ReviewCurrent neuropharmacology2022
Class A and C GPCR Dimers in Neurodegenerative Diseases.
Review in Current neuropharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed.
- Mechanistic and therapeutic insights into class A GPCR dimers in neuropsychiatric disorders.npj drug discovery · 2026Review
- Dopamine D2 Receptor Isoform Heteroreceptor Complexes with the Growth Hormone Secretagogue Receptor 1a Reveals Isoform-Specific Interaction Interface Dynamics.Journal of chemical information and modeling · 2026Article
- The GPCR Connection: Linking Alzheimer's Disease and Glioblastoma.Journal of cellular and molecular medicine · 2026Review
- GPR75 in glutamatergic neurons regulates body weight.Cell reports · 2026Article
- GPCR Heterodimers: Implications for Biased Signaling.Handbook of experimental pharmacology · 2026Review
- GPCR-A17 MAAP: mapping modulators, agonists, and antagonists to predict the next bioactive target.Journal of cheminformatics · 2025Article
- Leveraging Artificial Intelligence in GPCR Activation Studies: Computational Prediction Methods as Key Drivers of Knowledge.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Molecular insights into the activation mechanism of GPR156 in maintaining auditory function.Nature communications · 2024Article
- MUG: A mutation overview of GPCR subfamily A17 receptors.Computational and structural biotechnology journal · 2023Article
- The World of GPCR dimers - Mapping dopamine receptor DComputational and structural biotechnology journal · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Neurodegenerative diseases affect over 30 million people worldwide with an ascending trend. Most individuals suffering from these irreversible brain damages belong to the elderly population, with onset between 50 and 60 years. Although the pathophysiology of such diseases is partially known, it remains unclear upon which point a disease turns degenerative. Moreover, current therapeutics can treat some of the symptoms but often have severe side effects and become less effective in long-term treatment. For many neurodegenerative diseases, the involvement of G proteincoupled receptors (GPCRs), which are key players of neuronal transmission and plasticity, has become clearer and holds great promise in elucidating their biological mechanism. With this review, we introduce and summarize class A and class C GPCRs, known to form heterodimers or oligomers to increase their signalling repertoire. Additionally, the examples discussed here were shown to display relevant alterations in brain signalling and had already been associated with the pathophysiology of certain neurodegenerative diseases. Lastly, we classified the heterodimers into two categories of crosstalk, positive or negative, for which there is known evidence.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.