biological aging =
​senescence

6. Reduction in Proteostasis:
Proteins must be properly folded in order to be                  functional. Age related proteostatic reduction leads to an accumulation of misfolded         proteins linked to neurodegenerative diseases          such as Alzheimer's/Parkinson's.

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 NIH/Mayo Clinic identify several primary mechanisms, called hallmarks,  that drive senescence:

biological aging =
​senescence

2. Genomic Instability:
accumulative damage to our DNA damage due to external factors (such as radiation) and internal factors
(such as oxidative stress) leads to mutations and impaired DNA repair mechanisms.

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 chronological age =
    the actual time passed        since you were born

biological vs chronological aging
aging is not a uniform process.
although we all age through specific pathways, the speed of aging is influenced by many factors such as diet, the environment, and even anxiety and stress.

        senescence is the time dependent   progressive decline in physiological function due to:

*an accumulation of cellular damage coupled with                    stem cell exhaustion
*exposure to environmental stressors like toxins and               UV radiation
* genetic factors such as genes which help manage                    stress and repair mechanisms.

5. Epigenetic Modifications:
Changes to the epigenomic tags (like methylation) affect gene expression and contribute to reduced cellular function.

the science of aging

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              biological age =
  the functional age of your cells                   (older or younger)
         depending on health, the               environment, and genetics.

1. Mitochondrial Dysfunction:
cells produce less energy alongside an increase in the generation of reactive oxygen species (ROS). 

mechanisms which promote senescence

4. Cell Senescence:
Zombie cells have stopped dividing but refuse to die, secreting damaging inflammatory factors.

3. Telomere Erosion:
 Telomeres are DNA sequences at the ends of our         chromosomes that serve as their protective caps. Telomeres shorten with each cell division so at one point they become so short that the cell stops dividing and becomes a senescent (zombie) cell.