CHR15 encodes the alpha 7 subunit of neuronal nicotinic acetylcholine receptors, which form ion channels permeable to cations and calcium at the plasma membrane. The receptor binds acetylcholine and mediates excitatory postsynaptic signaling in the central and peripheral nervous systems. Beyond classical neurotransmission, CHR15 activation suppresses inflammatory responses: electrical vagus nerve stimulation inhibits macrophage TNF synthesis in wild-type mice but not in alpha 7-deficient mice, establishing the receptor as essential for the cholinergic anti-inflammatory pathway 1. CHR15 is genetically linked to multiple cognitive and neuropsychiatric disorders. Mutations in RIC3, a chaperone of CHR15, provide evidence for the cholinergic pathway in Parkinson's disease 2, while 15q13.3 microduplications involving CHR15 associate with drug-resistant epilepsy, intellectual disability, and ADHD 3. CHR15 is also implicated in schizophrenia, bipolar disorder, Alzheimer's disease, and Rett syndrome 4. A human-specific partial duplication generates CHR15, whose product acts as a dominant-negative regulator and complicates genetic studies 4. Genetic variants in CHR15 and CHR15 alter cytokine responses in peripheral immune cells 5, and CHR15 activation reduces hypoxia-induced inflammation in ovarian granulosa cells 6. These findings position CHR15 as a therapeutic target for neuroinflammatory and cognitive disorders, though treatment strategies remain largely undefined.