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Natural Product Compounds from Plants in Neurodegenerative Diseases
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Priya Darshani, Md TanjimAlam, Prem P. Tripathi, V.S. Pragadheesh
ALS is an irreversible and progressive neurodegenerative disease associated with selective motor neuron death in the spinal cord, brain stem and motor cortex. The progressive loss of motor neurons leads to muscle weakening, atrophy and dysfunction, resulting in final respiratory failure. ALS affects the nerve cells in the CNS and PNS (peripheral nervous system), causing loss of muscle control. Protein aggregates of TAR DNA-binding protein 43 (TDP-43) have been reported in patients with ALS (Van Es et al., 2017). Mutation of the superoxide dismutase-1 (SOD1) gene has been attributed to the development of this disease (Ciesler and Youssef, 2013).
Immunomodulatory Effect of Plant-Based Extracts on Neurodegeneration
Published in P. Mereena Luke, K. R. Dhanya, Didier Rouxel, Nandakumar Kalarikkal, Sabu Thomas, Advanced Studies in Experimental and Clinical Medicine, 2021
Koel Sinha, Chitrangada Das Mukhopadhyay
ALS, another neurodegenerative disease has got a beneficial effect of WS. The misfolded aggregation of TAR DNA binding protein-43 (TDP-43) is the main feature of ALS pathology. TDP-43 generally binds and coactivates the P-65 subunit of nuclear factor kappa beta (NF-κB). This NF-κB acts as a vital factor in disease pathology. On administration of the potent bioactive constituent withaferin-A in transgenic mouse model showed a marked improvement in ALS pathology whereas, this withaferin-A acts as an antagonist to NF-κB showed a remarkable reduction in the inflammatory response in the transgenic mice model [48]. Other observations suggested a marked improvement in ALS mice model by administration of withaferin-A which delayed the disease onset and progression. Later on, the root extract of WS with human TDP-43 mutation showed clearance of abnormal TDP-43 in neurons and showed improvement in motor as well as cognitive functions. Therefore, this adverse situation can be overcome by the administration of WS extract on neurodegenerative patients.
Rab11-mediated recycling endosome role in nervous system development and neurodegenerative diseases
Published in International Journal of Neuroscience, 2021
Jiajia Zhang, Gang Su, Qionghui Wu, Jifei Liu, Ye Tian, Xiaoyan Liu, Juanping Zhou, Juan Gao, Wei Chen, Deyi Chen, Zhenchang Zhang
The main pathological feature of ALS is the progressive loss of motor neurons [65, 66]. The loss of Rab11 endosome is associated with the complex regulation of MAPK/ERK/AKT signals in postmortem spinal cord specimens of patients [67]. TAR DNA-binding protein 43 (TDP-43) is a RNA‐binding protein in both healthy and diseased neurons.TDP-43 dysfunction is related to ALS and TDP‐43 knockdown attenuates Rab11-dependent endosome recycling process [68, 69]. Two ALS-linked molecules, optineurin (OPTN) and ubiquilin 2 gene (UBQLN2), localized to Rab11 endosomal vesicles. OPTN+/UBQLN2+ vesicles contribute to protein homeostasis in the endosomal system via Rab11-mediated autophagy, and an ALS-linked mutation disrupts the function of OPTN+/UBQLN2+ vesicles leading to the development of ALS [70, 71].
Progressive deterioration of sensory cortex excitability in advanced amyotrophic lateral sclerosis with invasive ventilation
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2020
Toshio Shimizu, Yuki Nakayama, Asuka Funai, Ryo Morishima, Kentaro Hayashi, Kota Bokuda, Yasuhiro Nakata, Eiji Isozaki
This case demonstrates that the increased amplitude of N20-P25 during the early stage of ALS, indicating hyperexcitability of the sensory cortex, gradually decreases during the advanced stages of ALS. One possible pathomechanism underlying the enlarged N20-P25 is a neuroplastic change of the sensory cortex excitability that is induced by increased excitability of the motor cortex via cortico-cortical neural connections (2). Another possibility are the early ALS-specific neuropathological changes within the sensory cortex (2). Previous studies have shown that ALS is a multisystem neurodegenerative disorder and that inclusions of TAR DNA-binding protein-43 (TDP-43) are widespread in cortical and subcortical areas as well as in the brainstem (5,6). In addition, neuronal loss in the sensory cortex of ALS patients was reported to be proportional to that in the motor cortex (7). Taken together, ALS-specific lesions might have primarily caused the sensory cortex hyperexcitability.
Interaction between genetic factors, Porphyromonas gingivalis and microglia to promote Alzheimer’s disease
Published in Journal of Oral Microbiology, 2020
Microglia can also develop functional defects as seen in other neurodegenerative disorders [35]. During the early stages of AD, they play a key role in the clearance of Aβ and reducing the plaque burden [36]. However, Aβ plaques and extracellular tau peptides can eventually become surrounded by glial cells with dysfunctional homeostatic control and as a result acquire a proinflammatory phenotype amplifying neuronal damage [37]. Similarly, cytokines and proinflammatory molecules secreted by microglia that initially have a neuroprotective role can subsequently become the cause of further neurodegeneration [37]. If microglia become overactive, they can initiate the biosynthesis of complement proteins and with the appropriate trigger, activate the complement cascade [38]. This can lead to their aberrant digestion of nerve synapses [39]. This is observed in mice lacking the TAR DNA-binding protein 43 (TPD-43) [40]. A complement-microglial axis has been found to drive synapse loss in AD [41] and is a plausible issue for deteriorating memory.