Specific alterations in the circulating levels of the SIRT1, TLR4, and IL7 proteins in patients with dementia

Kılıç, Ülkan; Elibol, Birsen; Uysal, Ömer; Kılıç, Ertuğrul; Yuluğ, Burak; Sakul, Ayse Arzu; Yildiz, Gulsen Babacan

doi:10.1016/j.exger.2018.07.018

Cited by 17 publications

(9 citation statements)

References 76 publications

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“…In addition, it was observed that brains of AD patients have consistently reduced NAD+ levels and SIRT1 transcription and/or protein levels involved in chronic inflammation that can also be altered by increased levels of the activated proinflammatory transcription factor NF-κB ( 77 – 79 ). In one of our studies, we found a significant increase in the SIRT1 level of dementia patients ( 80 ). Furthermore, in the patients with Huntington's disease (HD), Baldo and his colleagues found higher expression of SIRT1 protein level in the most affected brain regions, especially hypothalamic regions important for metabolic regulation, compared to brain regions which were less affected from the mutant huntingtin protein ( 28 ).…”

Section: Sirt1 and Age-related Neurodegenerative Diseasesmentioning

confidence: 48%

High Levels of SIRT1 Expression as a Protective Mechanism Against Disease-Related Conditions

2018

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SIRT1 protein, a member of Silent Information Regulator 2 (Sir2) protein family, have gained considerable attention as epigenetic regulators for a great area in the human physiology. Changes in sirtuin expression are critical in several diseases, including metabolic syndrome, cardiovascular diseases, cancer and neurodegeneration. Here, we provide an overview of the association of the increasing level of SIRT1 protein for regulating some disease related conditions such as obesity, cardiovascular diseases and neurodegeneration. This review also provides a detailed molecular understanding of the interaction of the some basic molecules with increasing SIRT1 levels rather than reduction of the SIRT1 expression. In this context, the current approaches to enhancing the expression of SIRT1 points the importance of epigenetics in several age-related diseases to provide a healthy aging by developing novel therapies which can prevent or damp the progression of some diseases.

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Section: Sirt1 and Age-related Neurodegenerative Diseasesmentioning

confidence: 48%

High Levels of SIRT1 Expression as a Protective Mechanism Against Disease-Related Conditions

2018

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“…A clinical study conducted in Northern Han Chinese populations demonstrated an increased plasma level of TLR4 in the peripheral blood mononuclear cells (PBMCs) along with elevated TLR4 mRNA and protein levels in LOAD patients compared to healthy controls [98]. On the contrary, a downregulation of TLR4 protein expression was observed in plasma/serum of AD patients who had more Aβ plaques than in patients with other dementia-related diseases [99]. A population study in northern Italy including 626 AD patients also reported that the +896A TLR4 pro-inflammatory allele was overrepresented in AD patients, suggesting that TLR4 single nucleotide polymorphism (SNP) may be a genetic marker of AD susceptibility [100].…”

Section: Hmgb1 Rage and Tlr4 As Potential Clinical Biomarkers Of Admentioning

confidence: 99%

Impact of HMGB1, RAGE, and TLR4 in Alzheimer’s Disease (AD): From Risk Factors to Therapeutic Targeting

Paudel

Angelopoulou

Piperi

et al. 2020

Cells

160

136

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Alzheimer’s disease (AD) is a devastating neurodegenerative disorder and a leading cause of dementia, with accumulation of amyloid-beta (Aβ) and neurofibrillary tangles (NFTs) as defining pathological features. AD presents a serious global health concern with no cure to date, reflecting the complexity of its pathogenesis. Recent evidence indicates that neuroinflammation serves as the link between amyloid deposition, Tau pathology, and neurodegeneration. The high mobility group box 1 (HMGB1) protein, an initiator and activator of neuroinflammatory responses, has been involved in the pathogenesis of neurodegenerative diseases, including AD. HMGB1 is a typical damage-associated molecular pattern (DAMP) protein that exerts its biological activity mainly through binding to the receptor for advanced glycation end products (RAGE) and toll-like receptor 4 (TLR4). RAGE and TLR4 are key components of the innate immune system that both bind to HMGB1. Targeting of HMGB1, RAGE, and TLR4 in experimental AD models has demonstrated beneficial effects in halting AD progression by suppressing neuroinflammation, reducing Aβ load and production, improving spatial learning, and inhibiting microglial stimulation. Herein, we discuss the contribution of HMGB1 and its receptor signaling in neuroinflammation and AD pathogenesis, providing evidence of its beneficial effects upon therapeutic targeting.

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“…As modulators of histone modifications, many dietary polyphenols hold promise to be effective for prevention and therapy of neurodegeneration [382].…”

Section: Impact Of Dietary Factors On Histone Post-translational Modimentioning

confidence: 99%

Functional Foods: An Approach to Modulate Molecular Mechanisms of Alzheimer’s Disease

Atlante

Amadoro

Bobba

et al. 2020

Cells

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A new epoch is emerging with intense research on nutraceuticals, i.e., “food or food product that provides medical or health benefits including the prevention and treatment of diseases”, such as Alzheimer’s disease. Nutraceuticals act at different biochemical and metabolic levels and much evidence shows their neuroprotective effects; in particular, they are able to provide protection against mitochondrial damage, oxidative stress, toxicity of β-amyloid and Tau and cell death. They have been shown to influence the composition of the intestinal microbiota significantly contributing to the discovery that differential microorganisms composition is associated with the formation and aggregation of cerebral toxic proteins. Further, the routes of interaction between epigenetic mechanisms and the microbiota–gut–brain axis have been elucidated, thus establishing a modulatory role of diet-induced epigenetic changes of gut microbiota in shaping the brain. This review examines recent scientific literature addressing the beneficial effects of some natural products for which mechanistic evidence to prevent or slowdown AD are available. Even if the road is still long, the results are already exceptional.

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Specific alterations in the circulating levels of the SIRT1, TLR4, and IL7 proteins in patients with dementia

Cited by 17 publications

References 76 publications

High Levels of SIRT1 Expression as a Protective Mechanism Against Disease-Related Conditions

High Levels of SIRT1 Expression as a Protective Mechanism Against Disease-Related Conditions

Impact of HMGB1, RAGE, and TLR4 in Alzheimer’s Disease (AD): From Risk Factors to Therapeutic Targeting

Functional Foods: An Approach to Modulate Molecular Mechanisms of Alzheimer’s Disease

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