A decisive factor in the progression of AD and the development of manifest cognitive disorders is the functional failure of the Tau protein due to its hyperphosphorylation at different sites of the molecule (e.g. p-tau 181 or p-tau 217). As mentioned at various points in the updates here, this change in the phosphorylation pattern of the Tau molecule is a process that is apparently modified or even initiated by lifestyle over time.
Tau regulation takes place during sleep, see above under The role of sleep & EEG and there (Holth & Fritschi, 2019). Irregularities in sleep caused by tau regulation in AD can be measured by EEG. An early AI-based prediction of AD is highly probable by EEG together with the new blood tests currently being developed in the Swedish BIOFINDER study, the reliability of which has been validated, which allow a differentiated detection of phosphorylations of the tau protein in Alzheimer's patients, see (Janelidze, 2020) and (Palmqvist, 2020), and by detecting this harbinger of later possible Alzheimer's dementia, a very early diagnosis and prognosis with an appropriate therapy, e.g. Gamma Entrainment, is possible.
- Janelidze, S., Mattson, N., Palmqvist, S., Smith, R., Beach, Th.G., Serrano, G.E., Chai, X., Proctor, N.K., Eichenlaub, U., Zetterberg, H., Blennow, K., Reiman, E.M., Stomrud, E., Dage, J.L., Hansson, O., (2020), Plasma P-tau181 in Alzheimer’s disease: relationship to other biomarkers, differential diagnosis, neuropathology and longitudinal progression to Alzheimer’s dementia. Nature Medicine, https://www.nature.com/articles/s41591-020-0755-1