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This creates a massive cytorheological gradient of free cytoplasmic norepinephrine, which is subsequently extruded into the synaptic cleft via transporter-mediated reverse transport (facilitated exchange diffusion) through NET (Solanki et al, 2014)

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According to the A-tau interaction hypothesis, A and tau pathology, which results in synaptic dysfunction, neuronal death, and cognitive impairment (96), is determined by the intrinsic interaction with A and tau (A42 enhances tau phosphorylation, truncation, and aggregation, while tau can increase A synthesis)

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