Increased levels of which compound can produce demyelination in the spinal cord, peripheral nerves, and brain?

Increased levels of propionyl CoA are associated with several metabolic disorders that can lead to nerve damage, including demyelination in the spinal cord, peripheral nerves, and brain. Propionyl CoA is a key intermediate in several metabolic pathways, including the metabolism of odd-chain fatty acids and certain amino acids. When there is an accumulation of propionyl CoA, especially in conditions like propionic acidemia, it can lead to toxic effects on neuronal tissues.

The accumulation of propionyl CoA can disrupt normal cellular processes and contribute to neurological damage, in part by inducing metabolic imbalances and promoting mitochondrial dysfunction. This dysfunction can lead to the generation of reactive oxygen species (ROS) and subsequent oxidative stress, which is known to contribute to demyelination in the nervous system.

Understanding the role of propionyl CoA in metabolic pathways and its potential toxic effects can highlight its significance in neurological disorders and demyelination processes. This makes it a key compound when examining causes of demyelination linked to metabolic disturbances.