Mitochondrial dysfunction and neurological disorders: A narrative review and treatment overview

Alshial, Eman E.; Abdulghaney, Muhammad Idris; Wadan, Al-Hassan Soliman; Abdellatif, Mohamed Abdelfatah; Ramadan, Nada E.; Suleiman, Aya Muhammed; Waheed, Nahla; Abdellatif, Maha; Mohammed, Haitham S.

doi:10.1016/j.lfs.2023.122257

Cited by 29 publications

(3 citation statements)

References 419 publications

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“…The occurrence of mitochondrial abnormalities has been demonstrated in studies of MS patients as well as in various animal models of MS. These abnormalities include accumulation of reactive ROS, altered mitochondrial dynamics, and mitochondrial autophagy ( Alshial et al, 2023 ).…”

Section: A Link Between Ms and Gut Microbiotamentioning

confidence: 99%

The role of the “gut microbiota-mitochondria” crosstalk in the pathogenesis of multiple sclerosis

Tian,

Huang,

Wang

et al. 2024

Front. Microbiol.

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Multiple Sclerosis (MS) is a neurologic autoimmune disease whose exact pathophysiologic mechanisms remain to be elucidated. Recent studies have shown that the onset and progression of MS are associated with dysbiosis of the gut microbiota. Similarly, a large body of evidence suggests that mitochondrial dysfunction may also have a significant impact on the development of MS. Endosymbiotic theory has found that human mitochondria are microbial in origin and share similar biological characteristics with the gut microbiota. Therefore, gut microbiota and mitochondrial function crosstalk are relevant in the development of MS. However, the relationship between gut microbiota and mitochondrial function in the development of MS is not fully understood. Therefore, by synthesizing previous relevant literature, this paper focuses on the changes in gut microbiota and metabolite composition in the development of MS and the possible mechanisms of the crosstalk between gut microbiota and mitochondrial function in the progression of MS, to provide new therapeutic approaches for the prevention or reduction of MS based on this crosstalk.

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Section: A Link Between Ms and Gut Microbiotamentioning

confidence: 99%

The role of the “gut microbiota-mitochondria” crosstalk in the pathogenesis of multiple sclerosis

Tian,

Huang,

Wang

et al. 2024

Front. Microbiol.

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“…This mitochondrial dysfunction is also an important aspect in the pathogenesis of AD, which diminishes ATP production, disrupts neurotransmitter imbalance, amplifies ROS levels, hinders the removal of damaged mitochondria, thereby affecting synaptic activity and plasticity. This disruption damages synaptic function, hinders neurotransmission, and may even lead to neuronal apoptosis, contributing to the development of AD ( Alshial et al, 2023 ).…”

Section: The Pathogenesis Of Ceramide and Admentioning

confidence: 99%

A review of the mechanisms of abnormal ceramide metabolism in type 2 diabetes mellitus, Alzheimer’s disease, and their co-morbidities

Pan,

Li,

Lin

et al. 2024

Front. Pharmacol.

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The global prevalence of type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD) is rapidly increasing, revealing a strong association between these two diseases. Currently, there are no curative medication available for the comorbidity of T2DM and AD. Ceramides are structural components of cell membrane lipids and act as signal molecules regulating cell homeostasis. Their synthesis and degradation play crucial roles in maintaining metabolic balance in vivo, serving as important mediators in the development of neurodegenerative and metabolic disorders. Abnormal ceramide metabolism disrupts intracellular signaling, induces oxidative stress, activates inflammatory factors, and impacts glucose and lipid homeostasis in metabolism-related tissues like the liver, skeletal muscle, and adipose tissue, driving the occurrence and progression of T2DM. The connection between changes in ceramide levels in the brain, amyloid β accumulation, and tau hyper-phosphorylation is evident. Additionally, ceramide regulates cell survival and apoptosis through related signaling pathways, actively participating in the occurrence and progression of AD. Regulatory enzymes, their metabolites, and signaling pathways impact core pathological molecular mechanisms shared by T2DM and AD, such as insulin resistance and inflammatory response. Consequently, regulating ceramide metabolism may become a potential therapeutic target and intervention for the comorbidity of T2DM and AD. The paper comprehensively summarizes and discusses the role of ceramide and its metabolites in the pathogenesis of T2DM and AD, as well as the latest progress in the treatment of T2DM with AD.

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“…The importance of mitochondrial dysfunction in the pathogenesis of AD has prompted the exploration of new treatment strategies designed to improve mitochondrial function [178][179][180]. A major focus has been on correcting oxidative stress imbalances using mitochondrial-targeted antioxidant therapies, and many studies have been conducted in rodent models showing efficacy [181][182][183].…”

Section: Mitochondria In the Treatment Of Admentioning

confidence: 99%

Mitochondria in Alzheimer’s Disease Pathogenesis

Reiss,

Gulkarov,

Jacob

et al. 2024

Life

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Alzheimer’s disease (AD) is a progressive and incurable neurodegenerative disorder that primarily affects persons aged 65 years and above. It causes dementia with memory loss and deterioration in thinking and language skills. AD is characterized by specific pathology resulting from the accumulation in the brain of extracellular plaques of amyloid-β and intracellular tangles of phosphorylated tau. The importance of mitochondrial dysfunction in AD pathogenesis, while previously underrecognized, is now more and more appreciated. Mitochondria are an essential organelle involved in cellular bioenergetics and signaling pathways. Mitochondrial processes crucial for synaptic activity such as mitophagy, mitochondrial trafficking, mitochondrial fission, and mitochondrial fusion are dysregulated in the AD brain. Excess fission and fragmentation yield mitochondria with low energy production. Reduced glucose metabolism is also observed in the AD brain with a hypometabolic state, particularly in the temporo-parietal brain regions. This review addresses the multiple ways in which abnormal mitochondrial structure and function contribute to AD. Disruption of the electron transport chain and ATP production are particularly neurotoxic because brain cells have disproportionately high energy demands. In addition, oxidative stress, which is extremely damaging to nerve cells, rises dramatically with mitochondrial dyshomeostasis. Restoring mitochondrial health may be a viable approach to AD treatment.

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Mitochondrial dysfunction and neurological disorders: A narrative review and treatment overview

Cited by 29 publications

References 419 publications

The role of the “gut microbiota-mitochondria” crosstalk in the pathogenesis of multiple sclerosis

The role of the “gut microbiota-mitochondria” crosstalk in the pathogenesis of multiple sclerosis

A review of the mechanisms of abnormal ceramide metabolism in type 2 diabetes mellitus, Alzheimer’s disease, and their co-morbidities

Mitochondria in Alzheimer’s Disease Pathogenesis

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