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Can we slow down the physical breakdown in old age?

Can we slow down the physical breakdown in old age?


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What role do mitochondria play in physical breakdown?

The human body continues to degrade, especially in old age. It is therefore very important to develop measures that we can slow down such degradation to prevent negative health effects and dangerous falls. A key mechanism has now been identified that drives the removal of damaged mitochondria. This could contribute to the development of drug therapies that help older adults maintain their skeletal muscle mass and physical performance for longer.

The recent study by the University of Birmingham found that a newly identified key mechanism could allow older adults to prevent their skeletal muscle mass and physical functions from breaking down. The results of the study were published in the English-language journal "FASEB".

What are mitochondria?

The researchers at the University of Birmingham examined the dynamic machinery in the cells, the so-called mitochondria. These act as a power plant in every cell and help supply all living beings with energy. A newly identified key mechanism appears to be promoting the removal of damaged mitochondria.

Mitochondrial breakdown changes with age

Because the mitochondria are so important for energy supply, they are constantly synthesized and dismantled to meet the energy needs. In older people, however, the way in which mitochondria are naturally broken down in cells begins to change. This leads to an accumulation of damaged mitochondria or old mitochondria, which no longer function optimally.

Decreased muscle function due to damaged mitochondria?

The researchers believe that these changes could contribute to the decline in muscle function in older people, which in turn reduces their physical abilities. The team therefore wanted to find out more about the breakdown of mitochondria in the muscle. Factors that control this degradation were also examined.

AMPK stimulates the breakdown of mitochondria

With a new method, the mitochondria in the muscle cells can be examined with the help of fluorescent labels. Networks of mitochondria appear golden in healthy cells, but turn red when they dissolve. With this experimental setup, the research group discovered that the activation of the so-called AMP-activated protein kinase (AMPK) stimulates the degradation of the mitochondria.

Movement stimulates removal of damaged mitochondria

This result suggests that other well-known AMPK activators, such as exercise, can stimulate the removal of damaged mitochondria, keeping the mitochondria in the muscle healthy and maintaining the physical ability of older people for longer.

AMPK activation has positive effects on type 2 diabetes

There had already been considerations to treat AMPK with drugs in a targeted manner. Results from various studies on this topic show, for example, that AMPK activation in muscles triggers positive effects for the treatment of type 2 diabetes. Many pharmaceutical companies are currently working on the development of preclinical compounds that activate AMPK.

Development of new drugs in prospect?

The results of the current investigation could possibly accelerate the development of drugs that are aimed at activating this key molecule in the muscle, the researchers hope.

Exercise and healthy nutrition protect against the loss of muscle mass

Exercise and healthy eating can help people maintain their muscle mass and physical abilities later in life. When a better understanding of why muscle wasting occurs with aging, targeted pharmacological interventions can be developed that help people stay physically fit longer. (as)

Author and source information

This text corresponds to the specifications of the medical literature, medical guidelines and current studies and has been checked by medical doctors.

Swell:

  • Alex P. Seabright, Nicholas HF Fine, Jonathan P. Barlow, Samuel O. Lord, Ibrahim Musa et al .: AMPK activation induces mitophagy and promotes mitochondrial fission while activating TBK1 in a PINK1 ‐ Parkin independent manner, in FASEB (published 22.03. 2020), FASEB


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