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Effects of idebenone on cognitive function and serum biomarkers in patients with amnestic mild cognitive impairment

European Journal of Medical Research volume 29, Article number: 600 (2024) Cite this article

Abstract

Objectives

This retrospective study aimed to investigate the effects of idebenone on cognitive function and serum levels of superoxide dismutase (SOD) and high-sensitivity C-reactive protein (hs-CRP) in individuals with amnestic mild cognitive impairment (aMCI).

Methods

Retrospective data were collected from the Neurology outpatient department of Liaocheng People’s Hospital from January 2021 to June 2023. Patients with a newly diagnosed aMCI who received treatment were included in the idebenone treatment group. The treatment group took 30 mg of oral idebenone three times a day for 6 months. A control group of 51 MCI patients who did not receive cholinesterase inhibitors or other cognitive-enhancing drugs during the period was selected. Cognitive function assessments and serum Biomarkers were conducted before and after treatment in both groups.

Results

MoCA scores were significantly improved after 6 months of idebenone treatment, and the difference was statistically significant. The delayed recall score was significantly improved, and the difference was statistically significant; The level of SOD increased and the level of high-sensitivity C-reactive protein decreased after the treatment, but there was no significant change in the control group.

Conclusions

The results of this study demonstrate that idebenone treatment significantly improves cognitive function in individuals with aMCI, particularly in the domain of delayed memory. In addition, idebenone reduces the degree of inflammation and oxidative stress and improves antioxidant levels. These findings suggest that idebenone may be a promising intervention for the management of cognitive impairments associated with aMCI.

Graphical Abstract

Introduction

With the increasing aging population, cognitive impairment has become one of the major health issues globally, and Alzheimer’s disease (AD) is the most common type [1]. Amnestic mild cognitive impairment (aMCI), characterized by decline in memory function while maintaining basic daily living abilities, is a cognitive impairment state that lies between normal aging and AD [2, 3]. However, there is currently no targeted treatment for aMCI, and researches on aMCI mainly focus on finding preventive or delaying measures for MCI progression to dementia [4].

In recent years, antioxidant therapy has gained significant attention in the medical field due to its potential therapeutic benefits in various diseases. Among them, idebenone (IDB) had been shown to have potential in the treatment of mitochondrial dysfunction and neurodegenerative diseases [5,6,7,8]. In Parkinson's disease research, idebenone had been shown to reduce lipid peroxidation levels and increase the expression of glutathione peroxidase, thereby mitigating oxidative damage [9]. Idebenone had also demonstrated significant clinical effects in treating hypertrophic cardiomyopathy caused by Friedreich’s ataxia [10]. It also had shown some effectiveness in treating mitochondrial myopathy and encephalopathy with lactic acidosis and stroke-like episodes as well [11]. In addition, IDB had been used to treat hereditary diseases resulting from mitochondrial dysfunction, such as Leber's hereditary optic neuropathy (LHON), the use of IDB exhibited certain therapeutic benefits [12].

Preclinical research had shown that IDB could cross the blood–brain barrier and protect neurons from oxidative damage, indicating its direct role in protecting cognitive function [13, 14]. IDB could protect primary neuronal mitochondria from oxidative stress, inhibit the formation of mitochondrial superoxide, and regulate important signaling pathways associated with cell survival and synaptic plasticity, which may contribute to its neuroprotective properties [14, 15]. Related clinical studies also suggested that IDB could effectively reduce blood inflammatory factor levels, increase antioxidant factor levels, reduce the degree of inflammation and oxidative stress reactions, and improve cognitive function [16,17,18].

Therefore, this study aims to investigate the effect of IDB treatment on cognitive function and the levels of superoxide dismutase (SOD) and high-sensitivity C-reactive protein (hs-CRP) in aMCI patients while also evaluating the efficacy and safety of IDB and providing a reference for clinical intervention of MCI.

Materials and methods

Retrospective data were collected from the Neurology outpatient department of Liaocheng People’s Hospital from January 2021 to June 2023. Patients with a newly diagnosed aMCI.

Each enrolled patient underwent relevant blood tests, cranial magnetic resonance imaging (MRI), and neuropsychological assessments to confirm the diagnosis of cognitive impairment.

Inclusion criteria

  • Age between 50 and 80 years.

  • Meet the clinical MCI diagnostic criteria established by the National Institute on Aging (NIA) and the Alzheimer’s Association (AA) in 2011, with a focus on AD-related amnestic MCI (aMCI).

  • Neuropsychological evaluation meeting the criteria of the Mini-Mental State Examination (MMSE) for normal cognitive function (elementary education level score > 20, middle school education level or above score > 24), Clinical Dementia Rating (CDR) score of 0.5 (memory = 0.5).

  • Normal daily living activities evaluated by the Activities of Daily Living (ADL) scale.

  • Proficiency in spoken Mandarin Chinese (non-illiterate).

  • No previous use of cholinesterase inhibitors, NMDA receptor antagonists, memantine, or other cognitive enhancers.

Exclusion criteria

Patients meeting any of the following criteria were excluded from the study:

  • Diagnosed with dementia at baseline assessment.

  • History of clear cerebrovascular stroke with symptoms or signs of neurological deficit at onset and corresponding responsible lesions on neuroimaging.

  • Severe white matter lesions (Fazekas score ≥ 3).

  • Consciousness impairment due to any cause.

  • Severe aphasia or physical disability preventing completion of neuropsychological examination.

  • Current diagnosis of psychiatric disorders such as major depression (Hamilton Depression Rating Scale score > 8) or schizophrenia.

  • History of alcoholism, substance abuse, traumatic brain injury, epilepsy, normal-pressure hydrocephalus, or other cognitive impairment-causing neurological diseases.

  • Presence of systemic diseases that could lead to mild cognitive impairment, such as hepatic or renal insufficiency, endocrine disorders, vitamin deficiency, or anemia.

All procedures performed in this study involving human participants were in accordance with the ethical standards of the institution and the National Research Council and the Declaration of Helsinki (revised in 2013). The medical ethics committee of Liaocheng People's Hospital approved this study [Approval No: 2024019].

Study design

After the diagnosis was confirmed, the patients were divided into two groups: the IDB treatment group and control group: (1) IDB group: patients took 30 mg of oral IDB three times a day for 6 months. (2) The control group included patients who visited the outpatient department during the same period and did not use cholinesterase inhibitors or other cognitive enhancers throughout the study.

According to the study criteria, the treatment group included 50 subjects while50 subjects were included in the control group finally. The screening process is shown in Fig. 1.

Fig. 1
figure 1

Flow chart of the study participants

Full size image

Patients with comorbidities such as hypertension, diabetes, or dyslipidemia continued their original treatment plans during the study.

Outcome measures: (1) Mini-Mental State Examination Scale (MMSE); MoCA; scores before and 6 months after treatment. (2) Levels of serum inflammatory factors were measured before and 6 months after treatment or observation. hs-CRP levels were measured using nephelometry. (3) Levels of oxidative stress indicators were calculated before and 6 months after treatment or observation in both groups, SOD were determined using enzyme-linked immunosorbent assay.

Statistical analysis

Statistical analysis was performed using SPSS 23.0 software. Normally distributed data were presented as mean ± standard deviation. Independent sample t tests were used for between-group comparisons, and paired I tests were used for within-group comparisons. Non-normally distributed data were presented as median and interquartile range. Count or categorical data were presented as numbers or rates, and between-group comparisons were made using the chi-square test. Descriptive statistics were used to summarize the clinical characteristics and cognitive assessments of all participants. Wilcoxon and Mann–Whitney U tests were used to compare within-group and between-group differences using nonparametric rank sum tests. A significance level of P < 0.05 was considered statistically significant for differences between the two groups.

Results

Comparison of baseline data

There was no significant difference in the baseline data between the two groups (P > 0.05) (Table 1).

Table 1 Comparison of baseline data of the two group patients
Full size table

Comparison of cognitive function

MMSE and MoCA scores were compared between the two groups at baseline and after 6 months. The MoCA score significantly improved in the IDB group, while no significant change was observed in the control group Table 2.

Table 2 Comparison of cognitive function between the two groups
Full size table

Comparison of subdomains of MoCA

We further analyzed the subdomains of MoCA before and after IDB treatment, and found that the improvement in delayed memory impairment was the most significant, with a statistically significant difference Table 3.

Table 3 Comparison of subdomains of MoCA
Full size table

Comparison of SOD and hs-CRP

We conducted a comparative analysis of oxidative stress markers and serum inflammatory factors before and after treatment in both patient groups. We found that after IDB treatment, there was a significant increase in serum SOD level and a significant decrease in hs-CRP levels, which were statistically significant (p < 0.05). However, no such changes were observed in the control group Table 4.

Table 4 Comparison of SOD and hs-CRP
Full size table

These findings indicate that IDB treatment significantly increases SOD levels and decreases hs-CRP levels in the serum of patients with aMCI, suggesting a reduction in oxidative stress.

Safety assessment results

No serious adverse events occurred throughout the observational period. In the IDB treatment group, three patients experienced insomnia characterized by difficulty falling asleep. During their 1 month follow-up visit, they were advised to take the medication at 4 PM, which resulted in alleviation of their symptoms. three patients of the IDB group, and four patients of the control group, had comorbid hyperlipidemia and were concurrently taking statin medications. Mild liver transaminase abnormalities were observed during the liver function reevaluation at 3 months. However, after discontinuing the statin medications, these abnormalities returned to normal. The use of IDB did not have any significant impact on patients with comorbid conditions such as hypertension, diabetes, or hyperlipidemia. No adverse reactions such as nausea, vomiting, or skin allergies were reported in either group. There was no significant difference in the incidence of adverse reactions between the two groups.

Discussion

In this study, we found that the use of IDB in patients with aMCI improved their cognitive function in MoCA scores, especially in the domain of delayed memory. AD is the most common type of dementia in the elderly, but to date, there are no effective interventions that could reverse or halt the continuous progression of AD [19]. Recent research has focused on interventions and treatments in the preclinical stages of AD. aMCI is highly associated with AD pathology [4].

IDB, as a synthetic analogue of coenzyme Q10, had garnered significant attention in the research of various neurodegenerative diseases due to its unique molecular mechanisms. Studies have demonstrated that IDB exerts its neuroprotective effects through multiple pathways. First, IDB had been found to activate the autophagy process, thereby facilitating the degradation of alpha-synuclein. This mechanism was achieved by inhibiting the AKT–mTOR signaling pathway, which plays a crucial role in the progression of Parkinson's disease. In SH-SY5Y cell models, idebenone enhanced autophagy and reduced the accumulation of synuclein, suggesting a potential therapeutic strategy against Parkinson’s disease [20, 21]. Second, IDB has also been shown to modulate amyloid beta (Aβ) pathology in Alzheimer’s disease model mice, decreasing the number of Aβ plaques. Research indicates that IDB significantly improves Aβ-related pathological changes by regulating the RAGE/caspase-3 signaling pathway and enhancing the expression of Aβ degrading enzymes, neprilysin and alpha-secretase. Furthermore, IDB suppressed the hyperphosphorylation of tau protein in the 5xFAD mouse model, further supporting its potential in the treatment of AD [22]. The antioxidant properties of IDB also make it a focal point of research. It protects neurons from damage by modulating mitochondrial function and alleviating neuroinflammatory responses and oxidative stress. Relevant studies have shown that in LPS-induced neuroinflammation models, IDB reduces the activation of the NLRP3 inflammasome, consequently diminishing glial cell responses and the release of pro-inflammatory cytokines [13].

Several clinical studies [6, 18, 23, 24] had shown that IDB could improve cognitive function and quality of life in AD patients, while a few studies have suggested that IDB failed to slow down the decline in cognitive ability in AD [25], This discrepancy may be related to the source of the selected study subjects, dosage and duration of medication, and the severity of cognitive impairment. In addition to AD, IDB has also been used to treat other diseases associated with cognitive impairments, such as vascular cognitive impairment and Parkinson’s disease-related cognitive impairment, and has shown protective effects on cognitive function [18, 26]. Previous research had yielded inconsistent results regarding the protective effects of IDB on cognitive function in these conditions as well as in patients with MCI [27].

In this study, we found that using IDB for 6 months in aMCI patients improved their cognitive function, as evidenced by an improvement in MoCA scores, particularly in the domain of delayed memory. However, there were no significant changes observed in MMSE scores before and after treatment in both patient groups. In the subdomain analysis of MoCA scores, we found a significant improvement in delayed memory scores. This result reveals the beneficial effect of IDB in improving memory impairment, especially short-term and delayed memory, in aMCI patients. Enhancing delayed memory capacity is of great significance for improving the quality of life and daily living abilities in MCI patients, as memory decline is often one of the earliest and most troublesome symptoms in patients with aMCI [28, 29].

Furthermore, this study also focused on the changes in SOD and hs-CRP levels in the serum after IDB treatment. SOD is an important antioxidant enzyme that scavenges superoxide anions in the body and protects cells from oxidative damage [30, 31], Supplementing SOD can prevent cognitive decline by reducing lipid peroxidation and maintaining neurogenesis in the hippocampus [32]. hs-CRP is an inflammatory marker, and increased levels often indicates the presence of an inflammatory response in the body. Moreover, hs-CRP levels are significantly elevated in AD patients as a non-specific biomarker [33]. In this study, we observed a significant increase in SOD levels and a significant decrease in hs-CRP levels after IDB treatment, suggesting that IDB enhances the antioxidant capacity and reduces oxidative stress and inflammatory response in aMCI patients. In previous studies, AD was closely associated with oxidative stress, which lead to increased production of Aβ and aberrant phosphorylation of tau protein, Excessive production of reactive oxygen species(ROS) resulted in lipid peroxidation of unsaturated fatty acids in cell membranes, causing functional impairment, aging, and apoptosis of neuronal cells, ultimately leading to memory and cognitive dysfunction [34]. IDB could inhibit the activation of mitochondrial permeability transition pores, thereby protecting mitochondrial membrane potential and ATP production [35]. IDB mitigated mitochondrial oxidative stress and offers protection against Aβ-mediated neurotoxicity. Excessive intracellular free radicals inhibit the activation of protein kinase Avia (PKA) oxidative modification of thiol groups in cysteine residues, while a large amount of ROS released during mitochondrial oxidative stress could further exacerbate this inhibition [20], IDB protected PKA from oxidative damage by suppressing the generation and accumulation of mitochondrial ROS [36]. IDB influenced the levels of SOD and hs-CRP through the above mechanisms. These combined mechanisms contribute to the improvement of cognitive function in MCI patients [15], though specific mechanisms require further experimental research for confirmation.

However, this study has several limitations. First, it was a retrospective study, which may lead to selection bias and did not account for other factors that could contribute to cognitive decline, such as lifestyle variables. Second, the sample size in this study was relatively small, which may limit the generalizability of the findings regarding the efficacy of IDB in the treatment of MCI. In addition, because this study is retrospective in nature, the control group did not utilize a placebo. Future research will incorporate a placebo-controlled design. In further studies, we intend to increase the sample size, include more inflammatory and oxidative stress markers, and extend the duration of treatment observation. We will design a prospective, multi-center, randomized, double-blind, placebo-controlled study protocol, to accurately evaluate the efficacy and safety of IDB in the treatment of MCI.

In conclusion, the results of this study demonstrate that IDB treatment has a significant positive impact on cognitive function, especially in improving delayed memory in patients with aMCI. In addition, IDB can reduce the extent of oxidative stress and inflammation in aMCI patients, indicating the potential of IDB as an intervention for treating mild cognitive impairments. These findings provide new insights into the treatment of aMCI. They also require further research and evaluation.

Availability of data and materials

No datasets were generated or analysed during the current study.

Abbreviations

AD:

Alzheimer’s disease

SOD:

Superoxide dismutase

hs-CRP:

High-sensitivity C-reactive protein

MCI:

Mild cognitive impairment

aMCI:

Amnestic mild cognitive impairment

IDB:

Idebenone

ADL:

Activities of daily living

CDR:

Clinical dementia rating

MMSE:

Mini-mental state examination

ROS:

Reactive oxygen species

Aβ:

Amyloid-beta

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Funding

This study was supported by Key Research and Development Program Policy-guided Project of Liaocheng City (2022YDSF20).

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Author notes

  1. Huiting Wang and Xiaoling Wang are co-first authors.

Authors and Affiliations

  1. Department of Neurology, Liaocheng People’s Hospital, No. 67 Dongchang West Road, Liaocheng, 252000, Shandong Province, People’s Republic of China

    Huiting Wang, Xiaoling Wang, Weiwei Wang & Depeng Feng

  2. Department of Neurology, Liaocheng People’s Hospital, Shandong University, Jinan, 250012, Shandong, People’s Republic of China

    Huiting Wang

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Contributions

HW: writing—original draft, writing—review & editing, funding acquisition; XW: data curation, writing—original draft, writing—review & editing; WW: writing—original draft, writing—review & editing; DF: writing—original draft, writing—review & editing.

Corresponding authors

Correspondence to Weiwei Wang or Depeng Feng.

Ethics declarations

Ethics approval and consent to participate

All procedures involving human participants in this study complied with the ethical standards set by relevant institutions and/or national research committees, as well as the principles outlined in the Helsinki Declaration of 1964 and its later amendments or similar ethical standards. The research had obtained approval from the Ethics Review Committee of Liaocheng People's Hospital [Approval No: 2024019].

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Wang, H., Wang, X., Wang, W. et al. Effects of idebenone on cognitive function and serum biomarkers in patients with amnestic mild cognitive impairment. Eur J Med Res 29, 600 (2024). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s40001-024-02184-w

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European Journal of Medical Research

ISSN: 2047-783X

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