Investigation of coenzyme Q10 status, serum amyloid-β, and tau protein in patients with dementia

Chang, Po-Sheng; Chou, Hsi-Hsien; Lai, Te-Jen; Yen, Chi-Hua; Pan, Ji-Cyun; Lin, Ping-Ting

doi:10.3389/fnagi.2022.910289

Cited by 5 publications

(3 citation statements)

References 62 publications

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“…Interestingly, using in-depth proteomics we found lower levels of CoQ10 in skeletal muscle from prematurely aging mtDNA mutator mice, which were normalized with exercise, thus suggesting that CoQ supplementation, perhaps together with exercise, could be used to treat patients with mitochondrial dysfunction [ 154 ]. Moreover, AD patients with low CoQ10 levels were found to have high serum Aβ and Aβ 40/42 ratio levels [ 297 ]. The impact of CoQ10 supplementation has been widely investigated within rodent models and has been found to improve the symptoms associated with various brain aging disorders.…”

Section: Dietary Supplementsmentioning

confidence: 99%

Mitochondrial Dysfunction: A Key Player in Brain Aging and Diseases

Bartman,

Coppotelli,

Ross

2024

CIMB

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Mitochondria are thought to have become incorporated within the eukaryotic cell approximately 2 billion years ago and play a role in a variety of cellular processes, such as energy production, calcium buffering and homeostasis, steroid synthesis, cell growth, and apoptosis, as well as inflammation and ROS production. Considering that mitochondria are involved in a multitude of cellular processes, mitochondrial dysfunction has been shown to play a role within several age-related diseases, including cancers, diabetes (type 2), and neurodegenerative diseases, although the underlying mechanisms are not entirely understood. The significant increase in lifespan and increased incidence of age-related diseases over recent decades has confirmed the necessity to understand the mechanisms by which mitochondrial dysfunction impacts the process of aging and age-related diseases. In this review, we will offer a brief overview of mitochondria, along with structure and function of this important organelle. We will then discuss the cause and consequence of mitochondrial dysfunction in the aging process, with a particular focus on its role in inflammation, cognitive decline, and neurodegenerative diseases, such as Huntington’s disease, Parkinson’s disease, and Alzheimer’s disease. We will offer insight into therapies and interventions currently used to preserve or restore mitochondrial functioning during aging and neurodegeneration.

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Section: Dietary Supplementsmentioning

confidence: 99%

Mitochondrial Dysfunction: A Key Player in Brain Aging and Diseases

Bartman,

Coppotelli,

Ross

2024

CIMB

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“…Similarly, CoQ10 administration attenuates Aβ accumulation and reduces tau phosphorylation, mitigating AD phenotypes [246][247][248]. Moreover, CoQ10 levels significantly correlated with Aβ accumulation in dementia patients [249], and they were associated with a high risk of developing dementia [250]. Many studies also focused on the efficacy of natural compounds, able not only to scavenge oxidants but also to potentiate endogenous antioxidant systems [12,251].…”

Section: Use Of Antioxidants As Targeted Therapeuticsmentioning

confidence: 99%

Redox Imbalance as a Common Pathogenic Factor Linking Hearing Loss and Cognitive Decline

et al. 2023

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Experimental and clinical data suggest a tight link between hearing and cognitive functions under both physiological and pathological conditions. Indeed, hearing perception requires high-level cognitive processes, and its alterations have been considered a risk factor for cognitive decline. Thus, identifying common pathogenic determinants of hearing loss and neurodegenerative disease is challenging. Here, we focused on redox status imbalance as a possible common pathological mechanism linking hearing and cognitive dysfunctions. Oxidative stress plays a critical role in cochlear damage occurring during aging, as well as in that induced by exogenous factors, including noise. At the same time, increased oxidative stress in medio-temporal brain regions, including the hippocampus, is a hallmark of neurodegenerative disorders like Alzheimer’s disease. As such, antioxidant therapy seems to be a promising approach to prevent and/or counteract both sensory and cognitive neurodegeneration. Here, we review experimental evidence suggesting that redox imbalance is a key pathogenetic factor underlying the association between sensorineural hearing loss and neurodegenerative diseases. A greater understanding of the pathophysiological mechanisms shared by these two diseased conditions will hopefully provide relevant information to develop innovative and effective therapeutic strategies.

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“…Mitochondrial-targeted therapies aim at improving mitochondrial function and reducing accumulation of ROS through targeting specific mitochondrial components, such as the electron transport chain or mPTP. Several compounds that specifically target mitochondria have been investigated as potential treatments for AD [169,170]. These include mitochondria-targeted antioxidants, such as MitoQ, coenzyme Q10, alpha-lipoic acid, and vitamin E, and mitochondria-targeted SS peptides [171,172].…”

mentioning

confidence: 99%

The Major Hypotheses of Alzheimer’s Disease: Related Nanotechnology-Based Approaches for Its Diagnosis and Treatment

Cáceres,

Heusser,

Garnham

et al. 2023

Cells

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Alzheimer’s disease (AD) is a well-known chronic neurodegenerative disorder that leads to the progressive death of brain cells, resulting in memory loss and the loss of other critical body functions. In March 2019, one of the major pharmaceutical companies and its partners announced that currently, there is no drug to cure AD, and all clinical trials of the new ones have been cancelled, leaving many people without hope. However, despite the clear message and startling reality, the research continued. Finally, in the last two years, the Food and Drug Administration (FDA) approved the first-ever medications to treat Alzheimer’s, aducanumab and lecanemab. Despite researchers’ support of this decision, there are serious concerns about their effectiveness and safety. The validation of aducanumab by the Centers for Medicare and Medicaid Services is still pending, and lecanemab was authorized without considering data from the phase III trials. Furthermore, numerous reports suggest that patients have died when undergoing extended treatment. While there is evidence that aducanumab and lecanemab may provide some relief to those suffering from AD, their impact remains a topic of ongoing research and debate within the medical community. The fact is that even though there are considerable efforts regarding pharmacological treatment, no definitive cure for AD has been found yet. Nevertheless, it is strongly believed that modern nanotechnology holds promising solutions and effective clinical strategies for the development of diagnostic tools and treatments for AD. This review summarizes the major hallmarks of AD, its etiological mechanisms, and challenges. It explores existing diagnostic and therapeutic methods and the potential of nanotechnology-based approaches for recognizing and monitoring patients at risk of irreversible neuronal degeneration. Overall, it provides a broad overview for those interested in the evolving areas of clinical neuroscience, AD, and related nanotechnology. With further research and development, nanotechnology-based approaches may offer new solutions and hope for millions of people affected by this devastating disease.

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Investigation of coenzyme Q10 status, serum amyloid-β, and tau protein in patients with dementia

Cited by 5 publications

References 62 publications

Mitochondrial Dysfunction: A Key Player in Brain Aging and Diseases

Mitochondrial Dysfunction: A Key Player in Brain Aging and Diseases

Redox Imbalance as a Common Pathogenic Factor Linking Hearing Loss and Cognitive Decline

The Major Hypotheses of Alzheimer’s Disease: Related Nanotechnology-Based Approaches for Its Diagnosis and Treatment

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