Metabolism-Centric Overview of the Pathogenesis of Alzheimer's Disease.

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metabolic syndrome 1 endocrinologydiseases
obesity 21 endocrinologydiseases
Insulin 8 endocrinologydiseasesdrugs
hyperglycemia 2 endocrinologydiseases
hyperinsulinemia 2 endocrinologydiseases

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Insulin 11020 begun to study mechanistic links between these diseases; the most promising link has been insulin.[34] Insulin is a major anabolic hormone that is secreted from pancreas beta cells in response to high glucose levels.
Insulin 11134 major anabolic hormone that is secreted from pancreas beta cells in response to high glucose levels. Insulin signals by binding to insulin receptors, thereby activating insulin receptor substrate 1, extracellular
Insulin 11331 extracellular signal-related kinase/mitogen activated protein kinase, and PI3 kinase/Akt pathways. Insulin also inhibits glycogen synthase kinase-3 (GSK-3).[35] Through these signals, insulin maintains glucose
Insulin 11683 Accordingly, impairment of insulin secretion or function is considered a primary cause of diabetes.[36] Insulin resistance refers to the reduced ability of insulin on target tissues, including liver, muscle, and
Insulin 13220 downstream cascade, insulin mediates long-term potentiation, learning, and memory processes.[44][45] Insulin signaling in specific brain regions, such as the limbic system and hypothalamus, has been found to be
Insulin 14020 pathologies, such as cognitive defects, accumulation of Aβ, and hyperphosphorylated tau in ICR mice.[51] Insulin affects Aβ accumulation and the phosphorylation of tau as well. Insulin-degrading enzyme (IDE) is known
Insulin 14093 hyperphosphorylated tau in ICR mice.[51]Insulin affects Aβ accumulation and the phosphorylation of tau as well. Insulin -degrading enzyme (IDE) is known to degrade excess insulin and other substrates, such as Aβ (Fig. 2).
Insulin 25433 progressively causes Alzheimer's disease.Fig. 2Brain insulin resistance causes Alzheimer's disease. (A) Insulin signaling maintains normal neuronal functions through IRS, ERK/MAPK, PI3K/AKT, and GSK3 signals. (B)
Select Disease Character Offset Disease Term Instance
hyperglycemia 4330 in the pancreas can falter, causing patients to suffer from relative hypoinsulinemia, which leads to hyperglycemia .[7]A large number of research has proven that obesity in middle age individuals can be an index of mild
hyperglycemia 14272 substrates, such as Aβ (Fig. 2). IDE knockout mice display accumulation of Aβ, hyperinsulinemia, and hyperglycemia .[52] As insulin levels are raised, IDE expression is activated to prevent the long-term activation of
hyperinsulinemia 4184 diseases. As obesity causes insulin resistance, it is one of the major risk factor for T2DM. After years of hyperinsulinemia , insulin secretory function in the pancreas can falter, causing patients to suffer from relative hypoinsulinemia,
hyperinsulinemia 14250 insulin and other substrates, such as Aβ (Fig. 2). IDE knockout mice display accumulation of Aβ, hyperinsulinemia , and hyperglycemia.[52] As insulin levels are raised, IDE expression is activated to prevent the long-term
metabolic syndrome 15584 damaging effects on many organ systems,[59] because many changes induced by obesity are related to metabolic syndrome , characterized by excess weight, high triglyceride levels, and insulin resistance. Moreover, the incidences
obesity 1205 metabolic alterations to find effective therapeutics for AD. Aging is associated with not only AD but also obesity and type 2 diabetes (T2DM). AD, obesity, and T2DM share demographic profiles, risk factors, and clinical
obesity 1245 therapeutics for AD. Aging is associated with not only AD but also obesity and type 2 diabetes (T2DM). AD, obesity , and T2DM share demographic profiles, risk factors, and clinical and biochemical features in common.
obesity 1744 found to have an effect on AD treatment. In addition, adiponectin is decreased in the patients with obesity and T2DM. This reduction induces metabolic dysfunction both in the body and the brain, leading to AD
obesity 2227 the world. Aging societies are faced with various chronic diseases, such as Alzheimer's disease (AD), obesity , and type 2 diabetes (T2DM). Globally, an estimated 422 million adults over the age of 18 years suffered
obesity 2649 were diagnosed with AD, with an estimated two-fold increase therein every 20 years. Interestingly, obesity , T2DM, and AD are reported to be related with each other.[2]AD is a degenerative brain disease and the
obesity 3239 Development of AD treatment could potentially benefit from seeking to consider the relationships among AD, obesity , and T2DM.According to the Mayo Clinic Alzheimer Disease Patient Registry, 80% of AD patients show impairment
obesity 4089 risk factor for various diseases, ranging from metabolic diseases to neurodegenerative diseases. As obesity causes insulin resistance, it is one of the major risk factor for T2DM. After years of hyperinsulinemia,
obesity 4390 relative hypoinsulinemia, which leads to hyperglycemia.[7]A large number of research has proven that obesity in middle age individuals can be an index of mild cognitive impairment at later years.[8] Even when
obesity 4736 linked to reduced cognitive function and an increased risk for developing dementia, including AD.[10]AD, obesity , and T2DM share similar demographic profiles, risk factors, and clinical and biochemical features.[11]
obesity 5405 and phosphorylated tau proteins, as well as cognitive impairment.[14][15]Given the relationship among obesity , T2DM, and AD, understanding the mechanistic links among them is essential to developing effective strategies
obesity 5605 effective strategies for AD prevention and treatment. Until now, inflammation has been thought to link obesity , T2DM, and AD.[1][16] Considering AD as a metabolic disease, however, we suggest that metabolic alterations
obesity 10052 Lacking energy, these neurons cannot survive and cause dementia.Metabolic diseases, such as T2DM and obesity , are reported to be related with AD, meaning that AD is a kind of metabolic disease (Fig. 1). Therefore,
obesity 15415 target for AD.ALZHEIMER'S DISEASE: REDUCED LEVELS OF ADIPONECTIN INDUCED BY OBESITYThe incidence of obesity is steadily rising throughout the world.[58] Obesity can have damaging effects on many organ systems,[59]
obesity 15561 world.[58] Obesity can have damaging effects on many organ systems,[59] because many changes induced by obesity are related to metabolic syndrome, characterized by excess weight, high triglyceride levels, and insulin
obesity 15758 levels, and insulin resistance. Moreover, the incidences of cognitive decline and AD are increased with obesity .[60]In normal adipose tissue, adipocytes secrete bioactive molecules, termed adipokines, including leptin,
obesity 16188 distribution, hemostasis, blood pressure, neuroendocrine regulation, and function of the immune system.[62]In obesity , adipocytes become bigger, and hypertrophic adipocytes lead to the development of a pro-inflammatory
obesity 17041 and decreased levels of adiponectin.[65] Overexpression of adiponectin prevents high-fat diet-induced obesity in rodents, and genetically eliminating adiponectin in obese mice facilitates increased fat in the liver.[66]
obesity 22459 initiates lipid peroxidation and a series of reactions, producing ROS.[87]ROS levels are increased in obesity .[88] Many studies have demonstrated that reduced insulin signals and adipokines dysregulation in T2DM
obesity 23979 accumulation of lipid is commonly observed in patients with AD.[98]Considering the noted relationships among obesity , T2DM, and AD, it is possible that increased ROS induced by metabolic alterations can cause AD pathologies
obesity 25248 disease.Fig. 1Alteration of brain metabolism causes Alzheimer's disease. Aging and metabolic diseases, such as obesity and diabetes, can alter brain metabolism. Alteration of brain metabolism progressively causes Alzheimer's
obesity 26196 and oxidases fatty acids in the brain in normal conditions. (B) Hypertrophic adipose cells induced by obesity elicit a pro-inflammatory environment and reduce adiponectin production. Reduced adiponectin causes

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