NDA1 Antibody

Synaptic Plasticity Modulation

NMDAR1 antibodies influence long-term potentiation (LTP), a synaptic mechanism underlying memory formation. Peptide-purified anti-NMDAR antibodies inhibit LTP induction at hippocampal Schaffer collateral-CA1 synapses, causing synaptic NMDAR hypofunction .

Pathological Implications

• Autoimmune Disorders: Anti-NMDAR antibodies are implicated in autoimmune encephalitis and epilepsy, where they disrupt receptor function .

• Leukemia Support: While not directly targeting leukemia, NMDAR1-related pathways intersect with ID1-regulated mechanisms in acute myeloid leukemia (AML) microenvironment cells, which promote leukemic progression via ANGPTL7 .

Experimental Tools

• Immunocytochemistry: Validated in HEK293 cells transfected with GluN1 and primary cortical neurons, showing colocalization with neuronal markers .

• Electrophysiology: Used in Xenopus oocyte voltage-clamp assays and hippocampal slice LTP studies to assess functional impacts .

Table 2: Key Validation Data

Therapeutic Potential

• Neurological Diseases: Targeting specific GluN1 epitopes (e.g., ATD region near N368/G369) may mitigate antibody-mediated synaptic dysfunction .

• Cancer Microenvironment: Indirect links to AML via ID1/ANGPTL7 axis suggest broader therapeutic avenues .