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    Neuroinflammation in Alzheimer�s Disease: Current Progress in Molecular Signaling and Therapeutics
    (Springer, 2022-08-20T00:00:00) Thakur, Sujata; Dhapola, Rishika; Sarma, Phulen; Medhi, Bikash; Reddy, Dibbanti HariKrishna
    Alzheimer�s disease, a neurodegenerative disease with amyloid beta accumulation as a major hallmark, has become a dire global health concern as there is a lack of clear understanding of the causative agent. It is a major cause of dementia which is increasing exponentially with age. Alzheimer�s disease is marked by tau hyperphosphorylation and amyloid beta accumulation that robs people of their memories. Amyloid beta deposition initiated a spectrum of microglia-activated neuroinflammation, and microglia and astrocyte activation elicited expressions of various inflammatory and anti-inflammatory cytokines. Neuroinflammation is one of the cardinal features of Alzheimer�s disease. Pro-inflammatory cytokine signaling plays multifarious roles in neurodegeneration and neuroprotection. Induction of proinflammatory signaling leads to discharge of immune mediators which affect functions of neurons and cause cell death. Sluggish anti-inflammatory system also contributes to neuroinflammation. Numerous pathways like NF?B, p38 MAPK, Akt/mTOR, caspase, nitric oxide, and COX are involved in triggering brain immune cells like astrocytes and microglia to secrete inflammatory cytokines such as tumor necrosis factor, interleukins, and chemokines and participate in Alzheimer�s disease pathology. PPAR-? agonists tend to boost the phagocytosis of amyloid beta and decrease the inflammatory cytokine IL-1?. Recent findings suggest the cross-link between gut microbiota and neuroinflammation contributing in AD which has been explained in this study. The role of cellular, molecular pathways and involvement of inflammatory mediators in neuroinflammation has also been described; targeting them could be a potential therapeutic strategy for treatment of AD. � 2022, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
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    Neurobiology of traumatic brain injury
    (Taylor and Francis Ltd., 2021-09-06T00:00:00) Bagri, Kajal; Kumar, Puneet; Deshmukh, Rahul
    Traumatic brain injury (TBI) involves structural damage to the brain regions causing death or disability in patients with lifelong sufferings. Accidental injuries to the brain, besides structural damage, if any, cause activation of various deleterious pathways leading to subsequent neuronal death and permanent dysfunction. However, immediate medical management/treatments could reduce the chances of disability and suffering to the patients. The objective of the current review is to review triggered molecular pathways following TBI and discuss possible targets that could restore brain functions. Understanding the pathologic process is always useful to device novel treatment strategies and may rescue the patient with TBI from death or associated co-morbidities. The current review significantly contributes to improve our understanding about the molecular pathways and neuronal death following TBI and helps us to provide possible targets that could be useful in the management/treatment of TBI. � 2021 Taylor & Francis Group, LLC.
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    Targeting mitochondria in the regulation of neurodegenerative diseases: A comprehensive review
    (John Wiley and Sons Inc, 2022-07-20T00:00:00) Maurya, Shashank Kumar; Gupta, Suchi; Bakshi, Amrita; Kaur, Harpreet; Jain, Arushi; Senapati, Sabyasachi; Baghel, Meghraj Singh
    Mitochondria are one of the essential cellular organelles. Apart from being considered as the powerhouse of the cell, mitochondria have been widely known to regulate redox reaction, inflammation, cell survival, cell death, metabolism, etc., and are implicated in the progression of numerous disease conditions including neurodegenerative diseases. Since brain is an energy-demanding organ, mitochondria and their functions are important for maintaining normal brain homeostasis. Alterations in mitochondrial gene expression, mutations, and epigenetic modification contribute to inflammation and neurodegeneration. Dysregulation of reactive oxygen species production by mitochondria and aggregation of proteins in neurons leads to alteration in mitochondria functions which further causes neuronal death and progression of neurodegeneration. Pharmacological studies have prioritized mitochondria as a possible drug target in the regulation of neurodegenerative diseases. Therefore, the present review article has been intended to provide a comprehensive understanding of mitochondrial role in the development and progression of neurodegenerative diseases mainly Alzheimer's, Parkinson's, multiple sclerosis, and amyotrophic lateral sclerosis followed by possible intervention and future treatment strategies to combat mitochondrial-mediated neurodegeneration. � 2022 Wiley Periodicals LLC.