Clinical and Pathological Benefit of Twendee X in Alzheimer's Disease Transgenic Mice with Chronic Cerebral Hypoperfusion

Liu, Xia; Yamashita, Toru; Shang, Jingwei; Shi, Xiaowen; Morihara, Ryuta; Huang, Yong; Sato, Kota; Hishikawa, Nozomi; Ohta, Yasuyuki

doi:10.1016/j.jstrokecerebrovasdis.2019.03.029

Cited by 21 publications

(25 citation statements)

References 26 publications

(27 reference statements)

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“…The therapeutic effect of TwX was also examined in nude mice that underwent inoculation of colon or gastric cancer cells: TwX reduced tumor growth, increased antioxidants measured by the d-ROMs test, and reduced natural killer cell activity, suggesting that TwX significantly reduced tumor growth and inhibited metastasis by reducing oxidative stress [107]. In ischemic stroke model mice, we demonstrated that pretreatment of TwX (20 mg/kg/d for 14 days) reduced infarct size as well as the expression of both oxidative stress markers such as 8-OHdG, 4-HNE and Nε-(carboxymethyl) lysine (an advanced glycation end product) and inflammatory markers such as Iba-1, tumor necrosis factor α (TNF-α) and monocyte chemotactic protein [108,109].…”

Section: Twendee Xmentioning

confidence: 97%

Prevention of Cognitive Decline in Alzheimer’s Disease by Novel Antioxidative Supplements

Tadokoro

Ohta

Inufusa

et al. 2020

IJMS

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Oxidative stress plays a crucial role in Alzheimer's disease (AD) from its prodromal stage of mild cognitive impairment. There is an interplay between oxidative stress and the amyloid β (Aβ) cascade via various mechanisms including mitochondrial dysfunction, lipid peroxidation, protein oxidation, glycoxidation, deoxyribonucleotide acid damage, altered antioxidant defense, impaired amyloid clearance, inflammation and chronic cerebral hypoperfusion. Based on findings that indicate that oxidative stress plays a major role in AD, oxidative stress has been considered as a therapeutic target of AD. In spite of favorable preclinical study outcomes, previous antioxidative components, including a single antioxidative supplement such as vitamin C, vitamin E or their mixtures, did not clearly show any therapeutic effect on cognitive decline in AD. However, novel antioxidative supplements can be beneficial for AD patients. In this review, we summarize the interplay between oxidative stress and the Aβ cascade, and introduce novel antioxidative supplements expected to prevent cognitive decline in AD.

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Section: Twendee Xmentioning

confidence: 97%

Prevention of Cognitive Decline in Alzheimer’s Disease by Novel Antioxidative Supplements

Tadokoro

Ohta

Inufusa

et al. 2020

IJMS

Self Cite

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“…It has been reported that chronic cerebral hypoperfusion (CCH) induces oxidative stress and neuroinflammation, potentially contributing to the progression of neurodegenerative diseases [70,71]. Thus, recent studies have examined whether an antioxidant supplement, Twendee X (TwX), exhibits beneficial effects in a mouse model of AD with CCH [72,73]. TwX contains the antioxidants coenzyme Q10, niacin amid, L-cystine, ascorbic acid, succinic acid, fumaric acid, L-glutamine, and riboflavin [72][73][74].…”

Section: Preclinical Findings Obtained By Twendee X Administrationmentioning

confidence: 99%

“…Thus, recent studies have examined whether an antioxidant supplement, Twendee X (TwX), exhibits beneficial effects in a mouse model of AD with CCH [72,73]. TwX contains the antioxidants coenzyme Q10, niacin amid, L-cystine, ascorbic acid, succinic acid, fumaric acid, L-glutamine, and riboflavin [72][73][74]. One study administered TwX by oral gavage to APP23 mice, which overexpress the human APP Swedish mutant gene, that were treated with ameroid constrictors on bilateral common carotid arteries to induce CCH development [72,73].…”

Section: Preclinical Findings Obtained By Twendee X Administrationmentioning

confidence: 99%

“…TwX contains the antioxidants coenzyme Q10, niacin amid, L-cystine, ascorbic acid, succinic acid, fumaric acid, L-glutamine, and riboflavin [72][73][74]. One study administered TwX by oral gavage to APP23 mice, which overexpress the human APP Swedish mutant gene, that were treated with ameroid constrictors on bilateral common carotid arteries to induce CCH development [72,73]. Immunohistochemical analyses revealed that TwX reduced oxidative stress levels in the brain [72].…”

Section: Preclinical Findings Obtained By Twendee X Administrationmentioning

confidence: 99%

“…One study administered TwX by oral gavage to APP23 mice, which overexpress the human APP Swedish mutant gene, that were treated with ameroid constrictors on bilateral common carotid arteries to induce CCH development [72,73]. Immunohistochemical analyses revealed that TwX reduced oxidative stress levels in the brain [72]. Furthermore, it reduced parenchymal and vascular Aβ deposition levels, microglial activation, and neuroinflammation in the brain [72].…”

Section: Preclinical Findings Obtained By Twendee X Administrationmentioning

confidence: 99%

See 2 more Smart Citations

Potential Therapeutic Approaches for Cerebral Amyloid Angiopathy and Alzheimer’s Disease

Tanaka

Saitô

Inoue

et al. 2020

IJMS

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Cerebral amyloid angiopathy (CAA) is a cerebrovascular disease directly implicated in Alzheimer’s disease (AD) pathogenesis through amyloid-β (Aβ) deposition, which may cause the development and progression of dementia. Despite extensive studies to explore drugs targeting Aβ, clinical benefits have not been reported in large clinical trials in AD patients or presymptomatic individuals at a risk for AD. However, recent studies on CAA and AD have provided novel insights regarding CAA- and AD-related pathogenesis. This work has revealed potential therapeutic targets, including Aβ drainage pathways, Aβ aggregation, oxidative stress, and neuroinflammation. The functional significance and therapeutic potential of bioactive molecules such as cilostazol and taxifolin have also become increasingly evident. Furthermore, recent epidemiological studies have demonstrated that serum levels of a soluble form of triggering receptor expressed on myeloid cells 2 (TREM2) may have clinical significance as a potential novel predictive biomarker for dementia incidence. This review summarizes recent advances in CAA and AD research with a focus on discussing future research directions regarding novel therapeutic approaches and predictive biomarkers for CAA and AD.

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Cognitive Impairments and blood-brain Barrier Damage in a Mouse Model of Chronic Cerebral Hypoperfusion

et al. 2022

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Chronic cerebral hypoperfusion (CCH) is commonly involved in various brain diseases. Tight junction proteins (TJs) are key components constituting the anatomical substrate of the blood-brain barrier (BBB). Changes in cognitive function and BBB after CCH and their relationship need further exploration. To investigate the effect of CCH on cognition and BBB, we developed a bilateral common carotid artery stenosis (BCAS) model in Tie2-GFP mice. Mice manifested cognitive impairments accompanied with increased microglia after the BCAS operation. BCAS mice also exhibited increased BBB permeability at all time points set from D1 to D42. Furthermore, BCAS mice showed reduced expression of TJs 42 d after the operation. In addition, correct entrances of mice in radial arm maze test had a moderate negative correlation with EB extravasation. Our data suggested that BCAS could lead to cognitive deficits, microglia increase and BBB dysfunction characterized by increased BBB permeability and reduced TJs expression level. BBB permeability may be involved in the cognitive impairments induced by CCH.

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Clinical and Pathological Benefit of Twendee X in Alzheimer's Disease Transgenic Mice with Chronic Cerebral Hypoperfusion

Cited by 21 publications

References 26 publications

Prevention of Cognitive Decline in Alzheimer’s Disease by Novel Antioxidative Supplements

Prevention of Cognitive Decline in Alzheimer’s Disease by Novel Antioxidative Supplements

Potential Therapeutic Approaches for Cerebral Amyloid Angiopathy and Alzheimer’s Disease

Cognitive Impairments and blood-brain Barrier Damage in a Mouse Model of Chronic Cerebral Hypoperfusion

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