Abstract
The pathological hallmarks of Alzheimer’s disease (AD) are extracellular β-amyloid deposition and intracellular tau inclusions. While β-amyloid deposition does not correlate with clinical progression of AD, the diffusion of neurofibrillary tangles (NFTs) from the entorhinal cortex to the neocortex, followed by neuronal and synapse loss, matches well with the clinical progression of AD symptomatology. Therefore, blocking the formation of NFTs is considered to be a promising approach to halt the progression of AD dementia.
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Takashima, A. (2015). Toxic Tau Aggregation in AD. In: Vlamos, P., Alexiou, A. (eds) GeNeDis 2014. Advances in Experimental Medicine and Biology, vol 822. Springer, Cham. https://doi.org/10.1007/978-3-319-08927-0_2
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DOI: https://doi.org/10.1007/978-3-319-08927-0_2
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