2013
DOI: 10.3233/jad-130602
|View full text |Cite
|
Sign up to set email alerts
|

Hyperphosphorylation Results in Tau Dysfunction in DNA Folding and Protection

Abstract: Hyperphosphorylation of tau occurs in preclinical and clinical stages of Alzheimer's disease (AD), and hyperphosphorylated tau is the main constituent of the paired helical filaments in the brains of mild cognitive impairment and AD patients. While most of the work described so far focused on the relationship between hyperphosphorylation of tau and microtubule disassembly as well as axonal transport impairments, both phenomena ultimately leading to cell death, little work has been done to study the correlation… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

1
46
0

Year Published

2014
2014
2023
2023

Publication Types

Select...
6
4

Relationship

2
8

Authors

Journals

citations
Cited by 45 publications
(47 citation statements)
references
References 73 publications
1
46
0
Order By: Relevance
“…Treatment with PNS did not ameliorate the toxic effect of FA ( Figure 6E). Similar to what has been shown previously [25], FA-treated cells grew many short processes and the cell density was significantly decreased (P0.01, n=3) (Figure S2 in Supporting Information). In general, GP and TLJN did not seem to ameliorate the changes in the F-actin morphology induced by FA.…”
Section: Morphology and Cell Numbers Are Restored Following Treatmentsupporting
confidence: 87%
“…Treatment with PNS did not ameliorate the toxic effect of FA ( Figure 6E). Similar to what has been shown previously [25], FA-treated cells grew many short processes and the cell density was significantly decreased (P0.01, n=3) (Figure S2 in Supporting Information). In general, GP and TLJN did not seem to ameliorate the changes in the F-actin morphology induced by FA.…”
Section: Morphology and Cell Numbers Are Restored Following Treatmentsupporting
confidence: 87%
“…In a similar vein, unphosphorylated tau, the major constituent of the neurofibrillary tangle, binds to the minor groove of the DNA double helix where its presence protects DNA from oxidative damage 171,172 . Phosphorylation of tau reduces its ability to prevent DNA thermal denaturation and reduces its protection of DNA from reactive oxygen species 173 . Finally, accumulation of α-synuclein in Parkinson disease is associated with increased mtDNA deletions and oxidative DNA damage 174 .…”
Section: Perspectives and Conclusionmentioning
confidence: 99%
“…In humans, endogenous formaldehyde is typically present in the brain, blood, urine, and other tissues [15,16] . According to the "formaldehyde stress" hypothesis [17] , the abnormal accumulation of endogenous formaldehyde can cause abnormal changes in proteins, resulting in neuronal responses such as tau hyperphosphorylation [18] , DNA damage [19] , reduced long-term potentiation [20] and even cell death [21] , followed by associated dysfunctions. The concentration of endogenous formaldehyde tends toward equilibrium under normal physiological conditions.…”
Section: Introductionmentioning
confidence: 99%