Gaba B Receptor Protein is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
| GABA-B Receptor | GABA-B Receptor Protein | GABBR1 | UniProt | 864 aa | 96.4 kDa | Postsynaptic Membrane | GPCR Family |
GABA-B Receptor Protein is a protein involved in neuronal function and signaling relevant to neurodegenerative diseases. It plays important roles in synaptic transmission, ion channel regulation, or cellular metabolism that are critical for neuronal health and function.
Dysregulation of this protein's function or expression contributes to the pathogenesis of Alzheimer's disease, Parkinson's disease, and related neurodegenerative disorders through effects on synaptic plasticity, energy metabolism, or cellular stress response.
GABA-B Receptor is a 864 aa 96.4 kDa Postsynaptic Membrane protein belonging to the GPCR Family. The protein is a G protein-coupled receptor (GPCR) with 7 transmembrane domains.
Metabotropic GABA receptor, slow inhibition, G protein signaling, anxiolytic target. These receptors are essential for inhibitory neurotransmission in the brain.
Alzheimer's Disease: Glutamate receptor dysfunction contributes to excitotoxicity. Dopaminergic receptors are affected in AD with dementia.
Parkinson's Disease: D2 receptor agonists are mainstays of treatment. NMDA receptor antagonists (amantadine) help dyskinesias.
ALS: Excitotoxicity via glutamate receptors is a key mechanism. Riluzole targets glutamate transmission.
Schizophrenia: D2 receptor antagonists are antipsychotics. NMDA receptor dysfunction implicated.
The study of Gaba B Receptor Protein has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.