As Alzheimer's disease progresses, RNA splicing, the process responsible for protein assembly, is disrupted. These changes lead to the formation of dysfunctional proteins that trigger neuronal death. An international team of scientists has discovered that the molecule NAD⁺ (nicotinamide adenine dinucleotide) can protect the brain from neurodegenerative damage, reports New Atlas.
Experiments have shown that NAD⁺ can correct editing errors via the EVA1C protein, which regulates splicing. NAD⁺ is known to help regulate cellular metabolism and DNA repair, and its levels naturally decline with age.
Scientists initially tested the new approach in laboratory models: adding NAD⁺ precursors did indeed improve symptoms. For example, improved memory and motor function were observed, coupled with significant splicing changes. Similar results were also obtained in pilot clinical trials.
In metabolism, NAD is involved in redox reactions, transferring electrons from one reaction to another. Thus, in cells, NAD exists in two functional states: its oxidized form, NAD+, is an oxidizing agent and takes electrons from another molecule, being reduced to NADH, which then serves as a reducing agent and donates electrons. In living organisms, NAD is synthesized de novo (a term meaning the synthesis of complex molecules from the simplest possible) from the amino acids aspartate or tryptophan. Other precursors of the coenzyme are supplied to the body exogenously, such as niacin (vitamin B3) through food.
Since higher NAD⁺ levels are associated with increased lifespan and improved health with age, scientists see great potential for this discovery as a potential treatment for Alzheimer's disease. Maintaining NAD⁺ levels at a certain level may likely help preserve neuronal function.
The nature of dementia and other neurodegenerative diseases is very complex, so there is currently no single treatment strategy. Another study previously showed that clearing the brain of toxic proteins is not enough to defeat Alzheimer's disease.
