Alzheimer’s Disease (AD) cognitive decline there is the targeting of synapses by small Ab and tau oligomers, which results in synaptic dysfunction and later disruption that underscore disease progression. Recent failures of Aβ‐directed therapeutics in multi‐center clinical trials suggest that Ab may not be playing a critical role in later disease stages, when clinical features of AD become manifest; rather, tau, which occurs later in the AD brain, may be the primary synaptotoxic element at that advanced stage. While attention is being currently given to the development of tau‐directed therapies for clinical AD, the mechanisms by which tau becomes the prevalent driver of synaptic dysfunction at later disease stages is still unknown.