Prosopagnosia

Introduction of Prosopagnosia

Prosopagnosia can be developed or acquired. Some of the most common causes of acquired prosopagnosia include destructive conditions such as posterior cerebral artery stroke or hematoma. Developmental prosopagnosia (DP) is a cognitive disorder characterized by severe facial recognition defects without any known impairments, neurological diseases, or low-level visual or intellectual impairments. It is estimated that about 2% of adults and children have experienced DP or “face blindness”. This situation can seriously affect daily life, and even produce devastating consequences, such as avoiding social interactions, interpersonal problems, damage to careers, and even depression.

Prosopagnosia is Related to Cortical Damage

Damage to specific areas of the cerebral cortex leads to many high visual processing disorders, which have specific roles in processing certain aspects of vision. Face recognition is supported by the collaboration of multiple facial reaction areas in the brain. A neural model is proposed based on the normal face recognition brain area, the occipital face area (OFA), the fuzzy face area (FFA), and the face-selective posterior superior temporal sulcus (pSTS) are used as the core face network (CFN), and the rest of the face response area serves as an extended surface network (EFN). By exploring the resting functional connection (FC) between the facial response areas of patients with DPs, we found that these interrupted FCs are related to DP's behavioral defects in face recognition.

NMDA Receptor Play a Role in Prosopagnosia

Anti-N-methyl-D-aspartate (NMDA) receptor encephalitis is an autoimmune disease that exhibits various neurological symptoms, including behavioral changes, memory deficits, seizures, and static form prosopagnosia. The patient can recognize the form of moving objects, but not the form of stationary objects. NMDA receptor encephalitis involves antibodies against the GluN1 subunit of the NMDA receptor. These antibodies may cause the binding, capping, and cross-connection of NMDA receptors, leading to the internalization of neuronal membrane surface receptors, and the dysfunction of signal transmission mediated by glutamine synapses. Therefore, drug mediated signaling pathways related to NMDA receptors may be available regulatory pathways for the treatment of prosopagnosia.

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