Table.

Characterization of narcolepsy in human, dog and mice.

		Onset	Symptoms/Phenotype	Transmission	Association with HLA / DLA	Abnormality in Hypocretin system
Human	Sporadic	Adolescent	EDS, Cataplexy, SP, HH SOREMPs, Sleep Fragmentation Obesity (+)	?	DQB1*0602 (+) (90-95%)	Hypocretin Ligand Deficiency (∼90%)
	Familial	Earlier onset than sporadic cases	EDS, Cataplexy, SP, HH SOREMPs, Sleep Fragmentation Obesity (+)	?	DQB1*0602 (+) (75-80%)	Hypocretin Ligand Deficiency (∼75%)
	Hypocretin Mutant (the only one case is identified)	Extremely early onset (6 mo)	EDS Severe Cataplexy	DeNovo Mutant (?) Dominant	DQB1*0602 (−)	Mutation in Preprohypocretin Gene Hypocretin ligand deficiency
Dog	Sporadic (17 breeds)	7wk-7yr	Cataplexy Short Sleep Latency SOREMPs	?	(−)	Hypocretin Ligand Deficiency
	Familial Dobermans, Laboradors, Dachshund	earlier than 6 mo	Cataplexy Short Sleep Latency SOREMPs	Autosomal Recessive 100% of penetrance	(−)	Mutation in Hcrtr2 gene
Mice	Hypocretin KO	∼4wk	Cataplexy, SOREMPs Short Sleep Latency Obesity (?)	Autosomal Recessive 100% of penetrance		Hypocretin Ligand Deficiency
	Hypocretin Cell Death Hypocretin/Ataxin-3 transgenic	∼6wk	Cataplexy, SOREMPs Short Sleep Latency Obesity (++)	Autosomal Dominant 100% of penetrance		Hypocretin/Dynorphin Deficiency
	Hcrtr1 KO		Fragmented Sleep Obesity (?)			Absence of Hcrtr1
	Hcrtr2 KO		Cataplexy, SOREMPs Short Sleep Latency Obesity (?)	Autosomal Recessive 100% of penetrance		Absence of Hcrtr2
	Double Receptor KO		Same Sleep Phenotype as that of Preprohypocretin KOMice, Obesity (?)	Recessive for each receptor gene		Absence of Hcrtr1 and 2

EDS, Excessive Daytime Sleepiness, SP, Sleep Paralysis; HH, Hypnagogic Hallucination; SOREMPs, Sleep onset REM periods; KO,knockout; HLA, Human leukocyto antigen' DLA, Dog Leukocyto Antigen.