The Strategies for Engineered Negligible Senescence (SENS) approach aging as the accumulation of cellular damage. Key forms of damage include stem cell decline, DNA mutations, cross-linking of molecules, metabolic waste buildup, protein misfolding, and senescent cell accumulation. This damage leads to downstream dysfunction, resulting in age-related degeneration and mortality. SENS proposes repairing this damage to slow or reverse aging. Addressing multiple forms of damage is crucial, as seen in the case of Parkinson’s disease. By targeting specific forms of damage, such as neuron loss and protein aggregates, researchers are making progress in rejuvenation therapies.
Parkinson’s Disease in the SENS View of Damage Repair
Parkinson’s disease, characterized by motor symptoms due to neuron loss, affects a significant portion of the elderly population. To combat this neurodegenerative disorder, researchers are exploring cellular and molecular aging damage-repair therapies. Neuron transplants and AmyloSENS therapies show promise in restoring function and reducing symptoms in Parkinson’s patients. Additionally, efforts to target intracellular protein aggregates and prevent mitochondrial DNA mutations offer potential treatments for this age-related condition. The SENS approach to damage repair holds great promise in combating Parkinson’s disease and other neurodegenerative disorders.