N-acetyl-aspartyl-glutamate (NAAG)

N-acetyl-aspartyl-glutamate (NAAG) is the most abundant endogenous dipeptide neuropeptide in the mammalian brain, primarily found in neurons. It is synthesized from N-acetyl-aspartate and glutamate, and rapidly hydrolyzed by glutamate carboxypeptidase II. NAAG acts as a neuromodulator at glutamatergic synapses by activating presynaptic metabotropic glutamate receptor 3 (mGluR3), thereby reducing excessive glutamate release and providing neuroprotection. It can also interact with NMDA receptors, showing context-dependent weak agonist/antagonist properties. Altered NAAG levels have been linked to neurological and psychiatric conditions, including neurodegenerative diseases, stroke, brain injury, epilepsy, pain states, and schizophrenia. Because NAAG is not a receptor, enzyme, or transporter, but a neurotransmitter/neuromodulator, it is not itself a direct "drug target," but enzymes involved in its metabolism (notably glutamate carboxypeptidase II) are considered therapeutic targets[1][2][4]. Key Point: NAAG is not itself a therapeutic target such as a receptor or enzyme; instead, it is a **signaling molecule** (neuropeptide) whose metabolic enzymes or receptors it acts upon are considered targets for drug development. This query likely confounds a **molecule** with a **target** (hence, is_incorrect: true)[2][1].

Other names

N-acetylaspartylglutamic acidN-acetyl-Asp-GluAc-Asp-Gluisospaglumic acid

Agonist at metabotropic glutamate receptor 3 (mGluR3) - Antagonist (or weak agonist/antagonist, depending on context) at NMDA receptor