TABLE 2.

Overview of the involvement of Semaphorins or their receptors in neuropsychiatric/neurological diseases.

Disease	Human mutation	Expression changes in human brain	Mutant mice that develop the disease or  modulation of gene  expression in mice
Schizophrenia	PlexinA2	↑ Sema3A ↑ Sema4D ↑ PlxnB1 ↓ PlxnA1 ↓ Sema3D	PlxnA2 -/- mice
Anxiety	PlexinA2	–	Sema3F -/- mice
Depression (comorbidity with alcohol dependence)	Sema3A	–	–
Epilepsy	–	↓ CRMP-1 ↓ CRMP-2	Sema3F -/- mice Npn-2 -/- mice
Autism	Sema5A	↓ Sema5A	Sema5A -/- mice Sema3F -/- mice Npn-2 -/- mice
Multiple sclerosis	–	↑ Sema3A ↑ Sema3F ↑ Sema4D ↑ Sema7A ↑ Npn ↑ PlexinA1	Milder symptoms/increased remyelination: - In Npn-1 -/- mice; - In Sema7A -/- mice; - After inhibition of Sema3A signaling; - After overexpression of Sema3F; - After infusion of anti-Sema4D antibodies More severe symptoms/decreased remyelination: - After overexpression of Sema3A
ALS	–	↑ Sema3A	–
Alzheimer’s disease	–	↑ PlexinA4 ↑ PlexinB1	–