INETA-BOTROPIC RECEPTORS: A REVIEW OF THEIR ROLE IN NEURODEGENERATIVE DISEASES
Neurodegenerative diseases are characterized by progressive deterioration of neurons and their synapses, eventually leading to the death of neurons. They are a major cause of death and disability worldwide, accounting for more than 6 million deaths annually. In recent years, there has been increasing research on the role of interneuronal communication in the development and progression of these diseases. In particular, the role of metabotropic glutamate receptors (mGluRs) has been extensively studied. One such receptor, the ineta-botropic receptor (iGluR), has been identified as playing a significant role in the regulation of neuronal signaling, and in particular, in the context of neurodegenerative diseases. This review aims to summarize the current understanding of the role of iGluRs in neurodegenerative diseases, with a focus on their potential therapeutic implications.
The iGluR family is composed of five members, all of which are G-protein coupled receptors (GPCRs). They are divided into two subtypes: the ionotropic (iGluR1-3) and metabotropic (iGluR4-5) receptors. iGluRs are found in both the central and peripheral nervous systems, and are highly expressed in the hippocampus, striatum, and hypothalamus. They have been implicated in numerous physiological processes, such as learning and memory, fear response, and the regulation of neurotransmitter release.
Recent studies have suggested that iGluRs may play a key role in the development and progression of several neurodegenerative diseases. In Alzheimer’s disease (AD), iGluRs have been implicated in the accumulation of amyloid-beta (Aβ) peptides, which are thought to be a major contributor to the disease’s symptoms. Additionally, iGluRs have been linked to the pathogenesis of Parkinson’s disease (PD) and Huntington’s disease (HD). In PD, iGluRs have been found to be involved in the regulation of dopaminergic neuron death, while in HD, they have been associated with the formation of aggregates of the mutant huntingtin protein.
The potential therapeutic implications of targeting iGluRs in neurodegenerative diseases are also being explored. One approach is to use drugs that modulate iGluR activities. Several compounds have been identified that modulate iGluR activity, including antagonists, agonists, and allosteric modulators. These compounds have been tested in preclinical models of neurodegenerative diseases, with promising results. For example, in a mouse model of AD, treatment with a iGluR antagonist was found to reduce Aβ deposition and improve cognitive function.
In summary, iGluRs have been identified as playing a role in the development and progression of several neurodegenerative diseases. Furthermore, several compounds have been identified that modulate iGluR activity, and these have shown promising results in preclinical models of neurodegenerative diseases. Further research is needed to better understand the role of iGluRs in these diseases, and to identify potential therapeutic targets.
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