Lifestyle Modifications and Nutritional Interventions in Aging-Associated Cognitive Decline and Alzheimer’s Disease

Frontiers in Aging Neuroscience, Journal Year: 2020, Volume and Issue: 11

Published: Jan. 10, 2020

Alzheimer's disease (AD) is one of the incurable neurodegenerative diseases characterised by accumulation amyloid-beta (plaques) and tau hyperphosphorylation (neurofibrillary tangles) in brain followed neuronal death, cognitive decline memory loss. The high prevalence AD developed world has become a major public health challenge associated with social economic burden on individuals society. Due to limited options early diagnosis exact pathophysiology AD, finding effective therapeutic strategies great challenge. Several possible risk factors pathology have been identified; however their conclusive role still unknown. Recent clinical trials drugs targeting are failing any cure for pathology. Therefore preventive should be reduce exponential increase dementia, especially AD. Although search new targets scientific community, lifestyle interventions nutraceuticals prevention many metabolic highly appreciated literature. In this article, we summarised molecular mechanisms involved ameliorative action nutritional including diet, exercise, calorie restrictions, various bioactive compounds dementia. This article will provide insights into non-pharmacologic modulation pathology, which may offer benefit improving quality life reducing incident

Language: Английский

---

Nutritional prevention of cognitive decline and dementia.

PubMed, Journal Year: 2018, Volume and Issue: 89(2), P. 276 - 290

Published: June 7, 2018

Cognitive impairment results from a complex interplay of many factors. The most important independent predictor cognitive decline is age but other contributing factors include demographic, genetic, socio-economic, and environmental parameters, including nutrition. number persons with dementia will increase in the next decades parallel aging world population. Effective pharmaceutical treatments for age-related are lacking, emphasizing importance prevention strategies. There extensive evidence supporting relationship between diet functions. Thus, nutritional approaches to prevent or slow could have remarkable public health impact. Several dietary components supplements been examined relation their association development decline. A studies role patterns on late-life cognition, accumulating that combinations foods nutrients may act synergistically provide stronger benefit than those conferred by individual components. Higher adherence Mediterranean pattern has associated decreased incident AD. Another neuroprotective actions Dietary Approach Stop Hypertension (DASH). combination these two slower rates significant reduction This review evaluates effects some components, supplements, as neuroprotective, potential delay onset dementia.

Language: Английский

---

Bidirectional interactions between diabetes and Alzheimer's disease

Neurochemistry International, Journal Year: 2017, Volume and Issue: 108, P. 296 - 302

Published: May 24, 2017

Language: Английский

---

Polyunsaturated fatty acids and endocannabinoids in health and disease

Nutritional Neuroscience, Journal Year: 2017, Volume and Issue: 21(10), P. 695 - 714

Published: July 7, 2017

Polyunsaturated fatty acids (PUFAs) are lipid derivatives of omega-3 (docosahexaenoic acid, DHA, and eicosapentaenoic EPA) or omega-6 (arachidonic ARA) synthesized from membrane phospholipids used as a precursor for endocannabinoids (ECs). They mediate significant effects in the fine-tune adjustment body homeostasis. Phyto- synthetic cannabinoids also rule daily life billions worldwide, they involved obesity, depression drug addiction. Consequently, there is growing interest to reveal novel active compounds this field. Cloning cannabinoid receptors 90s identification endogenous mediators arachidonylethanolamide (anandamide, AEA) 2-arachidonyglycerol (2-AG), led characterization endocannabinoid system (ECS), together with their metabolizing enzymes transporters. Today, ECS known be diverse functions such appetite control, food intake, energy balance, neuroprotection, neurodegenerative diseases, stroke, mood disorders, emesis, modulation pain, inflammatory responses, well cancer therapy. Western diet restriction micronutrients acids, could related altered production pro-inflammatory (e.g. eicosanoids) ECs, contributing progression cardiovascular diabetes, impairing conditions, Alzheimer' s disease. Here we review how diets based PUFAs might linked maintenance central peripheral metabolism, brain plasticity, memory learning, blood flow, genesis neural cells.

Language: Английский

---

The Triangle of Death in Alzheimer's Disease Brain: The Aberrant Cross-Talk Among Energy Metabolism, Mammalian Target of Rapamycin Signaling, and Protein Homeostasis Revealed by Redox Proteomics

Antioxidants and Redox Signaling, Journal Year: 2016, Volume and Issue: 26(8), P. 364 - 387

Published: Sept. 14, 2016

Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder and represents one of the most disabling conditions. AD shares many features in common with systemic insulin resistance diseases, suggesting that it can be considered as metabolic disease, characterized by reduced insulin-stimulated growth survival signaling, increased oxidative stress (OS), proinflammatory cytokine activation, mitochondrial dysfunction, impaired energy metabolism, altered protein homeostasis. Recent Advances: Reduced glucose utilization metabolism have been associated buildup amyloid-β peptide hyperphosphorylated tau, OS, accumulation unfolded/misfolded proteins. Mammalian target rapamycin (mTOR), which aberrantly activated since early stages, plays key role during neurodegeneration by, on side, inhibiting signaling negative feedback mechanism and, other regulating homeostasis (synthesis/clearance).It likely concomitant mutual alterations metabolism-mTOR signaling-protein might represent self-sustaining triangle harmful events trigger degeneration death neurons development progression AD. Intriguingly, cross-talk between components such death, beyond altering redox neuron, further exacerbated levels OS impair pathways involved. Redox proteomic studies human samples animal models AD-like dementia led to identification oxidatively modified composing therefore revealing crucial fueling this aberrant vicious cycle.The compounds able restore function targeted damage valuable therapeutic approach slow or delay Antioxid. Signal. 26, 364-387.

Language: Английский

---