The Fairbairn Menstruation Science Fund will advance groundbreaking research at MIT on the function of the human uterus and its impact on sex-based differences in human immunology that contribute to gynecological disorders such as endometriosis, as well as other chronic systemic inflammatory diseases that disproportionately affect women, such as Lyme disease and lupus.
Despite significant advances in aging research, translating these findings into clinical practice remains a challenge. Aging is a complex, multifactorial process shaped by many factors including genetic, metabolic, and environmental factors. While medical advancements have extended lifespan, healthspan remains constrained by cellular senescence, telomere attrition, and systemic inflammation—core hallmarks of biological aging. However, emerging evidence suggests that telomere dynamic is not inevitable but can be influenced by oxidative stress, lifestyle choices, and metabolic regulation. This review examines how telomere-based biomarkers and metabolic interventions can drive personalized longevity medicine, enabling targeted strategies to delay aging.
A surprising new study has uncovered over 200 misfolded proteins in the brains of aging rats with cognitive decline, beyond the infamous amyloid and tau plaques long blamed for Alzheimer’s. These shape-shifting proteins don’t clump into visible plaques, making them harder to detect but potentially just as harmful. Scientists believe these “stealth” molecules could evade the brain’s cleanup systems and quietly impair memory and brain function. The discovery opens a new frontier in understanding dementia and could lead to entirely new targets for treatment and prevention.
Degradation of proteostasis, mitochondrial function, and cellular stress resistance results in a build-up of damaged proteins, oxidative insult, and chronic inflammation, characteristic of aging. CHIP is essential for maintaining protein quality control and cellular homeostasis by having dual E3 ubiquitin ligase and co-chaperone activities. CHIP facilitates proteostasis by maintaining proteostasis in misfolded, aggregated proteins by promoting their degradation. Mitochondrial dysfunction, oxidative imbalance, and cellular senescence are caused by its age-associated decline and contribute to neurodegenerative, cardiovascular, and oncogenic disease pathogenesis. Examples of recent pharmacological and gene-based strategies to correct CHIP and restore stress resilience have been made.
A new study from Aarhus University turns our understanding of how running injuries occur upside down. The research project, which is the largest of its kind ever conducted, shows that running-related overuse injuries do not develop gradually over time, as previously assumed, but rather suddenly—often during a single training session. The research is published in the British Journal of Sports Medicine.
“Our study marks a paradigm shift in understanding the causes of running-related overuse injuries. We previously believed that injuries develop gradually over time, but it turns out that many injuries occur because runners make training errors in a single training session,” explains Associate Professor Rasmus Ø. Nielsen from the Department of Public Health at Aarhus University, who is the lead author of the study.
The study followed 5,205 runners from 87 countries over 18 months and shows that injury risk increases exponentially when runners increase their distance in a single training session compared to their longest run in the past 30 days. The longer the run becomes, the higher the injury risk.
Neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease, are devastating and incurable diseases. Although many neurodegenerative diseases are characterized by abnormal protein aggregation in the brain, a limited understanding of whether and how aggregated proteins cause brain cell dysfunction and death represents a major barrier to developing effective treatments.
Inspired by similar approaches in cardiovascular disease and cancer, the researchers focused on rare genetic forms of neurodegeneration as a powerful way to uncover fundamental mechanisms tying protein aggregation to brain disease. Thier work unexpectedly linked protein aggregation in genetic forms of neurodegeneration to disrupted processing of transfer RNAs (tRNAs), revealing an important mechanism that might be therapeutically targeted in these disorders.
The authors were interested in genetic forms of neurodegeneration caused by GGC trinucleotide repeat expansions (DNA sequence mutations caused by copying this 3-letter sequence too many times in a row). These mutations produce aggregation-prone proteins with long stretches of a single repeated amino acid (glycine).
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At-Home Metabolomics: https://www.iollo.com?ref=michael-lustgarten.
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NAD+ Quantification: https://www.jinfiniti.com/intracellular-nad-test/