Liver and Kidney Treatments Could Improve Due To An ‘Anti-Aging Molecule’

Nicotinamide adenine dinucleotide (NAD+) is a molecule that plays a role in cell metabolism and longevity. However, its activity gets limited due to an enzyme that is present in the liver and kidneys. Therefore scientists suggest that preserving the health of these organs can happen by blocking this enzyme, as per their research. It is also called as the “anti-aging molecule”, as the research has shown that its levels fall with age and that restoring them can extend years of good health and even longevity itself. The anti-aging molecule also has a vital responsibility for various other biological processes to energize cells and stay healthy, such as metabolism, DNA repair, gene expression, and cell signaling.

The molecule does not act alone but helps the enzymes that drive these vital cell processes, thus Scientists class NAD+ as a coenzyme. One family of enzymes that NAD+ has an ancient “intimate connection” with is the sirtuins. The tiny compartments that produce energy for the cell happen due to communication between the cell nucleus and its mitochondria. They are affected with a reduction in sirtuin activity with the decline in NAD+ ‘s age.

‘ACMSD controls NAD+ Levels in Cells’ being “Evolutionarily Conserved”

The École Polytechnique Fédérale de Lausanne (EPFL) in Switzerland featured their recent study in the journal Nature. It demonstrates Cells synthesize NAD+ from scratch using the amino acid tryptophan as the main building block. The presence of certain enzymes, including one called aminocarboxymuconate-semialdehyde decarboxylase (ACMSD) (which has the effect of limiting the production of NAD+), is needed for “de novo synthesis”. The team describes the way in which ACMSD controls NAD+ levels in cells as being “evolutionarily conserved.” The mechanism was the same in both Caenorhabditis elegans, a type of worm, and mice, and that blocking ACMSD increased both NAD+ and mitochondrial activity, as per the result of their investigation.

Blocking ACMSD also raised the activity of one of the sirtuins that NAD+ works with, as their research as shown. Also, a boost in the mitochondrial activity happened after the combination of elevated sirtuin activity and increased NAD+ synthesis. The team then tested the effect of two selective ACMSD blockers in animal models of nonalcoholic fatty liver disease and kidney damage, after working with TES Pharma. Results showed that both compounds seemed to preserve liver and kidney function.

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The first study author Elena Katsyuba, from the Interfaculty Institute of Bioengineering at EPFL, says

“Since the enzyme is mostly found in the kidneys and liver, we wanted to test the capacity of the ACMSD inhibitors to protect these organs from injury.”

This finding might open doors for a protective treatment that boosts NAD+ while other organs are not affects with it because ACMSD does not occur elsewhere in the body.

Elena Katsyuba says,

“Put simply, the enzyme will not be missed by an organ that does not have it anyway.”