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Abnormal insulin signaling in the brain has also been associated with nerve cell dysfunction and death, decreased levels of acetylcholine, and decreased levels of transthyretin, a protein that normally binds to and transports amyloid-beta proteins out of the brain.
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Despite the multiple beneficial actions of Glu in the central nervous system (CNS) of mammals, it is also true that excessive excitation of neurons by Glu can lead to nerve cell damage and neurological dysfunction [ 7].
In paralytic rabies patients, limb weakness is explained by peripheral nerve and not the anterior horn cell dysfunction [ 6, 7].
In EAE, as with MS, immune cells attack a nerve cell protein called myelin, causing symptoms ranging from impaired vision to severe motor dysfunction and even death.
Serial electrophysiologic studies of peripheral nerve in furious rabies patients revealed a sub-clinical evidence of anterior horn cell dysfunction in the spinal cord [ 6, 7].
That means when the dopamine released by one nerve cell is not entirely absorbed by the receiving nerve cell, the leftover dopamine is blocked from reentering the original nerve cell and stays in the gap between the two nerve cells.
Moreover, deficiencies in ISC-containing metabolic enzymes may attribute to the generation of reactive oxygen species (ROS) and mitochondria dysfunction, through which Ni induced significant cytotoxicity in nerve cells, as previously reported.
Alzheimer's disease (AD) is the most common neurodegenerative disorder, and is characterized by progressive cognitive dysfunction and memory loss that are caused by the death of nerve cells in several brain regions, including the cortex and hippocampus.
Neurodegenerative disorders encompass a condition where nerve cells of different parts of brain and spinal cord vanish leading to either functional loss or sensory dysfunction [ 1].
Nerve cells degenerate.
Start with nerve cells.
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