Category Archives: Increasing Lifespan

Are you a cyborg?

Are you a cyborg?

20140107 Kosta Schinarakis of Karlsruhe Institute of Technology —

Communication between man and machine – a fascinating area at the interface of chemistry, biomedicine, and engineering. (Figure: KIT/S. Giselbrecht, R. Meyer, B. Rapp)
Communication between man and machine – a fascinating area at the interface of chemistry, biomedicine, and engineering. Image by KIT/S. Giselbrecht, R. Meyer, B. Rapp

STORY HIGHLIGHTS

Now electronic implants based on microelectronics and semiconductor technology are used in cardiac pacemakers, retina implants, hearing implants, and implants for deep brain stimulation (pain or Parkinson therapies).
Future development area include highly complex neuroprostheses (brain-machine interfaces (BMI)) to allow for the direct physical contacting of the brain.
Future progress in releasing substances by implanted micro- and nanofluidic systems in a spatially or temporarily controlled manner for communication between technical devices and organisms.

They are known from science fiction novels and films – technically modified organisms with extraordinary skills, so-called cyborgs. This name originates from the English term “cybernetic organism”. In fact, cyborgs that combine technical systems with living organisms are already a reality. KIT researchers Professor Christof M. Niemeyer and Dr. Stefan Giselbrecht of the Institute for Biological Interfaces 1 (IBG 1) and Dr. Bastian E. Rapp, Institute of Microstructure Technology (IMT), point out that this especially applies to medical implants.

In recent years, medical implants based on smart materials that automatically react to changing conditions, computer-supported design and fabrication based on magnetic resonance tomography datasets or surface modifications for improved tissue integration allowed major progress to be achieved.

KIT scientists discuss the state of the art of research, opportunities, and risks.



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Intracellular Communication Breakdown May Be Reversible

Intracellular Communication Breakdown May Be Reversible

December 19, 2013 David Cameron of Harvard Medical School —

Sirt1 protein, red, circles the cell's chromosomes, blue.
Sirt1 protein, red, circles the cell’s chromosomes, blue. Image by Ana Gomes

STORY HIGHLIGHTS

• During aging, intracellular communication inside cells between the nucleus and mitochondria breaks down accelerating the aging process.
• This may be reversible.

Mitochondria are often referred to as the cell’s "powerhouse," generating chemical energy to carry out essential biological functions. These self-contained organelles, which live inside our cells and house their own small genomes, have long been identified as key biological players in aging. As they become increasingly dysfunctional overtime, many age-related conditions such as Alzheimer’s disease and diabetes gradually set in.

Researchers have generally been skeptical of the idea that aging can be reversed, due mainly to the prevailing theory that age-related ills are the result of mutations in mitochondrial DNA—and mutations cannot be reversed.

Sinclair and his group have been studying the fundamental science of aging—which is broadly defined as the gradual decline in function with time—for many years, primarily focusing on a group of genes called sirtuins. Previous studies from his lab showed that one of these genes, SIRT1, was activated by the compound resveratrol, which is found in grapes, red wine and certain nuts.

Ana Gomes, a postdoctoral scientist in the Sinclair lab, had been studying mice in which this SIRT1 gene had been removed. While they accurately predicted that these mice would show signs of aging, including mitochondrial dysfunction, the researchers were surprised to find that most mitochondrial proteins coming from the cell’s nucleus were at normal levels; only those encoded by the mitochondrial genome were reduced.

“This was at odds with what the literature suggested,” said Gomes.

As Gomes and her colleagues investigated potential causes for this, they discovered an intricate cascade of events that begins with a chemical called NAD and concludes with a key molecule that shuttles information and coordinates activities between the cell’s nuclear genome and the mitochondrial genome. Cells stay healthy as long as coordination between the genomes remains fluid. SIRT1’s role is intermediary, akin to a security guard; it assures that a meddlesome molecule called HIF-1 does not interfere with communication.

For reasons still unclear, as we age, levels of the initial chemical NAD decline. Without sufficient NAD, SIRT1 loses its ability to keep tabs on HIF-1. Levels of HIF-1 escalate and begin wreaking havoc on the otherwise smooth cross-genome communication. Over time, the research team found, this loss of communication reduces the cell’s ability to make energy, and signs of aging and disease become apparent.

“This particular component of the aging process had never before been described,” said Gomes.

While the breakdown of this process causes a rapid decline in mitochondrial function, other signs of aging take longer to occur. Gomes found that by administering an endogenous compound that cells transform into NAD, she could repair the broken network and rapidly restore communication and mitochondrial function. If the compound was given early enough—prior to excessive mutation accumulation—within days, some aspects of the aging process could be reversed.



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