Molecular Mechanisms of Cognitive Function and Dysfunction

Dear Colleagues,

Aim
Various molecular mechanisms facilitate cognitive processes, and the misfiring of neurons may lead to complications causing neuronal dysfunctions. Obtaining a better understanding of the importance of processes involving synaptic plasticity, neurotransmission, neuroinflammation, neurotransmitters, and inflammatory mediators is relevant for exploration in this field [1,2]. Also, important molecular players like NMDA [3] and NFkB [4] receptors are worth exploring.

Scope
This Special Issue takes into account the various cellular and molecular dynamics around optimal cognitive functions and explores the anomalies that lead to dysfunction.

Molecular Basis
Synaptic plasticity is mediated by NMDA, NFkB, and AMPA receptors. Studies around the molecular mechanisms of these receptors helps increase our understanding [5] about neurotransmission and molecular signalling cascades, encompassing glutamate, dopamine, serotonin, and acetylcholine [6,7].

Summary
Studies of these advancements help in the betterment of our understanding of cellular and molecular pathways. Such studies have the potential to evolve into studies [8,9] of targeted interventions [10,11] in neurodegenerative disorders and cognitive impairments.

References

1. Liu, J.; Chang, L.; Song, Y.; Li, H.; Wu, Y. The Role of NMDA Receptors in Alzheimer’s Disease. Neurosci. 2019, 13, 43, https://doi.org/10.3389/fnins.2019.00043.
2. Rao, J.S.; Kellom, M.; Kim, H.-W.; Rapoport, S.I.; Reese, E.A. Neuroinflammation and Synaptic Loss. Res. 2012, 37, 903–910, https://doi.org/10.1007/s11064-012-0708-2.
3. Zhou, Q.; Sheng, M. NMDA receptors in nervous system diseases. Neuropharmacology 2013, 74, 69–75, https://doi.org/10.1016/j.neuropharm.2013.03.030.
4. Ghosh, S.; Dass, J.F.P. Study of pathway cross-talk interactions with NF-κB leading to its activation via ubiquitination or phosphorylation: A brief review. Gene 2016, 584, 97–109. https://doi.org/10.1016/j.gene.2016.03.008.
5. Lin, M.T.; Beal, M.F. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. Nature 2006, 443, 787–795, https://doi.org/10.1038/nature05292.
6. Giese, K.P.; Mizuno, K. The roles of protein kinases in learning and memory. Mem. 2013, 20, 540–552, https://doi.org/10.1101/lm.028449.112.
7. Lindsay, H.G.; Hendrix, C.J.; Murcia, J.D.G.; Haynie, C.; Weber, K.S. The Role of Atypical Chemokine Receptors in Neuroinflammation and Neurodegenerative Disorders. J. Mol. Sci. 2023, 24, 16493, https://doi.org/10.3390/ijms242216493.
8. Ghosh, K.K.; Padmanabhan, P.; Yang, C.-T.; Wang, Z.; Palanivel, M.; Ng, K.C.; Lu, J.; Carlstedt-Duke, J.; Halldin, C.; Gulyás, B. An In Vivo Study of a Rat Fluid-Percussion-Induced Traumatic Brain Injury Model with [¹¹C]PBR28 and [¹⁸F]flumazenil PET Imaging. J. Mol. Sci. 2021, 22, 951, https://doi.org/10.3390/ijms22020951.
9. Zoey, F.L.; Ghosh, K.K.; Palanivel, M.; Gulyás, B.; Padmanabhan, P. Multifunctional Nanoparticles and Nanoclusters as a Theranostics and Symptoms Disappearing Agent for Traumatic Brain Injury. NanoBiomed Res. 2023, 3, https://doi.org/10.1002/anbr.202300010.
10. Liddelow, S.A.; Barres, B.A. Reactive Astrocytes: Production, Function, and Therapeutic Potential. Immunity 2017, 46, 957–967, https://doi.org/10.1016/j.immuni.2017.06.006.
11. Li, D.; Gao, X.; Ma, X.; Wang, M.; Cheng, C.; Xue, T.; Gao, F.; Shen, Y.; Zhang, J.; Liu, Q. Aging-induced tRNAGlu-derived fragment impairs glutamate biosynthesis by targeting mitochondrial translation-dependent cristae organization. 2024, https://doi.org/10.1016/j.cmet.2024.02.011.

Dr. Parasuraman Padmanabhan
Prof. Dr. Balázs Gulyás
Dr. Domokos Máthé
Guest Editors

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• cognition
• neurodevelopment
• neurotransmission
• molecular mecanisms
• signaling
• disorders
• therapy