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Telomerase Activity in the Various Regions of Mouse Brain: Non-Radioactive Telomerase Repeat Amplification Protocol TRAP Assay
Published on: September 2, 2014
Panic disorder aging characteristics: The role of telomerase reverse transcriptase gene and brain function
Huachen Ding1,2, Yuan Zhong3, Na Liu1,4
1Nanjing Brain Hospital Affiliated to Nanjing Medical University, Nanjing, China.
Panic disorder (PD) is linked to accelerated aging. Lower methylation of the TERT gene in PD patients correlates with memory and social function decline, suggesting TERT as a potential biomarker for PD aging.
Area of Science:
- Neuroscience
- Genetics
- Aging Research
Background:
- Panic disorder (PD) causes significant disability and accelerates aging.
- The molecular mechanisms linking PD, aging, and cognitive/social deficits are unclear.
- Telomerase reverse transcriptase (TERT) and telomere length (TL) are implicated in both aging and PD.
Purpose of the Study:
- To investigate the relationship between TERT gene expression, DNA methylation, and aging characteristics in PD.
- To explore the role of TERT in memory and social function within the context of PD-related aging.
Main Methods:
- Utilized TERT gene knockout mice to assess memory acquisition.
- Analyzed DNA methylation levels of the human TERT (hTERT) gene in PD patients and controls.
- Employed Regional Homogeneity (ReHo) analysis to examine brain function related to hTERT methylation and social function.
Main Results:
- TERT knockout mice showed impaired recent fear memory acquisition.
- PD patients exhibited significantly lower hTERT gene methylation compared to healthy controls.
- Decreased CpG methylation in the hTERT promoter region correlated with PD clinical characteristics.
- hTERT methylation influenced social function by modulating left postcentral gyrus activity.
Conclusions:
- The hTERT gene plays a crucial role in the pathological basis of PD-related aging.
- hTERT methylation may serve as a valuable biomarker for assessing accelerated aging in PD.
- Findings provide evidence for the genetic and pathological mechanisms underlying PD and its aging features.
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