: A proteome is defined as a comprehensive protein set either of an organ or an organism at a given time and under specific physiological conditions and accordingly, the study of nervous system’s proteomes is called Neuroproteomics. In the neuroproteomics process, various pieces of the nervous system are “fragmented” to understand the dynamics of each given sub-proteome in a much better way. Functional proteomics addresses the organisation of proteins into complexes, and formation of organelles from these multiprotein complexes that control various physiological processes. Current functional studies of neuroproteomics mainly talk about the synapse structure and its organisation, the major building site of the neuronal communication channel. The proteomes of synaptic vesicle, presynaptic terminal, and postsynaptic density, have been examined by various proteomics techniques. The objective of functional neuroproteomics is to solve the proteome of single neurons or astrocytes grown in cell cultures or from the primary brain cells isolated from tissues under various conditions; to identify set of proteins which characterize a specific pathogenesis; or to determine the group of proteins making up post-synaptic or pre-synaptic densities. It is very usual to try to solve a particular sub-proteome like the heatshock response proteome, or the proteome responding to inflammation. Posttranslational protein modifications alter their functions and interactions. The techniques to detect synapse phosphoproteome are available however, those for the analysis of ubiquitination and sumoylation, are under development.
Alzheimer’s disease (AD) is a commonly reported neurodegenerative disorder associated with dementia and cognitive impairment. The pathophysiology of AD comprises Aβ, hyperphosphorylated tau protein formation, abrupt cholinergic cascade, oxidative stress, neuronal apoptosis, and neuroinflammation. Recent findings have established the profound role of immunological dysfunction and microglial activation in the pathogenesis of AD. Microglial activation is a multifactorial cascade encompassing various signalling molecules and pathways such as Nrf2/NLRP3/NF-kB/p38 MAPKs/ GSK-3β. Additionally, deposited Aβ or tau protein triggers microglial activation and accelerates its pathogenesis. Currently, the FDA-approved therapeutic regimens are based on the modulation of the cholinergic system, and recently, one more drug, aducanumab, has been approved by the FDA. On the one hand, these drugs only offer symptomatic relief and not a cure for AD. Additionally, no targeted-based microglial medicines are available for treating and managing AD. On the other hand, various natural products have been explored for the possible anti-Alzheimer effect via targeting microglial activation or different targets of microglial activation. Therefore, the present review focuses on exploring the mechanism and associated signalling related to microglial activation and a detailed description of various natural products that have previously been reported with anti-Alzheimer’s effect via mitigation of microglial activation. Additionally, we have discussed the various patents and clinical trials related to managing and treating AD.
US Food and Drug Administration (USFDA) approved gabapentin as an adjuvant treatment for refractory partial seizures and several diverse disorders. The drug has a relatively safe profile and is well tolerated; however, awareness is required to monitor the patient's medication, its misuse, and how to approach better patient fate. Despite the enormous scientific hypothesis encircling the drug, there is a requisite to research further about the novelty of the drug. The review delineates the drug profile, synthesis, pharmacology, ADME properties, and computational study of gabapentin.
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