A glitch in the ability to move iron around in cells may underlie a disease known as Type IV mucolipidosis (ML4) and the suite of symptoms---mental retardation, poor vision and diminished motor abilities---that accompany it, new research at the University of Michigan shows.

Liwu Li, associate professor of biological sciences at Virginia Tech, has revealed a common connection between the cellular innate immunity network and human chronic inflammatory diseases, including atherosclerosis, Type 2 Diabetes, and neurodegenerative diseases.

Scientists have created a tool for mopping up the clumps of mutant protein that drive neurodegeneration in Huntington's disease. Emory University researchers engineered a virus to make an intracellular antibody or "intrabody" against huntingtin, the protein whose mutant forms poison the brain cells of people with Huntington's.

Expanding on prior research performed at the University of Pennsylvania, Penn biologists have determined that faulty RNA, the blueprint that creates mutated, toxic proteins, contributes to a family of neurodegenerative disorders in humans.

Gene therapy to replace the faulty CLN2 gene, which causes a neurodegenerative disease that is fatal by age 8-12 years, was able to slow significantly the rate of neurologic decline in treated children, according to a paper published online ahead of print in the May 2008 issue (Vol. 19 No. 5) of Human Gene Therapy, a peer-reviewed journal published by Mary Ann Liebert, Inc.

Researchers from the University of Pennsylvania School of Medicine are developing a novel approach to screen for drugs to combat neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease, using yeast cells. In recent months a number of mutations have been found in a disease protein called TDP-43, which is implicated in ALS and certain types of frontotemporal dementia (FTD).

Leaky blood vessels that lose their ability to protect the spinal cord from toxins may play a role in the development of amyotrophic lateral sclerosis, better known as ALS or Lou Gehrig’s disease, according to research published in the April issue of Nature Neuroscience.

Iron is vital to human life; for example, it is a component of hemoglobin, the substance that makes our blood red and supplies our cells with oxygen. However, iron can also cause heavy damage; it is thought that iron deposits in the brain contribute to certain forms of neurodegenerative diseases such as Parkinsons’s, Huntington’ s, and Alzheimer’s.

Prion infection of neurons increases the free cholesterol content in cell membranes. A new study published in the online open access journal BMC Biology suggests that disturbances in membrane cholesterol may be the mechanism by which prions cause neurodegeneration and could point to a role for cholesterol in other neurodegenerative diseases.

The amyloid plaques found in the brains of Alzheimer’s disease patients may form much more rapidly than previously expected.

Tauopathies are neurodegenerative diseases that involve dysfunction of the microtubule-associated protein Tau. For example, hyperphosphorylated Tau forms the paired helical filaments (PHFs) found in Alzheimer’s disease.

Working with fruit flies, researchers have discovered a new mechanism by which the abnormal protein in Huntington’s disease causes neurodegeneration.