Life & Medical Science

Scientists Discovered How To Slow Aging !

We can’t beat time in any aspect. Considering the life and aging, we can’t be the same and every passing second we are under the influence of aging and getting older. Our cells and tissues wouldn’t remain the same as we grow. But think ” Can We Really Slow Aging Or Even Stop It ?!”.

New research involving University of Minnesota Medical School faculty Paul D. Robbins and Laura J. Niedernhofer, recently published in Nature Medicine, shows there are types of small molecules called senolytics that can reverse the impact of aged, senescent cells.

Aging starts in our cells, and those aging cells can hasten cellular senescence, leading to tissue dysfunction and related health impacts.

“We’ve always thought of aging as a process, not a disease,” said Dr. Robbins, Associate Director of the newly founded Institute on the Biology of Aging and Metabolism (iBAM). “But what if we can influence the impacts of aging at a cellular level to promote healthy aging? That’s what senolytics seeks to achieve.”

The research determined whether introducing senescent cells to human and animal tissue would impact the cellular health of surrounding cells. Surprisingly, the transplant of a relatively small number of senescent cells caused persistent physical dysfunction as well as the spread of cellular senescence in previously healthy cells.

In addition, researchers found that a high fat diet, which causes a type of metabolic stress, or simply being old, enhances the physical dysfunction that comes from senescent cells.

“Previous research has shown that our immune system’s ability to eliminate or deal with senescent cells is based 30 percent on genetics and 70 percent on environment,” said Dr. Robbins, noting that what we eat and how often we exercise can affect senescence or aging of cells.

WHY DO WE GET AGED ?

Aging  is the process of becoming older. The term refers especially to human beings, many animals, and fungi, whereas for example bacteria, perennial plants and some simple animals are potentially immortal. In the broader sense, ageing can refer to single cells within an organism which have ceased dividing (cellular senescence) or to the population of a species (population ageing).

 

In humans, ageing represents the accumulation of changes in a human being over time,encompassing physical, psychological, and social changes. Reaction time, for example, may slow with age, while knowledge of world events and wisdom may expand. Ageing is among the greatest known risk factors for most human diseases: of the roughly 150,000 people who die each day across the globe, about two thirds die from age-related causes.

The causes of ageing are uncertain; current theories are assigned to the damage concept, whereby the accumulation of damage (such as DNA oxidation) may cause biological systems to fail, or to the programmed ageing concept, whereby internal processes (such as DNA methylation) may cause ageing. Programmed ageing should not be confused with programmed cell death (apoptosis).

FACTORS AFFECTING AGING

  • DNA damage theory of aging: DNA damage is thought to be the common basis of both cancer and ageing, and it has been argued that intrinsic causes of DNA damage are the most important drivers of ageing. Genetic damage (aberrant structural alterations of the DNA), mutations(changes in the DNA sequence), and epimutations (methylation of gene promoter regions or alterations of the DNA scaffolding which regulate gene expression), can cause abnormal gene expression. DNA damage causes the cells to stop dividing or induces apoptosis, often affecting stem cell pools and hence hindering regeneration. However, lifelong studies of mice suggest that most mutations happen during embryonic and childhood development, when cells divide often, as each cell division is a chance for errors in DNA replication.
  • Genetic instability: In heart muscle cells, dogs annually lose approximately 3.3% of the DNA in their heart muscle cells while humans lose approximately 0.6% of their heart muscle DNA each year. These numbers are close to the ratio of the maximum longevities of the two species (120 years vs. 20 years, a 6/1 ratio). The comparative percentage is also similar between the dog and human for yearly DNA loss in the brain and lymphocytes. As stated by lead author, Bernard L. Strehler, “… genetic damage (particularly gene loss) is almost certainly (or probably the) central cause of ageing.”
  • Accumulation of waste:
    • A buildup of waste products in cells presumably interferes with metabolism. For example, a waste product called lipofuscin is formed by a complex reaction in cells that binds fat to proteins. This waste accumulates in the cells as small granules, which increase in size as a person ages.
    • The hallmark of ageing yeast cells appears to be overproduction of certain proteins.
    • Autophagy induction can enhance clearance of toxic intracellular waste associated with neurodegenerative diseases and has been comprehensively demonstrated to improve lifespan in yeast, worms, flies, rodents and primates. The situation, however, has been complicated by the identification that autophagy up-regulation can also occur during ageing.  Autophagy is enhanced in obese mice by caloric restriction, exercise, and a low fat diet (but in these mice is evidently not related with the activation of AMP-activated protein kinase, see above).
  • Wear-and-tear theory: The very general idea that changes associated with ageing are the result of chance damage that accumulates over time.
  • Accumulation of errors: The idea that ageing results from chance events that escape proof reading mechanisms, which gradually damages the genetic code.
  • Cross-linkage: The idea that ageing results from accumulation of cross-linked compounds that interfere with normal cell function.
  • Studies of mtDNA mutator mice have shown that increased levels of somatic mtDNA mutations directly can cause a variety of ageing phenotypes. The authors propose that mtDNA mutations lead to respiratory-chain-deficient cells and thence to apoptosis and cell loss. They cast doubt experimentally however on the common assumption that mitochondrial mutations and dysfunction lead to increased generation of reactive oxygen species (ROS).

Conversely, the researchers determined that treatment with senolytic drugs, able to eliminate senescent cells, can reverse physical dysfunction and actually extend lifespan even when used in aged animal models.

“We saw greater activity, more endurance, and greater strength following use of senolytics,” said Dr. Robbins.

The paper notes that the results provide proof-of-concept evidence that improved health and lifespan in animals is possible by targeting senescent cells. The hope is that senolytics will prove effective in alleviating physical dysfunction and resulting loss of independence in older adult humans as well.

“This area of research is promising, not just to address the physical decline that comes with aging, but also to enhance the health of cancer survivors treated with radiation or chemotherapy – two treatments that can induce cell senescence,” said Laura Niedernhofer, Director of iBAM.

This study was done in collaboration with James Kirkland, MD, Ph.D., and Tamara Tchkonia, Ph.D., Mayo Clinic.

SOURCE – MED

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