A protein that promotes nerve cell healing in the peripheral nervous system has been discovered by Israeli researchers as a potential therapy for neurodegenerative illnesses.
An unexpected finding by a group of scientists at the Weizmann Institute of Science in Rehovot provides fresh light on neural regeneration and creates promising new avenues for treating long-untreatable disorders, including Alzheimer’s,
Parkinson’s, and ALS. Certain species of lizards, salamanders, and frogs, among other animals, have a greater public awareness of regeneration because their tails or limbs can regrow after being severed.
The ability to regenerate damaged nerve cells is a unique property of the peripheral nervous system, which connects the human brain and spinal cord to various organs.
Neurodegenerative disorders are irreversible and incurable because the central nervous system, which is made up of the brain and spinal cord, has limited regenerative capacity.
Scientists have been concentrating on figuring out how the peripheral nervous system can renew itself so efficiently up until now.
Research on regenerative medicine has focused on PTBP1, a protein that is known to drop dramatically as embryonic cells mature into adult nerve cells. Replicating this mechanism in non-neuronal cells by lowering PTBP1 levels was the goal of earlier research in an effort to regenerate neurons in the brains of patients with neurodegenerative disorders.
However, PTBP1 is not only found in embryonic cells, according to a new investigation performed by Stefanie Alber and doctoral candidate Pierluigi Di Matteo in the Weizmann Institute’s lab of Professor Mike Fainzilber.
Surprisingly, it is also expressed in adult peripheral nervous system neurons, refuting generalizations. The team’s research was only recently published in Science Advances, a peer-reviewed journal.
The discovery of PTBP1 in adult cells happened by accident; the research was originally intended to explore the control of KPNB1, a protein involved in message delivery inside neurons.
According to the study, KPNB1 acts as a “mail van,” allowing messages to be delivered from the far-flung branches of the neuron to the nucleus, where regeneration signals are started. PTBP1 efficiently attaches to the messenger RNA molecules that contain the instructions needed to build these messenger “vans.
The researchers looked at how neurons react to damage to understand how PTBP1 affects neuron function and regeneration.
Three days after damage, PTBP1 levels in cells started to rise, reaching their peak one week later. In parallel, the branches’ nerve cells started to regenerate.
Messenger RNA molecules associated with PTBP1 were sequenced to demonstrate its interaction with messenger RNA molecules encoding other proteins necessary for nerve cell regeneration, such as RHOA, an important regulator of cellular growth, in addition to KPNB1.
The researchers used genetic engineering to mute the expression of PTBP1 in order to more thoroughly research the function of adult cellsp. The peripheral nervous system’s ability to regenerate nerve cells that carry pain signals was diminished as a result of this alteration.
Additionally, muting PTBP1 increased sensitivity to mechanical and thermal stimuli, highlighting its function in maintaining and regenerating nerve cells.
Alzheimer’s disease is the most prevalent neurodegenerative condition, affecting 55 million people worldwide, according to the World Health Organization.
With 8.5 million individuals, Parkinson’s disease is the second most prevalent condition.