The phrase "alteration of tau" is correct and usable in written English.
It can be used in contexts related to changes or modifications involving the term "tau," which may refer to a variable, a concept in science, or a specific subject matter.
Example: "The alteration of tau in the experiment led to unexpected results that required further investigation."
Alternatives: "modification of tau" or "change in tau".
Understanding the precise molecular mechanisms underlying this pathological alteration of tau is critical to identify novel and effective neurotherapeutics for the treatment of AD and other tauopathies.
The results presented here support a plethora of data that show phosphorylation can affect tau toxicity but demonstrate that alteration of tau phosphorylation state is not required to modify tau toxicity.
Alteration of tau, p-tau (Ser396, Ser404, and Ser202/Thr205), GSK3β and CDK5 were either intermediate or consequent events in TSE pathogenesis and proposed the potential linkage of these bioactive proteins with the pathogenesis of prion diseases.
Furthermore, the above described alterations of tau and Aβ42 were highly significant both in AD patients with low and high scores on MMSE at baseline, when compared to the healthy controls (data not shown).
The folding of Tau into a paperclip-like structure, recognized by MC1 antibodies, occurs when the amino acids at residues 7 9 interact with residues 312 342, and is one of the earliest pathological alterations of Tau in Alzheimer disease, preceding the formation of neurofibrillary tangles in AD [48].
Alterations of tau and kinases in the brains of TSE animals during pathogenicity may consist of a complicate network.
Moreover, pathological alterations of tau are most likely not the result of a single post-translational modification, but instead a combination of structural and functional alterations that may ultimately contribute to determine tau pathogenicity.
These results indicate that iAβO-induced spine alteration is independent of tau.
We showed that iAβO-induced spine alteration is independent of tau (Fig 4), but it is unknown if this tau-independence extends to other cellular mechanisms such as intracellular transport.
In our study, however, we did not observe a significant alteration of phosphorylated levels of tau at serine-202 at the 1-week time point.
The link that has been postulated in the cascade hypothesis between the alteration of APP metabolism and tau accumulation has not been reproduced, and the reason for this failure is still unknown.
