Addiction is a treatable disease.

Neurochemical Pathways

A primary factor in the development of addiction is neurophysiologic reinforcement (reward). Evidence of at least one central reward-reinforcement pathway involving the neurotransmitter dopamine exists for drug self-administration in the human brain. This pathway involves dopaminergic neurons that originate in the ventral tegmental area and project into the nucleus accumbens and forebrain. Release of dopamine from these neurons onto the dopamine receptors in the nucleus accumbens produces positive reinforcement and drives craving and addictive behavior.

Conditioned responses that trigger craving for addictive substances motivate drug-seeking behaviors often leading to heavy use. Indeed, strong cravings can persist long after drug use has stopped. Alcohol and other addictive agents stimulate an increase in dopamine levels in the nucleus accumbens that mediates reward or reinforcement processes in brain.

ALDH2 inhibition is the key

ALDH2 inhibition restores normal dopamine levels by a use-dependent negative feedback mechanism.

Selective ALDH2 inhibition reduced self-administration of various addictive chemicals including alcohol, nicotine, cocaine, and opiates. Furthermore, ALDH2 inhibition reduces cue-reinstatement (craving relapse) of alcohol, cocaine, methamphetamine, and heroin and compulsive binge eating. These findings are important for the treatment of SUD given that SUD is commonly associated with, or co-dependent use, of other addictive substances or compulsive disorders. We also discovered that selective inhibition of ALDH2 can reduce anxiety. These results indicate that an orally bioavailable, selective, and reversible ALDH2 inhibitor may help patients reduce their use of addictive drugs and anxiety.

ALDH2 inhibition has shown to be effective in multiple models of Substance Use Disorders (SUD).

Studies by ANS scientists and others provide validation of ANS technology.