International Journal of Molecular Sciences

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Special Issue Information

Dear Colleagues,

Normal aging is an inevitable process of organisms over time. Brain aging is one of the most critical biological processes disturbing the physiological balance, and cognitive impairment including Alzheimer’s disease (AD) is one of the most common and disabling conditions in older people. Cognitive impairment is characterized by a considerable reduction in neural activity or neuronal death in the brain. Dementia refers to the loss of an individual’s mental abilities and ability to perform social activities severe enough to cause a person daily life impairment. Despite recent FDA-approved drug for AD, it is still equivocal in that of clinical effectiveness, and new therapeutic approaches are needed.

This Special Issue will present the current research approaches to understand the progression of cognitive impairment and external environment of the brain excavation according to controllable changes. This Issue will also present research on the identification of the changes in immune cells in the brain to control targets aggravating dementia due to lipid metabolism problems in the blood, to discover risk factors and early diagnostic biomarkers for dementia in other body organs outside the brain, and to explore therapeutic targets controlling cognitive impairment. We warmly welcome contributions in the form of original research articles, reviews, and communications.

Dr. KyoungJoo Cho
Guest Editor

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Keywords

cognitive impairment
aging
neurodegenerative disease
dementia
mild cognitive impairment
immune cells
brain

Published Papers (2 papers)

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Research

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17 pages, 2367 KiB

Open AccessArticle

Why Does the Antioxidant Complex Twendee X^® Prevent Dementia?

by Fukka You, Yoshiaki Harakawa, Toshikazu Yoshikawa and Haruhiko Inufusa

Int. J. Mol. Sci. 2023, 24(16), 13018; https://doi.org/10.3390/ijms241613018 - 21 Aug 2023

Cited by 4 | Viewed by 1778

Abstract

Alzheimer’s disease (AD) is a complex neurodegenerative disease characterized by cognitive and short-term memory impairments. The disease involves multiple pathological factors such as amyloid plaque formation, mitochondrial dysfunction, and telomere shortening; however, oxidative stress and diabetes mellitus are significant risk factors. The onset of AD begins approximately 20 years before clinical symptoms manifest; therefore, treating AD after symptoms become evident is possibly too late to have a significant effect. As such, preventing AD or using an effective treatment at an early stage is important. Twendee X^® (TwX) is an antioxidant formulation consisting of eight ingredients. TwX has been proven to prevent the progression to dementia in patients with mild cognitive impairment (MCI) in a multicenter, randomized, double-blind, placebo-controlled, prospective intervention trial. As well, positive data has already been obtained in several studies using AD model mice. Since both diabetes and aging are risk factors for AD, we examined the mechanisms behind the effects of TwX on AD using the spontaneous hyperglycemia model and the senescence model of aged C57BL/6 mice in this study. TwX was administered daily, and its effects on diabetes, autophagy in the brain, neurogenesis, and telomere length were examined. We observed that TwX protected the mitochondria from oxidative stress better than a single antioxidant. TwX not only lowered blood glucose levels but also suppressed brain neurogenesis and autophagy. Telomeres in TWX-treated mice were significantly longer than those in non-treated mice. There are many factors that can be implicated in the development and progression of dementia; however, multiple studies on TwX suggest that it may offer protection against dementia, not only through the effects of its antioxidants but also by targeting multiple mechanisms involved in its development and progression, such as diabetes, brain neurogenesis, telomere deficiency, and energy production. Full article

(This article belongs to the Special Issue Cognitive Dysfunction: Molecular Research and Novel Therapy)

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Review

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21 pages, 1607 KiB

Open AccessReview

Neutrophil-Mediated Progression of Mild Cognitive Impairment to Dementia

by KyoungJoo Cho

Int. J. Mol. Sci. 2023, 24(19), 14795; https://doi.org/10.3390/ijms241914795 - 30 Sep 2023

Viewed by 1632

Abstract

Cognitive impairment is a serious condition that begins with amnesia and progresses to cognitive decline, behavioral dysfunction, and neuropsychiatric impairment. In the final stage, dysphagia and incontinence occur. There are numerous studies and developed drugs for cognitive dysfunction in neurodegenerative diseases, such as Alzheimer’s disease (AD); however, their clinical effectiveness remains equivocal. To date, attempts have been made to overcome cognitive dysfunction and understand and delay the aging processes that lead to degenerative and chronic diseases. Cognitive dysfunction is involved in aging and the disruption of inflammation and innate immunity. Recent reports have indicated that the innate immune system is prevalent in patients with AD, and that peripheral neutrophil markers can predict a decline in executive function in patients with mild cognitive impairment (MCI). Furthermore, altered levels of pro-inflammatory interleukins have been reported in MCI, which have been suggested to play a role in the peripheral immune system during the process from early MCI to dementia. Neutrophils are the first responders of the innate immune system. Neutrophils eliminate harmful cellular debris via phagocytosis, secrete inflammatory factors to activate host defense systems, stimulate cytokine production, kill pathogens, and regulate extracellular proteases and inhibitors. This review investigated and summarized the regulation of neutrophil function during cognitive impairment caused by various degenerative diseases. In addition, this work elucidates the cellular mechanism of neutrophils in cognitive impairment and what is currently known about the effects of activated neutrophils on cognitive decline. Full article

(This article belongs to the Special Issue Cognitive Dysfunction: Molecular Research and Novel Therapy)

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