, Ghetti B There is considerable interest in the pathobiology of tau protein, given its potential role in neurodegenerative diseases and aging. , Wegmann acknowledged that there is more work to do, but noted that the increase in thioflavin S fluorescence was likely too great to be explained by rotational or vibration effects. Uryu K (2018) Sequential stages and distribution patterns of aging-related tau astrogliopathy (ARTAG) in the human brain. Schmitt FA Wegmann showed that at concentrations as low as 1.5 μM, the same range as in neurons, tau formed liquid droplets in vitro in the presence of crowding agents. , Hoffman SW Fulham MJ , Tau prions have yet to be re-derived and re-injected with phenotypic changes in subsequent passages, separating tau prions from conventional prion disease. Kwong LK Kadavath H, Jaremko M, Jaremko Ł, Biernat J, Mandelkow E, Zweckstetter M. , (2013) Amyloids and yeast prion biology. , In keeping with this idea, Wegmann reported that hexane1,6-diol, which destabilizes β-sheet structures, blocked tau liquid-liquid phase transitions. , IOS Press, Inc. Daneshvar DH , Kamboh MI Arendt T Kohler K Del Tredici K Martinez-Lage P Causal assertions from epidemiological studies remain hypothetical, however. Maeda S , Acta Neuropathol 130, 877–889. [221] studied 75 severely head-injured patients and found that patients often had dementia from TBI, with few surviving more than a decade. P-tau in postmortem brain may tend toward buried epitopes, insolubility, and limited biological meaning. This again suggests that the most readily identifiable postmortem lesions detected by immunohistochemistry may be the least biologically relevant. , , (2014) Tau mRNA is present in axonal RNA granules and is associated with elongation factor 1A. J Neurochem 105, 833–841. , , , , Hammond F It is noteworthy that classic studies of dementia pugilistica (DP) describe neurofibrillary degeneration in a similar distribution [174], which raises the possibility of coincidental p-tau pathology. , Interestingly, PART is a mixed 3R/4R tauopathy whereas ARTAG is a 4R tauopathy, suggesting some degree of cell type specificity. McKee A From Old Frisian twā. Schneider JA Mehrabian M Necula M Studies increasingly suggest a role for physiologic tau phosphorylation in synaptic function [59]. , Andreadis A Sahara N Select this link to jump to navigation, In navigation section. Galvin J The TBI component of the equation itself presents a significant challenge for study. , Ross CA , , “The low-complexity prion domain may be an evolutionary invention to protect the C terminal from aggregation under times of duress,” said Alberti. Hager H Acta Neuropathol 126, 537–544. Liu WK , Poyhonen M , , Cantu RC , , Baker A In fact, a paper from Anthony Hyman’s group bears this out. , Abramowski S , Freeman-Browne D Braak H Int J Mol Sci 17, pii: E189. Wegmann wondered if, in effect, the low-complexity domain acts like an internal chaperone, preventing the C terminal domain from aggregating. Tau phosphorylation by cyclin dependent kinases and mitogen activated protein kinases [103–105], emphasize the role of tau metabolism in cellular division and proliferation. (2002) What does it mean to be natively unfolded? Borisy , , Brain tissue interpretation may require expensive, labor-intensive research methodology that has yet to be validated for diagnostic purposes. , , Spires-Jones TL , Philos Trans R Soc B Biol Sci 369, 20130144. , , Giaccone G , PLoS Biol. Whether fibrillar or PHF tau signifies cytotoxicity, versus a productive response to the aging process or cellular stress, remains an open question [138]. Kalimo H Mukrasch MD, Bibow S, Korukottu J, Jeganathan S, Biernat J, Griesinger C, Mandelkow E, Zweckstetter M. , Nunomura A , Do Membraneless Organelles Host Fibril Nucleation? , , Klein M , (2015) Tau post-translational modifications in wild-type and human amyloid precursor protein transgenic mice. , Harris PLR Carlson GA Damianich A Sharma AM Mann DMA

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