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Purpose: Both aging and neurodegenerative illnesses are thought to be influenced by mitochondrial malfunction and free radical formation. Deformities of the energy metabolism, mitochondrial genome polymorphisms, nuclear DNA genetic abnormalities associated with mitochondria, modifications of mitochondrial fusion or fission, variations in shape and size, variations in transit, modified mobility of mitochondria, transcription defects, and the emergence of misfolded proteins associated with mitochondria are all linked to Parkinson's disease. Methods: This review is a condensed compilation of data from research that has been published between the years of 2014 and 2022, using search engines like Google Scholar, PubMed, and Scopus. Results: Mitochondrial transplantation is a one-of-a-kind treatment for mitochondrial diseases and deficits in mitochondrial biogenesis. The replacement of malfunctioning mitochondria with transplanted viable mitochondria using innovative methodologies has shown promising outcomes as a cure for Parkinson's, involving tissue sparing coupled with enhanced energy generation and lower oxidative damage. Numerous mitochondria-targeted therapies, including mitochondrial gene therapy, redox therapy, and others, have been investigated for their effectiveness and potency. Conclusion: The development of innovative therapeutics for mitochondria-directed treatments in Parkinson's disease may be aided by optimizing mitochondrial dynamics. Many neurological diseases have been studied in animal and cellular models, and it has been found that mitochondrial maintenance can slow the death of neuronal cells. It has been hypothesized that drug therapies for neurodegenerative diseases that focus on mitochondrial dysfunction will help to delay the onset of neuronal dysfunction. [ABSTRACT FROM AUTHOR]

A small, translucent nematode known as Caenorhabditis elegans, or C. elegans, is frequently utilized as a model organism in biomedical studies. These worms, which are around 1 mm long and feed on bacteria, are usually found in soil. For accessible and effective research on genetics, developmental biology, neuroscience, cell biology, and aging, C. elegans provide an ideal model. Its simplicity, which includes a translucent body and a nervous system with only 302 neurons, makes it possible to see cellular and developmental processes in great detail. Because of its special benefits, the worm Caenorhabditis elegans allows for a thorough characterization of the cellular and molecular processes causing age-related neurodegenerative diseases. This is a general review of the life cycle, experimental methodologies, and the use of C. elegans to model brain diseases, including those related to molecular and genetic factors that cause neurodegenerative diseases. Additionally, we go over how C. elegans is a perfect model organism for studying neurons in instances of prevalent age-related neurodegenerative illnesses due to a combination of its biological traits and new analytical techniques. The literature review process was carried out step-by-step using online search databases such as Web of Science, PubMED, Embase, Google Scholar, Medline, and Google Patents. In the first searches, keywords like C.elegans, disease modelling, and neuroprotective activity were employed. Because of C. elegans's physiological transparency, it is possible to track the development of neurodegeneration in aging organisms by using co-expressed fluorescent proteins. Importantly, a fully characterized connectome provides a unique ability to precisely connect cellular death with behavioural instability or phenotypic diversity in vivo, thus permitting a deep knowledge of the detrimental effect of neurodegeneration on wellbeing. In addition, pharmacological therapies and both forward and reverse gene screening speed up the discovery of modifiers that change neurodegeneration. These chemical-genetic investigations work together to determine important threshold states that either increase or decrease cellular stress in order to unravel related pathways., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Inflammatory, immune, and neurodegenerative diseases constitute a category of persistent and debilitating conditions affecting millions worldwide, with inter-twined pathophysiological pathways. Recent research has spotlighted naturally occurring compounds like naringenin for potential therapeutic applications across multiple ailments., Objective: This review offers an encompassing exploration of naringenin's anti-inflamma-tory, immune-protective, and neuroprotective mechanisms, elucidating its pharmacological targets, signal transduction pathways, safety profile, and insights from clinical investigations., Methods: Data for this review were amassed through the scrutiny of various published studies via search engines such as PubMed and Google Scholar. Content from reputable publishers including Bentham Science, Taylor and Francis, Nature, PLOS ONE, among others, was referenced., Results: Naringenin exhibits substantial anti-inflammatory effects by restraining the NF-κB signaling pathway. It activates Nrf2, renowned for its anti-inflammatory properties, inducing the release of hemeoxynase-1 by macrophages. Furthermore, naringenin treatment downregulates the expression of Th1 cytokines and inflammatory mediators. It also impedes xanthine oxidase, counteracts reactive oxygen species (ROS), scavenges superoxide radicals, mitigates the accessibility of oxygen-induced K+ erythrocytes, and reduces lipid peroxidation. Naringenin's antioxidant prowess holds promise for addressing neurological conditions., Conclusion: Extensive research has been undertaken to establish the anti-inflammatory, immunomodulatory, and neuroprotective attributes of naringenin across various medical domains, lending credence to its pharmacological utility. The principal obstacle to naringenin's adoption as a therapeutic agent remains the dearth of in vivo data. Efforts should focus on rendering naringenin delivery patient-friendly, economically viable, and technologically advanced., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Parkinson's disease is the second most common neurological ailment. It is also known that it affects practically all other brain components, although only gradually. Animal models are mostly used to test the efficacy of treatment against a specific enzyme and aid in creating a new drug dose., Objective: The purpose of this review is to highlight in vivo Parkinson's disease screening approaches, as well as the mechanism of action of each drug involved in Parkinson's disease development, and discuss the limitations of each model. In addition, it also sheds light on Parkinson's disease genetic models., Methods: The data for the publication was gathered from databases, such as PubMed, Bentham Science, Elsevier, Springer Nature, Wiley, and Research Gate, after a thorough examination of diverse research findings linked to Parkinson's disease and its screening models., Results: Each chemical or drug has a unique mechanism for causing disease, whether through the production of reactive oxygen species or the blockage of the dopamine receptor. Almost every disease symptom, whether physical or behavioral, is covered by each of the constructed models' unique set of indicators and symptoms., Conclusion: Animal models are typically used to assess a medicine's activity against a specific enzyme and aid in the creation of a new drug dose. The process, restrictions, and mechanisms interfering with the screening, as well as the level of animal suffering, must all be thoroughly reviewed before any model for screening for Parkinson's disease can be implemented., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)