Abstract
Despite the identification of Aβ plaques and NFTs as biomarkers for Alzheimer’s disease (AD) pathology, therapeutic interventions remain elusive, with neither an absolute prophylactic nor a curative medication available to impede the progression of AD presently available. Current approaches focus on symptomatic treatments to maintain AD patients’ mental stability and behavioral symptoms by decreasing neuronal degeneration; however, the complexity of AD pathology requires a wide range of therapeutic approaches for both preventive and curative treatments. In this regard, this review summarizes the role of receptors as a potential target for treating AD and focuses on the path of major receptors which are responsible for AD progression. This review gives an overall idea centering on major receptors, their agonist and antagonist and future prospects of viral mimicry in AD pathology. This article aims to provide researchers and developers a comprehensive idea about the different receptors involved in AD pathogenesis that may lead to finding a new therapeutic strategy to treat AD.
Highlights
We found that snake toxins inhibit nicotinic acetylcholine receptor in the central nervous system [26]
We address the ramifications amyloid plaques and tau proteins have on the working capacity of these receptors, the impact on synaptic signaling and cognitive functions that lead to neurodegeneration and cognitive impairments
It is believed that cerebellar granule neuron (CGN) in the presence of Aβ40 significantly induce the phosphorylation of extracellular signal regulated kinase (ERK) and mTOR, eventually increasing the expression of the GABAA α6 subunit, affecting the development of CGN in the rat models [147]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. In AD patients, the cell signaling mechanism is considered to be dysfunctional In this regard, receptors have a prominent relation with AD pathology, thereby, serving as a potential target for treating the disease [11,12]. The amyloid cascade hypothesis, earlier studies suggested that AD neurodegeneration AD is caused by the formation of extracellular Aβ peptide deposited in senile plaques, followed by the intracellular accumulation of malformed tau protein in NFTs [14]. Amyloid’s β-sheet structure binds to multiple sites and it is assumed that the Aβ peptide plays a role in decreasing the release of presynaptic ACh and impeding the coupling of postsynaptic muscarinic acetylcholine receptors (mAChR) to G proteins This action reduces both signal transduction and APP level modulation and, as a result, simultaneously increases the production of Aβ peptide and further decreases ACh levels [11]. Using receptors to develop AD therapies is an emerging effort driving our understanding of [50,51]
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