Drugs for aging-related diseases may modulate aging itself, but standard clinical trial designs cannot detect such effects. Aging clocks could close this gap, but epigenetic models often yield inconsistent, hard-to-interpret results. In contrast, proteomic clocks, by tracking the immediate effectors of biological chang...
Alex Zhavoronkov, F. Galkin, Shan Chen et al.· Nature Biotechnology· 1 citation
Overall, MA-5 suppresses neuroinflammation and reverses accelerated transcriptomic aging, supporting its potential as a therapeutic strategy for GD and other lysosomal storage disorders, as well as for diseases characterized by mitochondrial dysfunction, chronic inflammation, and pathological accumulation.
Y. Tongu, Tomoko Kasahara, Kohta Nakamura et al.· Research Square· 0 citations
Aging-related molecular damage accumulation can contribute to changes in mitochondrial morphology and metabolic dysfunction, particularly in tissues with high energy expenditures. Pharmacological compounds that ameliorate metabolic dysfunction and restore healthy, 'young' mitochondrial morphologies may thus represent e...
Wayne Mitchell, C. G. De Magalhães, P. Anekal et al.· Journal of Visualized Experi...· 0 citations
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