Aging, Cancer, and Neurodegenerative Diseases

Aging, cancer, and neurodegenerative diseases represent significant challenges to human health, sharing common biological mechanisms that reflect the progressive decline in cellular and tissue function over time. These hallmark processes include genomic instability, which arises from accumulated DNA damage, and epigenetic alterations that disrupt gene expression and cellular identity, contributing to cellular dysfunction. Mitochondrial dysfunction is also central to these conditions, as they disrupt energy production and metabolic balance. Chronic inflammation, often driven by persistent immune activation and oxidative stress, exacerbates tissue damage and disease progression. Cellular senescence is characterized by an irreversible growth arrest and the secretion of pro-inflammatory factors known as the senescence-associated secretory phenotype (SASP). While initially protective, the accumulation of senescent cells over time disrupts tissue homeostasis and promotes chronic inflammation. Understanding these hallmark processes and their interplay can offer new potential targets for therapeutic interventions aimed at mitigating age-related diseases and improving quality of life across the lifespan.

The goal of this Research Topic is to understand the molecular and cellular mechanisms underlying aging, cancer, and neurodegenerative diseases, focusing on how age-related cellular dysfunction, accumulation of DNA damage, and altered immune responses contribute to cancer initiation and progression. The topic aims to identify potential biomarkers and therapeutic targets to prevent or treat age-related cancers, ultimately improving cancer outcomes in older populations.

This Research Topic invites original research, reviews, and perspective articles focused on the intricate relationship between aging, cancer, and neurodegenerative diseases. These conditions share common biological mechanisms, such as DNA damage accumulation, mitochondrial dysfunction, chronic inflammation, and cellular senescence, all of which contribute to cellular and tissue dysfunction over time. Authors are encouraged to explore how these processes intersect at the molecular and cellular levels, providing insights into their roles in disease development and progression. Contributions that discuss therapeutic strategies targeting key mechanisms, such as DNA repair, epigenetic regulation, mitochondrial function, and inflammation, are particularly welcome. The goal is to identify novel approaches that could mitigate the effects of aging and offer new treatments for cancer and neurodegenerative diseases, ultimately improving human health and longevity.

Article types and fees

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Clinical Trial
• Data Report
• Editorial
• FAIR² Data
• FAIR² DATA Direct Submission
• General Commentary
• Hypothesis and Theory
• ... View all formats

Articles that are accepted for publication by our external editors following rigorous peer review incur a publishing fee charged to Authors, institutions, or funders.

Article types

This Research Topic accepts the following article types, unless otherwise specified in the Research Topic description:

• Brief Research Report
• Case Report
• Clinical Trial
• Data Report
• Editorial
• FAIR² Data
• FAIR² DATA Direct Submission
• General Commentary
• Hypothesis and Theory
• Methods
• Mini Review
• Opinion
• Original Research
• Perspective
• Review
• Systematic Review
• Technology and Code

Keywords: DNA damage, Mitochondrial Dysfunction, Cellular Senescence, Inflammation, Inflammaging

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.