GABBR1: A Potential Drug Target and Biomarker for Alzheimer's Disease

Target Name: GABBR1

NCBI ID: G2550

GABBR1

GABBR1: A Potential Drug Target and Biomarker for Alzheimer's Disease

Alzheimer's disease is a progressive neurological disorder that is characterized by a accumulation of neurofibrillary tangles and neuroplasmic senescent cells in the brain. It is the most common cause of dementia and affects millions of people worldwide. There is currently no cure for Alzheimer's disease, and the only treatment available is to manage symptoms with a combination of medications. However, researchers are constantly searching for new treatments and potential drug targets to slow the progression of the disease and improve treatment outcomes. In this article, we will discuss GABBR1, a gene that has potential as a drug target and biomarker for Alzheimer's disease.

GABBR1 is a gene that encodes a protein known as GABBR1. GABBR1 is a transmembrane protein that is expressed in many different tissues and cells in the body. It is involved in a variety of cellular processes, including cell signaling, neurotransmitter release, and synaptic plasticity. GABBR1 has been shown to be involved in the regulation of several key processes that are important for the development and progression of Alzheimer's disease.

One of the key functions of GABBR1 is its role in the regulation of neurotransmitter release. GABBR1 has been shown to play a role in the regulation of the release of several neurotransmitters, including dopamine, a neurotransmitter that is involved in motor function and mood regulation. Studies have shown that individuals with the GABBR1 gene variants are less likely to have amyloid plaques, a hallmark of Alzheimer's disease, and may be at a lower risk for developing the disease.

Another function of GABBR1 is its role in synaptic plasticity, which is the ability of the brain to change and adapt over time. GABBR1 has been shown to play a role in the regulation of synaptic plasticity, which may be important for the formation of new neural connections in the brain. This is important for maintaining cognitive function and may be important for the development of Alzheimer's disease.

In addition to its role in neurotransmitter release and synaptic plasticity, GABBR1 has also been shown to be involved in the regulation of cell signaling. GABBR1 has been shown to play a role in the regulation of several signaling pathways that are important for the development and progression of Alzheimer's disease. For example, GABBR1 has been shown to play a role in the regulation of the T-cell receptor, a signaling pathway that is important for the development of neurofibrillary tangles.

GABBR1 has also been shown to be involved in the regulation of inflammation. Inflammation is a key feature of the development and progression of Alzheimer's disease, and GABBR1 has been shown to play a role in the regulation of inflammation. For example, GABBR1 has been shown to play a role in the regulation of the production of pro-inflammatory cytokines, which are involved in the development of neurofibrillary tangles.

In conclusion, GABBR1 is a gene that has potential as a drug target and biomarker for Alzheimer's disease. Its involvement in the regulation of neurotransmitter release, synaptic plasticity, cell signaling, and inflammation makes it an attractive target for researchers to investigate further. While further research is needed to fully understand the role of GABBR1 in the development and progression of Alzheimer's disease, its potential as a drug target and biomarker is an exciting area of research that could lead to new and effective treatments for this debilitating disease.

Protein Name: Gamma-aminobutyric Acid Type B Receptor Subunit 1

Functions: Component of a heterodimeric G-protein coupled receptor for GABA, formed by GABBR1 and GABBR2 (PubMed:9872316, PubMed:9872744, PubMed:15617512, PubMed:18165688, PubMed:22660477, PubMed:24305054). Within the heterodimeric GABA receptor, only GABBR1 seems to bind agonists, while GABBR2 mediates coupling to G proteins (PubMed:18165688). Ligand binding causes a conformation change that triggers signaling via guanine nucleotide-binding proteins (G proteins) and modulates the activity of down-stream effectors, such as adenylate cyclase (PubMed:10906333, PubMed:10773016, PubMed:10075644, PubMed:9872744, PubMed:24305054). Signaling inhibits adenylate cyclase, stimulates phospholipase A2, activates potassium channels, inactivates voltage-dependent calcium-channels and modulates inositol phospholipid hydrolysis (PubMed:10075644). Calcium is required for high affinity binding to GABA (By similarity). Plays a critical role in the fine-tuning of inhibitory synaptic transmission (PubMed:9844003). Pre-synaptic GABA receptor inhibits neurotransmitter release by down-regulating high-voltage activated calcium channels, whereas postsynaptic GABA receptor decreases neuronal excitability by activating a prominent inwardly rectifying potassium (Kir) conductance that underlies the late inhibitory postsynaptic potentials (PubMed:9844003, PubMed:9872316, PubMed:10075644, PubMed:9872744, PubMed:22660477). Not only implicated in synaptic inhibition but also in hippocampal long-term potentiation, slow wave sleep, muscle relaxation and antinociception (Probable). Activated by (-)-baclofen, cgp27492 and blocked by phaclofen (PubMed:9844003, PubMed:9872316, PubMed:24305054)

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•   protein biological mechanisms;
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•   expression level;
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The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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