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Thank you for visiting nature. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Further, higher soluble p-tau concentrations are mainly related to faster accumulation of tau aggregates in the regions with strong functional connectivity to individual tau epicenters.
In this early stage, higher soluble p-tau concentrations is associated with cognitive decline, which is mediated by faster increase of tau aggregates. Our data suggest that therapeutic approaches reducing soluble p-tau levels might be most favorable in early AD, before widespread insoluble tau aggregates.
Among the earliest tau-related abnormalities in AD are increases in soluble hyperphosphorylated tau p-tau concentrations, which can reliably be detected in cerebrospinal fluid CSF 1 and precede the neocortical deposition of insoluble fibrillary tau pathology in AD 6 , 7 , 8.
Recent studies could show that levels of p-tau start increasing already at the preclinical stage of AD when persons are asymptomatic 11 , increase even further in early symptomatic AD and reach a plateau in patients with AD dementia 12 , Importantly, levels of soluble p-tau have been shown to correlate with neuropathological levels of insoluble fibrillar tau 14 , 15 , 16 , and preclinical studies found that soluble hyperphosphorylated p-tau seeds can induce a cascade of tau aggregation in animal models 4 , 17 , 18 , Therefore, increases in soluble p-tau may drive subsequent tau aggregation and spread in AD, suggesting p-tau as a potential treatment target to halt tau spread and the formation of toxic insoluble tau aggregates.
