![]() ![]() H1N1 Influenza and the associated Pandemrix ® vaccination is likely to be the specific environmental triggers for narcolepsy onset. Similarly, in China increased narcolepsy onsets were seen with natural pH1N1 infections. ![]() This increase was quickly traced back to a widespread vaccination campaign against pandemic H1N1 Influenza A (pH1N1) that used a vaccine brand called Pandemrix ®. In 2009–2010 a striking increase in narcolepsy cases was seen in Northern Europe, especially in children. ![]() These findings further support an autoimmune basis as the cause of hypocretin cell destruction. These findings were later complemented by genome-wide association studies (GWAS), which showed that narcolepsy associated with variants within genes that regulated immune system. In narcolepsy cases, 87–98% of patients are DQB1*06:02 positive, depending on population and inclusion criteria. Fine mapping of the HLA-DR2 revealed an association with HLA-DQB1*06:02. The first clue for an autoimmune disease etiology in narcolepsy was observed in 1980s when a strong association with HLA-DR2 haplotype was discovered. Furthermore, there is convincing genetic and epidemiological evidence suggesting an autoimmune mediated hypocretin neuronal loss. In humans, in the majority of cases, the loss of hypocretin is somewhat gradual and occurs postnatal. In addition, both hypocretin knockout mice as well as dogs with mutations in the hypocretin receptors manifest cataplexy and narcolepsy. A characteristic selective loss (>90%) of hypocretin producing neurons is seen in narcoleptic patients. Hypocretin is a wake promoting neurotransmitter, produced by neurons in the lateral hypothalamus. In almost all type 1 narcolepsy patients, the disease is caused by lack of hypocretin (orexin) neurotransmitter. Type 1 narcolepsy is a chronic neurological disorder defined by the presence of excessive daytime sleepiness and cataplexy, episodes of muscle weakness triggered by strong emotions. ![]()
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