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Brain Aging: Hsp90 and Neurodegenerative Diseases
Kun Wang1,2,3, Yu Shang1,2,3, Fei Dou4,5,6
1State Key Laboratory of Cognitive Neuroscience and Learning & IDG/McGovern Institute for Brain Research, College of Life Sciences, Beijing Normal University, Beijing, China.
Advances in Experimental Medicine and Biology
|September 21, 2018
Summary
Brain aging impairs heat shock protein function, disrupting protein balance and leading to neurodegenerative diseases. This review explores mechanisms like transcriptional changes and cell communication in brain aging.
Area of Science:
- Neuroscience
- Molecular Biology
- Aging Research
Background:
- The brain, central nervous system's core, lacks regeneration, making age a key risk for irreversible neurodegenerative diseases.
- Impaired molecular chaperone, primarily heat shock proteins, function contributes to brain aging by causing protein homeostasis imbalance.
Purpose of the Study:
- To review the mechanisms behind heat shock protein functional decline during brain aging.
- To elucidate the molecular and cellular factors contributing to age-related cognitive impairment.
Main Methods:
- Literature review focusing on mechanisms of heat shock protein impairment.
- Analysis of transcriptional regulation, posttranslational modifications, and intercellular communication in brain aging.
Main Results:
- Heat shock protein function is compromised through various regulatory pathways during brain aging.
- Dysregulation at transcriptional, posttranslational, and intercellular levels impacts protein homeostasis.
Conclusions:
- Understanding these mechanisms is crucial for addressing age-related cognitive decline and neurodegeneration.
- Targeting heat shock protein function may offer therapeutic strategies for brain aging.
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