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Myocardial Infarction in Neonatal Mice, A Model of Cardiac Regeneration
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Myocardial Infarction Predisposes Neurodegenerative Diseases
1Departments of Geriatric Medicine, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, Chengdu, China.
Journal of Alzheimer'S Disease : JAD
|February 18, 2020
Summary
Myocardial infarction (MI) may increase Alzheimer
Area of Science:
- Neuroscience and Cardiovascular Research
- Pathophysiology of Neurodegenerative Diseases
Background:
- Cardiovascular disorders like atherosclerosis and hypertension are linked to increased risk of dementia and Alzheimer's disease (AD).
- The specific impact of myocardial infarction (MI) on AD development remains unclear.
Purpose of the Study:
- To investigate whether myocardial infarction (MI) influences the development of Alzheimer's disease (AD) pathology and cognitive decline.
- To explore the underlying mechanisms linking MI to AD pathogenesis in a mouse model.
Main Methods:
- Myocardial infarction (MI) was induced in wild-type and AD-prone APP/PS1 mice.
- Cognitive functions were assessed using behavioral tests (social recognition, Morris water maze, plus-maze).
- Brain tissues were analyzed for Alzheimer's disease hallmarks, including amyloid-β deposition, tau phosphorylation, reactive oxygen species, and microglial activation.
Main Results:
- MI-treated mice exhibited impaired performance in cognitive and memory tasks compared to controls.
- MI induced increased deposition of amyloid-β and tau protein phosphorylation in the brain.
- MI led to elevated reactive oxygen species and a shift in microglial polarization towards a proinflammatory phenotype.
Conclusions:
- Myocardial infarction (MI) may act as a predisposing factor for Alzheimer's disease (AD) development.
- MI exacerbates key pathological features of AD, including amyloid and tau pathology, and neuroinflammation.
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