Publications by authors named "Emmy Sakakibara"
Article Synopsis
- - Dual specificity protein phosphatase 6 (DUSP6) is important in regulating late-onset Alzheimer's disease (AD), with lower DUSP6 levels linked to worse dementia ratings in humans and decreased levels observed in a mouse model of the disease.
- - Researchers injected AAV5-DUSP6 into the brains of 5xFAD mice to increase DUSP6 expression and found that it improved memory deficits and reduced amyloid plaques in male mice but not in female mice, while also decreasing microglial activation in both sexes.
- - Although DUSP6 overexpression helped reduce neuroinflammation and activated microglia in both male and female mice, the improvement in memory was sex-dependent, indicating different underlying mechanisms
Background: Dual specificity protein phosphatase 6 (DUSP6) was recently identified as a key hub gene in a causal network that regulates late-onset Alzheimer's disease. Importantly, decreased DUSP6 levels are correlated with an increased clinical dementia rating in human subjects, and DUSP6 levels are additionally decreased in the 5xFAD amyloidopathy mouse model.
Methods: AAV5-DUSP6 or AAV5-GFP (control) were stereotactically injected into the dorsal hippocampus (dHc) of female and male 5xFAD or wild type mice to overexpress DUSP6 or GFP.
Recent multiscale network analyses of banked brains from subjects who died of late-onset sporadic Alzheimer's disease converged on (non-acronymic) as a key hub or driver. Within this computational network, we identified the dual-specificity protein phosphatase 4 () [also known as mitogen-activated protein kinase (MAPK) phosphatase 2] as an important node. Importantly, gene expression, like that of , is downregulated in postmortem Alzheimer's disease (AD) brains.
View Article and Find Full Text PDFRecent studies suggest that bioactive dietary polyphenol preparation (BDPP) and individual polyphenolic compounds ameliorate stress-induced depression-like behaviors, but the underlying molecular mechanisms are incompletely understood. VGF (non-acronymic) in the dorsal hippocampus (dHc) has been shown to play a role in depression-like behaviors and antidepressant efficacy, and the VGF-derived peptide TLQP-62 (named by the N-terminal 4 amino acids and length) infused into dHc has been shown to have antidepressant efficacy that is BDNF-TrkB dependent. Here, we investigated whether BDPP influences VGF expression in the dHc, and whether dHc VGF is required for BDPP antidepressant efficacy.
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