Decoding Aging And Neurodegeneration

Decoding Aging and Neurodegeneration

This book focuses on the close relationship between aging and neurodegeneration. By highlighting the reversible nature of epigenetic changes, it provides a comprehensive overview of how these modifications can regulate gene expression without altering the DNA sequence, offering promising solutions for clinical intervention. Aging induces a gradual decline in cerebral function, leading to cognitive impairment, memory loss, motor dysfunction, and eventually functional decline and death. It is accompanied by the decline of organismal functions induced by whole genome alterations leading to neurodegeneration. Epigenetic modifications, including chromatin modifications, DNA methylation, and changes in regulatory RNAs, have a major impact on neurodegenerative disorders such as Alzheimer's disease, Parkinson's disease, and Huntington's disease. The chapters in this book address critical issues such as the contribution of epigenetic mechanisms to aging, the interaction between genetic and environmental factors in neurodegeneration, and the potential for epigenetic therapies to delay aging and mitigate disease progression. This volume, part of the RNA Technologies book series, is an invaluable resource for researchers and advanced students in genetics and neuroscience. It provides a deep understanding of the molecular basis of neurodegenerative diseases and offers innovative strategies to address the challenges of aging and neurodegeneration.

Protein Misfolding and Proteostasis Impairment in Aging and Neurodegeneration: From Spreading Studies to Therapeutic Approaches

The Metabolic-Inflammatory Axis in Brain Aging and Neurodegeneration

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.