Кафедра нервових хвороб

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https://repository.pdmu.edu.ua/handle/123456789/30

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Перегляд Кафедра нервових хвороб за Автор "Awuah, Wireko Andrew"

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    Документ
    Hereditary spastic paraplegia: Novel insights into the pathogenesis and management
    (SAGE, 2024-01) Awuah, Wireko Andrew; Tan, Joecelyn Kirani; Shkodina, Anastasiia D; Ferreira, Tomas; Adebusoye, Favour Tope; Mazzoleni, Adele; Wellington, Jack; David, Lian; Chilcott, Ellie; Huang, Helen; Abdul-Rahman, Toufik; Shet, Vallabh; Atallah, Oday; Kalmanovich, Jacob; Jiffry, Riaz; Madhu, Divine Elizabeth; Sikora, Kateryna; Kmyta, Oleksii; Delva, Mykhailo Yu.; Шкодіна, Анастасія Дмитрівна; Дельва, Михайло Юрійович
    Hereditary spastic paraplegia is a genetically heterogeneous neurodegenerative disorder characterised primarily by muscle stiffness in the lower limbs. Neurodegenerative disorders are conditions that result from cellular and metabolic abnormalities, many of which have strong genetic ties. While ageing is a known contributor to these changes, certain neurodegenerative disorders can manifest early in life, progressively affecting a person’s quality of life. Hereditary spastic paraplegia is one such condition that can appear in individuals of any age. In hereditary spastic paraplegia, a distinctive feature is the degeneration of long nerve fibres in the corticospinal tract of the lower limbs. This degeneration is linked to various cellular and metabolic processes, including mitochondrial dysfunction, remodelling of the endoplasmic reticulum membrane, autophagy, abnormal myelination processes and alterations in lipid metabolism. Additionally, hereditary spastic paraplegia affects processes like endosome membrane trafficking, oxidative stress and mitochondrial DNA polymorphisms. Disease-causing genetic loci and associated genes influence the progression and severity of hereditary spastic paraplegia, potentially affecting various cellular and metabolic functions. Although hereditary spastic paraplegia does not reduce a person’s lifespan, it significantly impairs their quality of life as they age, particularly with more severe symptoms. Regrettably, there are currently no treatments available to halt or reverse the pathological progression of hereditary spastic paraplegia. This review aims to explore the metabolic mechanisms underlying the pathophysiology of hereditary spastic paraplegia, emphasising the interactions of various genes identified in recent network studies. By comprehending these associations, targeted molecular therapies that address these biochemical processes can be developed to enhance treatment strategies for hereditary spastic paraplegia and guide clinical practice effectively.
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    Документ
    Targeting oxidative stress mechanisms to treat Alzheimer's and Parkinson's disease: a critical review
    (Hindawi, 2022) Aborode, Abdullahi Tunde; Pustake, Manas; Awuah, Wireko Andrew; Alwerdani, Mariam; Shah, Parth; Yarlagadda, Rohan; Ahmad, Shahzaib; Correia, Inês F. Silva; Chandra, Ayush; Nansubug, Esther Patience; Abdul-Rahman, Toufik; Mehta, Aashna; Ali, Omar; Amaka, Shekinah Obinna; Zuñiga, Yves Miel H.; Shkodina, A. D.; Inya, Oko Christian; Shen, Bairong; Alexiou, Athanasios; Шкодіна, Анастасія Дмитрівна
    Neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) are becoming more frequent as the age increases. Contemporary therapies provide symptom resolution instead of targeting underlying pathological pathways. Consequently, there is considerable heterogeneity in response to treatment. Research has elucidated multiple potential of pathophysiological mechanisms contributing to neurodegenerative conditions, among which oxidative stress pathways appear to be suitable drug targets. The oxidative stress pathway has given rise to numerous novel pharmacological therapies that may provide a new avenue for neurodegenerative diseases. For example, SKQ (plastoquinone), MitoVitE, vitamin E, SOD mimic, MitoTEMPO (SOD mimetic), and bioactive molecules like curcumin and vitamin C have indeed been examined. To better understand how oxidative stress contributes to neurodegenerative diseases (such as Alzheimer’s and Parkinson’s), we analyzed the medicinal qualities of medicines that target markers in the cellular oxidative pathways. The specific pathway by which mitochondrial dysfunction causes neurodegeneration will require more investigation. An animal study should be carried out on medications that tackle cellular redox mechanisms but are not currently licensed for use in the management of neurodegenerative conditions.