In a breakthrough finding, researchers have discovered to successfully switch off a key route for nerve fibre failure in debilitating neurodegenerative diseases such as Parkinson’s, glaucoma, and traumatic brain injury.
The study led by Institute for Glycomics and Disarm therapeutics at Griffith University explains the structural processes behind activation and inhibition of SARM1 – a major molecule for the damage of nerve fibers.
The understanding of action of SARM1 is important to help to treat several neurodegenerative conditions, which is a trigger for nerve fiber degeneration.
Importantly, the study demonstrates the molecular interactions that can switch SARM1 on and off. This provides a clear path for the design of new drug therapeutics.
Meanwhile, for neurodegenerative disorders such as Parkinson’s, peripheral neuropathy, traumatic brain injury, and glaucoma, the damage of nerve fibers activates SARM1.
This triggers a series of molecular processes that lead to self-destruction of axon of the nerve cell – the cable that transmits electric impulse away from one nerve cell to the other.
Anatomically, the axon is several times thinner than a human hair, but is up to a meter in length. It stretches from brain to the spinal cord, and its destruction can lead to serious dysfunction.
The SARM1 protein works like a sensor and responds to the environment. The molecule switches on when the levels of nicotinamide mononucleotide, which is a small activator molecule increases. The activator molecule attaches to the larger SARM1 protein like a key in a lock thereby initiating the process that lead to the breakdown of nerve fibers. SARM1 when unlocked is able to disintegrate another key molecule called nicotinamide adenine dinucleotide, which provides energy for nerve fibers to function and continue to live.
Consequent upon a study at the Institute of Pharmacology, Medical University of Vienna – a small protein molecule (peptide) from beetroot isolated. The peptide is able to inhibit a particular enzyme that is responsible for the disintegration of messenger molecules in the body.
In fact, beetroot features a stable molecular form and pharmacological characteristics. This potentially makes beetroot a good candidate for development of a drug to treat certain inflammatory diseases such as autoimmune and neurodegenerative diseases.
Anatomically, the peptide is present in the roots of beetroot plants. The peptide belongs to a class of molecules that plants use as a chemical protection against pests such as viruses, bacteria, or insects. Meanwhile, the analysis of a number of genomic data points led the team to define a number of new cysteine-rich peptides and keep them phylogenetically in the plant kingdom. In the interim, the attention of researchers drawn to a possible function so-called as protease inhibitors. “Therefore, beetroot peptide can inhibit enzymes that digest proteins, explains one of the researchers.”
Physiology of Beetroot Peptide helps regulate Infectious Diseases
In fact, the beetroot peptide specifically impedes prolyl oligopeptidase (POP). This prolyl oligopeptidase is involved in the disintegration of protein hormones in the body and is therefore able to regulate infectious diseases. Also, POP is extensively examined for inflammatory and neurodegenerative diseases such as multiple sclerosis and Alzheimer’s. This implies, ‘knottins’ – a group of plant peptides those found in beetroot – could be a potential drug bet for treating these diseases.
Not only root vegetables, the peptide can also be discovered in commercially available beetroot juices – though in very low concentrations. Whilst beetroot is a healthy vegetable, prevention of dementia with the regular consumption of beetroot is an unreasonable goal.