School Of Basic And Applied Sciences

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    miRNA in Parkinson's disease:�From pathogenesis to theranostic approaches
    (John Wiley and Sons Inc, 2022-12-11T00:00:00) Elangovan, Ajay; Venkatesan, Dhivya; Selvaraj, Priyanka; Pasha, Md. Younus; Babu, Harysh Winster Suresh; Iyer, Mahalaxmi; Narayanasamy, Arul; Subramaniam, Mohana Devi; Valsala Gopalakrishnan, Abilash; Kumar, Nachimuthu Senthil; Vellingiri, Balachandar
    Parkinson's disease (PD) is an age associated neurological disorder which is specified by cardinal motor symptoms such as tremor, stiffness, bradykinesia, postural instability, and non-motor symptoms. Dopaminergic neurons degradation in substantia nigra region and aggregation of ?Syn are the classic signs of molecular defects noticed in PD pathogenesis. The discovery of microRNAs (miRNA) predicted to have a pivotal part in various processes regarding regularizing the cellular functions. Studies on dysregulation of miRNA in PD pathogenesis has recently gained the concern where our review unravels the role of miRNA expression in PD and its necessity in clinical validation for therapeutic development in PD. Here, we discussed how miRNA associated with ageing process in PD through molecular mechanistic approach of miRNAs on sirtuins, tumor necrosis factor-alpha and interleukin-6, dopamine loss, oxidative stress and autophagic dysregulation. Further we have also conferred the expression of miRNAs affected by SNCA gene expression, neuronal differentiation and its therapeutic potential with PD. In conclusion, we suggest more rigorous studies should be conducted on understanding the mechanisms and functions of miRNA in PD which will eventually lead to discovery of novel and promising therapeutics for PD. � 2022 Wiley Periodicals LLC.
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    Dopamine, sleep, and neuronal excitability modulate amyloid-?-mediated forgetting in Drosophila
    (Public Library of Science, 2021-10-07T00:00:00) Kaldun, Jenifer C.; Lone, Shahnaz R.; Humbert Camps, Ana M.; Fritsch, Cornelia; Widmer, Yves F.; Stein, Jens V.; Tomchik, Seth M.; Sprecher, Simon G.
    Alzheimer disease (AD) is one of the main causes of age -related dementia and neurodegeneration. However, the onset of the disease and the mechanisms causing cognitive defects are not well understood. Aggregation of amyloidogenic peptides is a pathological hallmark of AD and is assumed to be a central component of the molecular disease pathways. Panneuronal expression of A?42 Arctic peptides in Drosophila melanogaster results in learning and memory defects. Surprisingly, targeted expression to the mushroom bodies, a center for olfactory memories in the fly brain, does not interfere with learning but accelerates forgetting. We show here that reducing neuronal excitability either by feeding Levetiracetam or silencing of neurons in the involved circuitry ameliorates the phenotype. Furthermore, inhibition of the Rac-regulated forgetting pathway could rescue the A?42 Arctic-mediated accelerated forgetting phenotype. Similar effects are achieved by increasing sleep, a critical regulator of neuronal homeostasis. Our results provide a functional framework connecting forgetting signaling and sleep, which are critical for regulating neuronal excitability and homeostasis and are therefore a promising mechanism to modulate forgetting caused by toxic A? peptides. � 2021 Kaldun et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.