Explore
The Metabolic-Inflammatory Axis in Brain Aging and Neurodegeneration
0 Ungluers have
Faved this Work
Login to Fave
Impairment of energy metabolism is a hallmark of brain aging and several neurodegenerative diseases, such as the Alzheimer’s disease (AD). Age- and disease-related hypometabolism is commonly associated with oxidative stress and they are both regarded as major contributors to the decline in synaptic plasticity and cognition. Neuroinflammatory changes, entailing microglial activation and elevated expression of inflammatory cytokines, also correlate with age-related cognitive decline. It is still under debate whether the mitochondrial dysfunction-induced metabolic deficits or the microglia activation-mediated neuroinflammation is the initiator of the cognitive changes in aging and AD. Nevertheless, multiple lines of evidence support the notion that mitochondrial dysfunction and chronic inflammation exacerbate each other, and these mechanistic diversities have cellular redox dysregulation as a common denominator. This research topic focuses on the role of a metabolic-inflammatory axis encompassing the bioenergetic activity, brain inflammatory responses and their redox regulation in healthy brain aging and neurodegenerative diseases. Dynamic interactions among these systems are reviewed in terms of their causative or in-tandem occurrence and how the systemic environment, –e.g., insulin resistance, diabetes, and systemic inflammation–, impacts on brain function.
This book is included in DOAB.
Why read this book? Have your say.
You must be logged in to comment.
Rights Information
Are you the author or publisher of this work? If so, you can claim it as yours by registering as an Unglue.it rights holder.Downloads
This work has been downloaded 84 times via unglue.it ebook links.
- 33 - mobi (CC BY) at Unglue.it.
- 25 - epub (CC BY) at Unglue.it.
- 26 - pdf (CC BY) at Unglue.it.
Keywords
- Alzheimer's disease
- Brain aging
- diabetes
- Energy Metabolism
- Mitochondria
- neurodegeneration
- neuroinflammation
- Perimenopause
- redox homeostasis
Links
DOI: 10.3389/978-2-88945-253-8Editions