| id |
c6211a75-83e7-4d05-aa2e-396e576cf3ad |
| user_id |
8684964a-bab1-4235-93a8-5fd5e24a1d0a |
| job_id |
vzblqkgd-9030 |
| base_model_name |
xevyo |
| base_model_path |
/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf... |
| model_name |
longevity by preventing |
| model_desc |
longevity by preventing the age |
| model_path |
/home/sid/tuning/finetune/backend/output/vzblqkgd- /home/sid/tuning/finetune/backend/output/vzblqkgd-9030/merged_fp16_hf... |
| source_model_name |
xevyo |
| source_model_path |
/home/sid/tuning/finetune/backend/output/xevyo-bas /home/sid/tuning/finetune/backend/output/xevyo-base-v1/merged_fp16_hf... |
| source_job_id |
xevyo-base-v1 |
| dataset_desc |
This scientific paper, published in PLOS Biology ( This scientific paper, published in PLOS Biology (2025), investigates how removing the protein Maf1—a natural repressor of RNA Polymerase III—in neurons can significantly extend lifespan and improve age-related health in Drosophila melanogaster (fruit flies). The study focuses on how aging reduces the ability of neurons to perform protein synthesis, and how reversing this decline affects longevity.
Core Scientific Insight
Maf1 normally suppresses the production of small, essential RNA molecules (like 5S rRNA and tRNAs) needed for building ribosomes and synthesizing proteins. Aging decreases protein synthesis in many tissues including the brain. This study shows that removing Maf1 specifically from adult neurons increases Pol III activity, boosts production of 5S rRNA, maintains protein synthesis, and ultimately promotes healthier aging and longer life.
Major Findings
Knocking down Maf1 in adult neurons extends lifespan, in both female and male flies, with larger effects in females.
Longevity effects are cell-type specific: extending lifespan works via neurons, not gut or fat tissues.
Neuronal Maf1 removal:
Delays age-related decline in motor function
Improves sleep quality in aged flies
Protects the gut barrier from age-related failure
Aging naturally causes a sharp decline in 5S rRNA levels in the brain. Maf1 knockdown prevents this decline.
Maf1 depletion maintains protein synthesis rates in old age, which normally fall significantly.
Longevity requires Pol III initiation on 5S rRNA—genetically blocking this eliminates the life-extending effect.
The intervention also reduces toxicity in a fruit-fly model of C9orf72 neurodegenerative disease (linked to ALS and FTD), highlighting potential therapeutic importance.
Biological Mechanism
Removing Maf1 → increased Pol III activity → restored 5S rRNA levels → increased ribosome functioning → maintained protein synthesis → improved neuronal and systemic health → extended lifespan.
Broader Implications
The study challenges the long-standing assumption that reducing translation always extends lifespan. Instead, it reveals a cell-type–specific benefit: neurons, unlike other tissues, require sustained translation for healthy aging. The findings suggest similar mechanisms may exist in mammals, potentially offering insights into combatting neurodegeneration and age-related cognitive decline.... |
| dataset_meta |
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| dataset_path |
/home/sid/tuning/finetune/backend/output/vzblqkgd- /home/sid/tuning/finetune/backend/output/vzblqkgd-9030/data/vzblqkgd-9030.json... |
| training_output |
null |
| status |
completed |
| created_at |
1764881164 |
| updated_at |
1764889789 |
| source_adapter_path |
NULL |
| adapter_path |
/home/sid/tuning/finetune/backend/output/vzblqkgd- /home/sid/tuning/finetune/backend/output/vzblqkgd-9030/adapter... |
| plugged_in |
False |