1
The levels of phosphorylated tau and caspase-cleaved tau were reduced by the ROCK inhibitors.
2
There was a modest reduction in phosphorylated tau in the cortex of P301S mice.
3
At the cellular level, diffuse staining for phosphorylated tau was detected in neurons with GVDs.
4
We show that Balpha specifically and markedly facilitates dephosphorylation of the phosphorylated Tau in our reconstituted assay.
5
We previously reported that pitavastatin decreases the total and phosphorylated tau protein using a cellular model of tauopathy.
6
However, in schizophrenia brain, MAPK- phosphorylated tau was unchanged compared to matched controls, despite similar expression levels to those in AD.
7
Significantly, analysis of secondary progressive multiple sclerosis brain tissue also revealed abnormally phosphorylated tau and the formation of insoluble tau.
8
Immunohistochemical analysis for phosphorylated tau protein revealed reduced staining in the frontal cortex, hippocampus, and striatum in animals treated with TA.
9
In addition, the accumulation of abnormally phosphorylated tau as soluble toxic oligomers and as neurofibrillary tangles is an essential part of the pathology.
10
In addition the accumulation of abnormally phosphorylated tau as soluble toxic oligomers and as neurofibrillary tangles is a critical part of the pathology.
11
It is characterized by the accumulation of amyloid β peptides and abnormally phosphorylated tau proteins that are associated with cognitive decline and dementia.
12
Results: The number of neurons with GVDs significantly increased with the level of phosphorylated tau accumulation in the hippocampal regions in non-AD neurodegenerative disorders.
13
Importantly, results from both tasks indicated that higher levels of tau and phosphorylated tau pathologies were associated with block-level overactivations of attentional control areas.
14
Moreover, deposits of abnormally phosphorylated tau that form soluble toxic oligomers and then accumulate as neurofibrillary tangles are an essential part of AD pathology.
15
The hallmark changes in AD include plaques, beta amyloid protein, neurofibrillary tangles, phosphorylated tau protein, and memory loss-all changes that can be caused by mercury.
16
Several lines of evidence have suggested that GVDs appear within hippocampal pyramidal neurons in AD when phosphorylated tau begins to aggregate into early-stage neurofibrillary tangles.