Surveys show a particular distribution pattern with large clusters and frequencies of gene mutations along the western European coastline. This led the development of the "Viking Hypothesis". Cluster locations and mapped patterns of this mutation correlate closely to the locations of Viking settlements in Europe established c.700 AD to c.1100 AD. The Vikings originally came from Norway, Sweden and Denmark. Viking ships made their way along the coastline of Europe in search of trade, riches, and land. Genetic studies suggest that the extremely high frequency patterns in some European countries are the result of migrations of Vikings and later Normans, indicating a genetic link between hereditary haemochromatosis and Viking ancestry. Modern times
In 1865, Armand Trousseau (a French internist) was one of the first to describe many of the symptoms of a diabetic patient with cirrhosis of the liver and bronzed skin color. The term haemochromatosis was first used by German pathologist Friedrich Daniel von Recklinghausen in 1889 when he described an accumulation of iron in body tissues. Identification of genetic factors
Although it was known most of the 20th century that most cases of haemochromatosis were inherited, they were incorrectly assumed to depend on a single gene.In 1935 J.H. Sheldon, a British physician, described the link to iron metabolism for the first time as well as demonstrating its hereditary nature.In 1996 Felder and colleagues identified the haemochromatosis gene, HFE gene. Felder found that the HFE gene has two main mutations, C282Y and H63D, which were the main cause of hereditary haemochromatosis.
In 2003 Teva partnered with Eisai, giving Eisai the right to jointly market the drug for Parkinsons in the US, and to co-develop and co-market the drug for Alzheimers and other neurological diseases.It was approved by the European Medicines Agency for Parkinsons in 2005 and in the US in 2006.: 255

Research
Rasagiline was tested for efficacy in people with multiple system atrophy in a large randomized, placebo-controlled, double-blind disease-modification trial; the drug failed.Teva conducted clinical trials attempting to prove that rasagiline did not just treat symptoms, but was a disease-modifying drug - that it actually prevented the death of the dopaminergic neurons that characterize Parkinsons disease and slowed disease progression. They conducted two clinical trials, called TEMPO and ADAGIO, to try to prove this. The FDA advisory committee rejected their claim in 2011, saying that the clinical trial results did not prove that rasagiline was neuroprotective. The main reason was that in one of the trials, the lower dose was effective at slowing progression, but the higher dose was not, and this made no sense in light of standard dose-response pharmacology. See also
Selegiline
Ladostigil

References
External links
"Rasagiline". Drug Information Portal. U.S. National Library of Medicine. "Rasagiline mesylate". Drug Information Portal. U.S. National Library of Medicine.