Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here?

Nature Reviews Neurology, Journal Year: 2020, Volume and Issue: 17(3), P. 157 - 172

Published: Dec. 14, 2020

Language: Английский

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Leaky gut: mechanisms, measurement and clinical implications in humans

Gut, Journal Year: 2019, Volume and Issue: 68(8), P. 1516 - 1526

Published: May 10, 2019

The objectives of this review on ‘leaky gut’ for clinicians are to discuss the components intestinal barrier, diverse measurements permeability, their perturbation in non-inflammatory ‘stressed states’ and impact treatment with dietary factors. Information ‘healthy’ or ‘leaky’ gut public domain requires confirmation before endorsing exclusions, replacement non-irritating foods (such as fermented foods) use supplements repair damage. barrier includes surface mucus, epithelial layer immune defences. Epithelial permeability results from increased paracellular transport, apoptosis transcellular permeability. Barrier function can be tested vivo using orally administered probe molecules vitro mucosal biopsies humans, exposing colonic mucosa rats mice cell layers extracts stool human patients. Assessment beyond layer. ‘Stress’ disorders such endurance exercise, non-steroidal anti-inflammatory drugs administration, pregnancy surfactants bile acids factors emulsifiers) increase Dietary reverse leakiness damage ‘stress’ disorders. Whereas inflammatory ulcerating diseases result leaky gut, no disease cured by simply normalising function. It is still unproven that restoring ameliorate clinical manifestations GI systemic diseases. Clinicians should aware potential dysfunction a target future therapy.

Language: Английский

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Molecular mechanisms of ROS production and oxidative stress in diabetes

Biochemical Journal, Journal Year: 2016, Volume and Issue: 473(24), P. 4527 - 4550

Published: Dec. 9, 2016

Oxidative stress and chronic inflammation are known to be associated with the development of metabolic diseases, including diabetes. stress, an imbalance between oxidative antioxidative systems cells tissues, is a result over production oxidative-free radicals reactive oxygen species (ROS). One outcome excessive levels ROS modification structure function cellular proteins lipids, leading dysfunction impaired energy metabolism, altered cell signalling cycle control, transport mechanisms overall dysfunctional biological activity, immune activation inflammation. Nutritional such as that caused by excess high-fat and/or carbohydrate diets, promotes evident increased lipid peroxidation products, protein carbonylation decreased antioxidant status. In obesity, underlying factors lead pathologies insulin resistance, dysregulated pathways diabetes cardiovascular disease through metabolism resulting in secretion, action responses. However, exercise may counter thus improve inflammatory outcomes. present article, we review molecular origins significance production, targets responses describing how affects secretion action, from point view possible application novel diabetic therapies based on redox regulation.

Language: Английский

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Brain insulin resistance in Alzheimer's disease and related disorders: mechanisms and therapeutic approaches

The Lancet Neurology, Journal Year: 2020, Volume and Issue: 19(9), P. 758 - 766

Published: July 27, 2020

Language: Английский

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<p>How Western Diet And Lifestyle Drive The Pandemic Of Obesity And Civilization Diseases</p>

Diabetes Metabolic Syndrome and Obesity, Journal Year: 2019, Volume and Issue: Volume 12, P. 2221 - 2236

Published: Oct. 1, 2019

Abstract: Westernized populations are plagued by a plethora of chronic non-infectious degenerative diseases, termed as "civilization diseases", like obesity, diabetes, cardiovascular cancer, autoimmune Alzheimer's disease and many more, diseases which rare or virtually absent in hunter-gatherers other non-westernized populations. There is growing awareness that the cause this amazing discrepancy lies profound changes diet lifestyle during recent human history. This paper shows transition from Paleolithic nutrition to Western diets, along with lack corresponding genetic adaptations, significant distortions fine-tuned metabolism has evolved over millions years evolution adaptation diets. With increasing spread worldwide, overweight civilization also rapidly developing countries. It suggested diet-related key developmental process include an increased production reactive oxygen species oxidative stress, development hyperinsulinemia insulin resistance, low-grade inflammation abnormal activation sympathetic nervous system renin-angiotensin system, all play pivotal roles civilization. In addition, epigenetic fetal programming important role. The pathomechanism able explain well-known but not completely understood close relationship between obesity wide range comorbidities, type 2 diabetes mellitus, disease, etc., same etiopathology. Changing our accordance makeup, including physical activity, may help prevent limit these diseases. Keywords: metabolic syndrome, hypersecretion, paleolithic diet, pathogenesis

Language: Английский

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Nutrients and Oxidative Stress: Friend or Foe?

Oxidative Medicine and Cellular Longevity, Journal Year: 2018, Volume and Issue: 2018, P. 1 - 24

Published: Jan. 1, 2018

There are different types of nutritionally mediated oxidative stress sources that trigger inflammation. Much information indicates high intakes macronutrients can promote and subsequently contribute to inflammation via nuclear factor-kappa B- (NF- κ B-) cell signaling pathways. Dietary carbohydrates, animal-based proteins, fats important highlight here because they may the long-term consequences Oxidative is a central player metabolic ailments associated with high-carbohydrate protein diets excessive fat consumption. Obesity has become an epidemic represents major risk factor for several chronic diseases, including diabetes, cardiovascular disease (CVD), cancer. However, molecular mechanisms complex poorly understood. Therefore, this review aimed explore how dietary choices exacerbate or dampen We also discussed implications in adipocyte glucose metabolism obesity-associated noncommunicable diseases (NCDs). Taken together, better understanding role obesity development obesity-related NCDs would provide useful approach. This be by both extrinsic intrinsic factors, hence providing plausible means prevention disorders.

Language: Английский

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Ketogenic Diet in Alzheimer’s Disease

International Journal of Molecular Sciences, Journal Year: 2019, Volume and Issue: 20(16), P. 3892 - 3892

Published: Aug. 9, 2019

At present, the prevalence of Alzheimer’s disease, a devastating neurodegenerative disorder, is increasing. Although mechanism underlying pathology not fully uncovered, in last years, there has been significant progress its understanding. This includes: Progressive deposition amyloid β-peptides plaques and hyperphosphorylated tau protein intracellular as neurofibrillary tangles; neuronal loss; impaired glucose metabolism. Due to lack effective prevention treatment strategy, emerging evidence suggests that dietary metabolic interventions could potentially target these issues. The ketogenic diet very high-fat, low-carbohydrate diet, which fasting-like effect bringing body into state ketosis. presence ketone bodies neuroprotective impact on aging brain cells. Moreover, their production may enhance mitochondrial function, reduce expression inflammatory apoptotic mediators. Thus, it gained interest potential therapy for disorders like disease. review aims examine role disease progression outline specific aspects nutritional profile providing rationale implementation therapeutic strategy

Language: Английский

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Diabetes mellitus and Alzheimer’s disease: GSK-3β as a potential link

Behavioural Brain Research, Journal Year: 2017, Volume and Issue: 339, P. 57 - 65

Published: Nov. 21, 2017

Language: Английский

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Vitamin D deficiency and diabetes

Biochemical Journal, Journal Year: 2017, Volume and Issue: 474(8), P. 1321 - 1332

Published: March 24, 2017

Vitamin D deficiency has been linked to the onset of diabetes. This review summarizes role in maintaining normal release insulin by pancreatic beta cells (β-cells). Diabetes is initiated resistance. The β-cells can overcome this resistance releasing more insulin, thus preventing hyperglycaemia. However, as hyperactivity increases, experience excessive Ca2+ and reactive oxygen species (ROS) signalling that results cell death contributes both initial subsequent diabetes caused β-cell death. acts reduce inflammation, which a major process inducing maintains resting levels ROS are elevated during also very significant epigenome. Epigenetic alterations feature many diabetes-related genes inactivated hypermethylation. prevent such hypermethylation increasing expression DNA demethylases multiple gene promoter regions genes. What remarkable just how cellular processes maintained D. When deficient, these begin decline sets stage for diseases

Language: Английский

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Very-low-calorie ketogenic diet (VLCKD) in the management of metabolic diseases: systematic review and consensus statement from the Italian Society of Endocrinology (SIE)

Journal of Endocrinological Investigation, Journal Year: 2019, Volume and Issue: 42(11), P. 1365 - 1386

Published: May 20, 2019

Language: Английский

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