Important Roles of GABA and Its Receptor Subtypes in Alzheimer’s Disease: A Mini Review

Abstract

This review is dedicated to a systematic evaluation of the involvement of Gamma-Aminobutyric Acid (GABA) and the three major receptor subtypes in the pathophysiology of Alzheimer’s disease. The core theme is how changes in GABAergic neurotransmission, receptor expression, synaptic inhibition, and network oscillatory dysfunction lead to cognitive decline, neurodegeneration, and disease progression. The review also outlines the therapeutic interventions designed to target the GABAergic signaling to lessen the Alzheimer's-related neuropathology. This review was conducted using a structured narrative approach to ensure a transparent and comprehensive synthesis of data on GABAergic mechanisms in Alzheimer’s disease. A systematic literature search was performed across PubMed, Scopus, Web of Science, and Google Scholar for studies published between 2000 and 2024. Search keywords included: “GABA AND Alzheimer’s disease,” “GABAergic dysfunction,” “GABA receptor subtypes,” “GABAA_AA receptors and AD,” “GABAB_BB signaling,” “GABAC_CC receptor function,” “inhibitory neurotransmission AND neurodegeneration.” GABA plays an important role in synchronization of neuronal transmission in brain and also functions for storing of memory. It performs physiological functions like production of controlling brain signals, interferon-γ production, and decrease the cell excitability. In this review article, we have shown the role of GABA and its types in Alzheimer’s disease AD.

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