Aging and Age-related Disease Research

Advancing aging research with precision genomics

BreakSight® provides cutting-edge tools to map and sequence DNA double-strand breaks, shedding light on the genomic instability that drives aging and age-related diseases.

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Why BreakSight?

Pinpoint where and why breaks occur during the aging process

Genomic instability lies at the root of multiple age-related diseases: in neurons (neurodegeneration), vascular cells (atherosclerosis, stiffness), immune cells (immunosenescence), and proliferative tissues (cancer). The cumulative burden of DNA lesions, mutations, and misrepair underlies much of age-associated decline.

With DNA damage being a central driver of aging and age-related disease, integrating BreakSight’s genome-wide break-mapping capabilities into research workflows can move the field from measuring aggregate damage to pinpointing where and why breaks occur — accelerating discovery of biomarkers, mechanisms, and interventions that promote healthy longevity.

Illustration representing DDsite technology for genomic instability analysis

Chart age-dependent break landscapes

Compare DNA break sites between young vs old tissue cells or model organisms. Chart changes in breakage frequency, genomic location, and motif biases with aging.

Monitor the effect of anti-aging treatments

Assess interventions that modulate DNA damage and delve into the mechanisms of developing treatments on DNA damage burden and repair efficacy. Quantify how the break landscape shifts as a function of treatment.

Discover genomic aging biomarkers and therapeutic targets

Gain actionable insights on DNA sequence vulnerabilities across the genome and pinpoint patterns of loci that correlate breakage with functional decline. Uncover specific DNA motifs or structural elements whose breakage correlates with disease phenotypes.

Connect break profiles to downstream functional outcomes

By correlating DNA break sites with transcriptomic, epigenomic, and chromatin data, one can infer how persistent DNA breaks may influence gene regulation, chromatin architecture, and cell fate. Dissect how the absence of certain repair mechanisms shifts break patterns, revealing mechanistic dissection of aging acceleration.

Ready to transform your aging research?

Release the full potential of the genome to advance age-related disease research and improve patient outcomes.

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