Doctors and genetic researchers at The University of Manchester have discovered that changes in a gene leads to severe nerve damage in children following a mild bout of infection.

Antonella Favit-Van Pelt, MD, PhD, discusses the use of neuromodulation and neuroplasticity for addressing gait deficits in patients with multiple sclerosis.

Replacing defective microglia can halt ALSP—a fatal neurodegenerative disease—in mice and humans, offering hope for broader brain therapies.

Conclusions MS causes progressive axonal loss in the optic nerve, regardless of a history of ON. This ganglion cell atrophy occurs in all eyes but is more marked in MS eyes than in healthy eyes.

Imaging studies at the NIH Clinical Center showed that chronic active lesions with a paramagnetic rim exerted ongoing tissue ...

Background Axonal loss is a major determinant of disability in multiple sclerosis (MS). While acute inflammatory demyelination is a principal cause of axonal transection and subsequent axonal ...

Demyelination resulting from diseases such as multiple sclerosis (MS) leads to neuronal dysfunction, namely deficits in signal propagation, subsequent axonal degeneration, and neuronal death. MS is ...

Changes in axonal excitability may be useful as an early biomarker of disease progression that could guide treatment in patients with ATTRv-PN.

In MS, demyelination is a driving factor that is a part of the biology of the disease. Loss of myelin of a previously myelinated axon is a threat to that axon and leads to axonal degeneration and ...

MRI is sensitive to the increase in axonal caliber due to pathology and was used to detect widespread increase in the average axonal caliber in multiple sclerosis brains with short disease duration ...

The efficient removal of damaged myelin was found to protect nerve cells against neurodegeneration in mouse models of myelin loss in a study.

A prime example is multiple sclerosis, a serious and frequent neurological disease in which immune cells drive demyelination, i.e., the loss of myelin.