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Recommended reading:
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A newly-published call-to-arms and technical exposition on the SENS approach to age-related disease
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An early study of one of the seven targets of SENS research
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What to do in the meantime:
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Full of diet and lifestyle tips based on current science, to preserve your health until better technology is developed
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Only 7 Pathogenic Age-related Precursors: Pathogenic Aggregations
Two of the seven early precursors of age-related pathology are accumulations of usually benign substances that, with time, reach a threshold beyond which a cascade of damage leads to the symptoms of aging and ultimately death. Even if the other five precursors were controlled or didn't exist, each of these two could still kill us.
These precursors are divided into two groups, depending on whether they develop inside the cell or outside.
The intracellular aggregates targeted by SENS relate to the function of the lysosomse, the body's garbage can of last resort. The problem is either that human lysosomal enzymes can't degrade them or that the aggregates prevent transport of degradable materials into the lysosome in the first place. The former problem appears to be behind atherosclerosis and age-related macular degeneration. Both problems appear to be behind the neurodegenerative disorders Alzheimer's, Parkinson's, and Huntington's disease.
LysoSENS, one of LMRF's beneficiaries, is currently targeting lysosomal build-up of the undegradable substance 7-ketocholesterol in artery walls. If the approach is successful, it will be turned on another recalcitrant substance that is associated with age-related macular degeneration. Neurodegenerative diseases are also targeted for the future.
The extracellular aggregates targeted by SENS are atherosclerotic plaques and amyloid that accumulates into plaques. The former relates to atherosclerosis, the latter to Alzheimer's.
If lysosomal dysfunction is the precursor of both however, as evidence indicates, then breaking down intracellular aggregates alone would take care of both problems, and pathogenic aggregation reduces to an intracellular problem. However, dissolving extracellular plaques could serve as a worthwhile adjunct to intracellular lysosomal enhancement.
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