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Updated: Feb 3, 2026

Analysis of β-Amyloid-induced Abnormalities on Fibrin Clot Structure by Spectroscopy and Scanning Electron Microscopy
Published on: November 30, 2018
Methamphetamine exposure induces neuropathic protein β-Amyloid expression
Lingling Chen1, Pengfei Yu2, Li Zhang1
1Children's Hospital of Nanjing Medical University, 72 Guangzhou Road, Nanjing, Jiangsu 210029, China; Key Lab of Modern Toxicology (NJMU), Ministry of Education, Department of Toxicology, School of Public Health, Nanjing Medical University, 101 Longmian Avenue, Nanjing, Jiangsu 211166, China.
Abstract:
Methamphetamine (METH) abusing contributes to dopaminergic neurons degeneration, resulting inParkinson's disease (PD)-like changes. More recently, the association between METH exposure and the Alzheimer's disease (AD)-like changes gained more attention, however, the underlying mechanisms remain poorly understood. In the present study, we aimed to investigate whether METH exposure promotes the formation of Aβ42, one of the key AD-like pathological proteins. With the cell model PC-12 cell line, it showed that METH treatment significantly increased the level of the precursor protein APP and its hydrolysates CTFs expression in a dose-dependent manner. In parallel, with the ELISA assay, we found that METH exposure contributed to an obvious elevation of the Aβ1-42 excretion in the cell culture supernatant. Therefore, we examined the expression of p-GSK3α and BACE-1, which were responsible for APP and Aβ1-42 generation respectively, it suggested in that METH obviously activated the p-GSK3α and increased the level of BACE-1, and the expression of BACE-1 was also detected by the immunofluorescence, with the significant elevation of the BACE-1 fluorescence intensity. In conclusion, METH treatment promotes the expression of Aβ precursor protein APP and its hydrolysis product CTFs and Aβ1-42, and p-GSK3α as well as BACE-1 may be involved in this process.
Insights
Methamphetamine (METH) use increases Alzheimer
Area of Science:
- Neuroscience
- Toxicology
- Cell Biology
Background:
- Methamphetamine (METH) abuse is linked to Parkinson's disease-like neurodegeneration.
- Emerging evidence suggests METH exposure may also induce Alzheimer's disease (AD)-like changes.
- The precise mechanisms underlying METH's association with AD pathology are not well understood.
Purpose of the Study:
- To investigate if METH exposure promotes the formation of amyloid-beta 42 (Aβ42), a key pathological protein in AD.
- To explore the molecular pathways involved in METH-induced Aβ42 production.
Main Methods:
- Utilized the PC-12 cell line as a cellular model for METH exposure.
- Quantified levels of amyloid precursor protein (APP) and its C-terminal fragments (CTFs) using dose-dependent METH treatment.
- Measured Aβ1-42 levels in cell culture supernatant via ELISA assay.
- Assessed the expression and activity of p-GSK3α and BACE-1, key enzymes in APP processing and Aβ generation.
- Visualized BACE-1 expression using immunofluorescence.
Main Results:
- METH treatment significantly increased APP and CTFs expression in a dose-dependent manner.
- METH exposure led to a marked elevation of Aβ1-42 in the cell culture supernatant.
- METH activated p-GSK3α and increased the expression of BACE-1.
- Immunofluorescence confirmed a significant elevation in BACE-1 fluorescence intensity.
Conclusions:
- METH treatment promotes the expression of APP, CTFs, and Aβ1-42.
- The molecular players p-GSK3α and BACE-1 are implicated in METH-induced Aβ production.
- These findings suggest a potential link between METH abuse and Alzheimer's disease-like pathology.
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