A new medicine study has identified a common link in the cause for all types of ALS.

The discovery by Northwestern University Feinberg School of medicine researchers, published in the journal Nature, provides a common target for drug therapy and shows that all types of ALS are linked to have a common cellular pathway.

Amyotrophic lateral sclerosis (ALS and Lou Gehrig's disease) is a fatal neurodegenerative disease that paralyzes individuals by attacking the nerve cells responsible for muscle controls. As many as 20,000-30,000 people in the United States have ALS, and an estimated 5,000 people in the United States are diagnosed with the disease each year. ALS most commonly strikes people between 40 and 60 years of age, but younger and older people also can develop the disease, according to the National Institutes of Health.

"This opens up a whole new field for finding an effective treatment for ALS," said senior author Teepu Siddique, M.D., the Les Turner ALS Foundation/Herbert C. Wenske Professor of the Davee Department of Neurology and Clinical Neurosciences at Northwestern's Feinberg School and a neurologist at Northwestern Memorial Hospital.

Siddique has been searching for the underlying mechanism of ALS for 25 years "It was one of the most difficult problems in neurology and the most devastating, a disease without any treatment or known cause."

Feinberg School of Medicine researchers discovered the protein ubiquilin2, was not functioning in people with ALS. The purpose of ubiquilin is to recycle damaged or misfolded proteins in motor and cortical neurons.

Ubiquilin in ALS patients accumulate in the motor neurons of the spinal cord and the brain. The accumulating protein takes on the appearance of "twisted skeins of yarn" which causes the degeneration of the neurons.

Researchers found the skein-like accumulations were present in people's brains and spinal cords in all forms of ALS and ALS/dementia, whether or not they had the gene mutation.

"This study provides robust evidence showing a defect in the protein degradation pathway causes neurodegenerative disease," said Han-Xiang Deng, M.D., lead author of the paper and associate professor of neurology at the Feinberg School.

"We can now test for drugs that would regulate this protein pathway or optimize it, so it functions as it should in a normal state." said Siddique.