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Published on: March 22, 2016
Alzheimer disease, the two-hit hypothesis: an update.
Xiongwei Zhu1, Hyoung-gon Lee, George Perry
1Department of Pathology, Case Western Reserve University, 2103 Cornell Road, Cleveland, OH 44106, USA. xiongwei.zhu@case.edu
Biochimica Et Biophysica Acta
|December 5, 2006
Summary
Alzheimer's disease may stem from a two-hit hypothesis involving oxidative stress and mitogenic dysregulation. Recent findings support this theory, suggesting it could be a common mechanism in neurodegenerative diseases.
Area of Science:
- Neuroscience
- Pathology
- Biochemistry
Background:
- Single-insult models have limitations in reflecting Alzheimer's disease pathogenesis.
- Previous research focused on oxidative stress and mitogenic signaling pathways.
Purpose of the Study:
- To review and strengthen the proposed two-hit hypothesis for Alzheimer's disease.
- To explore the hypothesis's relevance to other neurodegenerative diseases.
Main Methods:
- Review of recent scientific developments and predictions of the two-hit hypothesis.
- Analysis of potential mechanisms for steady-state achievement in sporadic Alzheimer's disease cases.
Main Results:
- Recent findings confirm key predictions of the two-hit hypothesis.
- New insights into mechanisms underlying sporadic Alzheimer's disease have emerged.
Conclusions:
- The two-hit hypothesis, involving oxidative stress and mitogenic dysregulation, is strengthened by recent evidence.
- This hypothesis may represent a common pathogenic mechanism for neurodegenerative diseases.
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