Aβ peptides stabilize GPCRs in inactive form and trigger inverse agonism in Alzheimer's disease

Amit Chaudhary; Ashutosh Mani

doi:10.1016/j.biochi.2022.07.005

Aβ peptides stabilize GPCRs in inactive form and trigger inverse agonism in Alzheimer's disease

Biochimie. 2022 Oct:201:75-78. doi: 10.1016/j.biochi.2022.07.005. Epub 2022 Jul 15.

Authors

Amit Chaudhary¹, Ashutosh Mani²

Affiliations

¹ Department of Biotechnology, Motilal Nehru National Institute of Technology, Allahabad, 211004, India.
² Department of Biotechnology, Motilal Nehru National Institute of Technology, Allahabad, 211004, India. Electronic address: amani@mnnit.ac.in.

PMID: 35839919
DOI: 10.1016/j.biochi.2022.07.005

Abstract

Several G-protein coupled receptors (GPCR) are upregulated in Alzheimer's Disease (AD), which ought to facilitate neurotransmission, and improve cognition. Yet, despite this upregulation, associated physiological effects are not observed in AD patients. This paradox solicits urgent attention to find a suitable justification for disturbed neurotransmission in AD. This article focuses on the role of Aβ granules and their possible interaction with GPCRs that modulate neurotransmission and AD progression.

MeSH terms

Alzheimer Disease* / drug therapy
Amyloid beta-Peptides
Cognition
Humans
Receptors, G-Protein-Coupled
Synaptic Transmission

Substances

Amyloid beta-Peptides
Receptors, G-Protein-Coupled