Fisiopatología Diabetes Mellitus Diabetes tipo 2. Se caracteriza por 3 alteraciones fisiopatologicas: Destrucción de los islotes. Diabetes tipo 1. Type 2 diabetes mellitus in the pathophysiology of Alzheimer’s disease. DIABETES MELLITUS TIPO 2 NA FISIOPATOLOGIA DA DOENÇA DE ALZHEIMER. fisiopatología 1º fisioterapia ucm marta fernández de piérola cuesta profesora: susana muñoz lasa año: unidad didáctica factores etiológicos de.
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Both Alzheimer’s disease AD and type 2 diabetes mellitus DM are two common forms of disease worldwide and many studies indicate that people with diabetes, especially DM, are at higher risk of developing AD. DM is a metabolic disorder characterized by hyperglycemia in the context of insulin resistance and relative lack of insulin. Both diseases also share common characteristics such as loss of fisiopatolkgia function and inflammation. Inflammation due to overnutrition induces insulin resistance fisiopatolohia consequently DM.
Memory deficit and a decrease in Fisiopattologia and hippocampal insulin signaling have been observed in animal models of insulin resistance. The objective of this review was to show the shared characteristics of AD and DM.
Many researchers have struggled to understand the molecular basis of the pathophysiology of Alzheimer’s disease AD because an exponential number of cases have been predicted for the coming decades and more effective treatments will be required to prevent or halt progression of the disease.
AD is characterized by insulinoeresistencia of cognitive function evolving to dementia and death. Despite decades of research, the etiology of the disease is still poorly understood and data have shown insulinorresisttencia type 2 diabetes mellitus DM is a risk factor for AD.
Neuroinflammation is one of the pathophysiological features of AD. Moreover, AD brains exhibit defective insulin signaling, and, more importantly, decreased responsiveness to insulin.
Alzheimer’s disease AD has been studied for decades. There is a sporadic form of the disease 1314 and average survival is about eight years. The typical AD symptomatology is severe and progressive impairment of cognitive function, 12 which includes memory loss and language problems 15 as well as non-cognitive dysfunction executive often followed by behavioral disorders such as agitation, aggressiveness and depression 1215 Table 1. Neocortex and hippocampus seem to be the areas most affected by specificity of the disease 12 and the loss of neurons in these areas is responsible for their atrophy, which is inherent to cognitive dysfunction, especially of memory, and the disease diagnosis.
The proinflammatory cytokines released by these cells bind to their receptor located in neurons and promote the activation of molecules such as JNK leading to serine phosphorylation of the IRS-1 receptor, thereby triggering insulin resistance and blocking of insulin action in neuron cells.
Tumour necrosis factor; IL-1, IL Interleukins 1 and 6; IKK: I kappa B kinase; PKR: Insulin bound in its receptor. APP, whose physiological function is yet not clearly elucidated, 30 has extracellular, membrane and cytoplasmic portions. Neuroinflammation is another feature that seems to be involved in the pathophysiology of AD. According to some reports, the interaction of environmental and genetic factors may trigger AD. Phosphorylation of Tau protein is regulated from fetal to adult life.
Tau insulinorresistencua decreases its affinity for microtubules 42 promoting neuronal dysfunction due to loss of normal cell morphology, axonal insulinorrsistencia, synaptic dysfunction and neurodegeneration. In addition, it has been reported that the hyperphosphorylation of Tau protein is associated with an increase in cytokine levels.
It is well established that there is degeneration of cholinergic neurons in Alzheimer’s patients. The neurotransmission promoted by the acetylcholine neurotransmitter, among other functions, is involved in cognition, particularly memory. Studies show a reduction in acetylcholinesterase and choline acetyltransferase ChAT activity in the brain of Alzheimer’s patients relative to the brains of normal individuals. DM is implicated as one of the risk factors for AD, 13 and data suggest that Alzheimer’s patients have a high risk of developing type 2 diabetes.
Diabetes mellitus is a group of insulinorresostencia diseases characterized by chronic hyperglycemia resulting from defects in insulin secretion or action. This test consists of fasting blood collection, followed by ingestion of 75 g of glucose and then repeat blood collection after two hours. Insulin is a peptide hormone consisting of 51 amino acids that metabolizes fisiiopatologia and promotes its uptake by cells. Its deficiency may generate metabolic abnormalities of these molecules.
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Insulin promotes its effect by binding to its receptors IRwhich belong to the tyrosine kinase receptor class. Insulin also promotes its effect by binding itself to insulin-like growth factor 1 IGF-1R. However, it has been suggested that neurons synthesize IGF-1 under physiological conditions, whereas fisuopatologia are produced after injuries. This is an insulinotropic hormone with neurotransmitter activity whose properties and functions are similar to insulin and IGF GLP-1 is secreted by intestinal cells and neurons, and its receptor, GLP-1R, is widely expressed in the brain, including the cerebral cortex and hippocampus.
Fisiopatologia by candelaria soto on Prezi
The main feature of the pathogenesis of DM is insulin resistance. These cytokines promote the activation, in neurons, of molecules such as JNK leading to serine phosphorylation of the IRS-1 receptor, inhibiting tyrosine phosphorylation and triggering insulin resistance Figure 1B. Once activated, they bind to their respective receptors and recruit several other proinflammatory mediators. The increase in proinflammatory cytokines induces a chronic inflammatory process and reactive oxygen species ROS production.
Research has shown that DM may develop due to a high fat diet and obesity. Also, some studies have indicated that chronic ingestion of high-fat diets and DM are some of the risk factors for decline in cognitive function and for a dementia similar to AD. In addition, another study showed, using a Senescence-accelerated mouse prone model SAMP8that animals subjected to experimental induction of type.
This memory deficit was observed using the Morris water maze. Also, other researchers showed that decreased sensitivity to insulin has been associated with reduced verbal fluency and with cortical volume reduction of temporal lobes in healthy elderly individuals.
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Type 2 diabetes is characterized by hyperglycemia, decreased production of insulin or its availability, and insulin resistance. Studies indicate a reduction in glucose metabolism as well as changes in brain energy metabolism and impaired neuronal insulin signaling in AD patients. In both conditions, type 2 diabetes and AD, increased oxidative stress 9394 and chronic inflammation 5794 occur Figure 3.
The response to injury in the peripheral nervous system PNS and CNS by the activation of microglia and astrocytes is a normal and beneficial response. Nevertheless, an intense inflammatory response may promote the production of excess cytokines and oxidative stress leading to cell death. The pathophysiology of both pathologies includes inflammation, increased oxidative stress, cognitive deficit and insulin resistance.
Cytokines and chemokines produced by both adipose tissue resident macrophages and by adipocytes of obese patients can cross the blood-brain barrier and contribute to the onset of brain inflammation. In the brain, these mediators join with pro-inflammatory mediators released by activated microglia and induce inflammation in the CNS leading to neurodegeneration.
The binding of these cytokines to their receptors located in neuronal cells induces the activation of kinases such as JNK and protein kinase double-stranded RNA-dependent PKRwhich phosphorylate IRS-1 at serine residues thereby inhibiting tyrosine phosphorylation.
Thus, there is blocking of the action of insulin in neuronal cells. Several types of studies, including epidemiological and genetic investigations, indicate a relationship among obesity, insulin resistance, type 2 diabetes and neurodegenerative disorders such as AD. Knowledge and understanding of the pathophysiology as well as inflammatory and type 2 diabetes mechanisms involved in AD are important for early diagnosis of the disease e.
Caloric intake and the risk of Alzheimer disease.
Shared links between type 2 diabetes mellitus and Alzheimer’s disease: Type 2 diabetes as a risk factor for Alzheimer’s disease: Memory impairment in obese Zucker rats: Obesity and central obesity as risk factors for incident dementia and its subtypes: Inflammatory mechanisms in Alzheimer’s disease.
The inflammatory response system of brain: Brain Res Brain Res Rev. Inflammation and Oxidative Stress: Diagnosis and Management of Diabetes: Insulin in central nervous system: The cholinergic hypothesis of Alzheimer’s disease: J Neurol Neurosurg Psychiatry. Intranasal insulin restores insulin signaling, increases synaptic proteins, and reduces Abeta level and microglia activation in the brains of 3xTg-AD mice.
Evolution of the diagnostic criteria for degenerative and cognitive disorders. Morphological criteria for the recognition of Alzheimer’s disease and the distribution pattern of cortical changes related to this disorder.
Some morphometric aspects of the brain in senile dementia of the Alzheimer type. Physical basis of cognitive alterations in Alzheimer’s disease: The history of the cholinergic hypothesis. Beta-amyloid peptides as direct cholinergic neuromodulators: Biogenesis and metabolism of Alzheimer’s disease Abeta amyloid peptides.
What the evolution of the amyloid protein precursor supergene family tells us about its function. Clearance mechanisms of Alzheimer’s amyloid-beta peptide: Truncated and modified amyloid-beta species.
Low cholesterol stimulates the nonamyloidogenic pathway by its effect on the alpha fisiopatologla ADAM Annu Rev Pharmacol Toxicol. Regulation of APP cleavage by alpha- beta- and gamma-secretases. Physiological functions of APP family proteins. Cold Spring Harb Perspect Med.
A beta oligomers – a decade of discovery. Innate immune system fisiopatologoa inflammation in Alzheimer’s disease: Inflammation, defective insulin signaling, and neuronal dysfunction in Alzheimer’s disease. The genetics of Alzheimer disease: Proposed nomenclature of apoE isoproteins, apoE genotypes, and phenotypes. Amyloid-associated proteins alpha 1-antichymotrypsin and apolipoprotein Insulinnorresistencia promote assembly of Alzheimer beta-protein into filaments.
Interaction of tau with the neural plasma membrane mediated by tau’s amino-terminal projection domain. The roles of microtubule-associated proteins in brain morphogenesis: Microheterogeneity of microtubule-associated tau proteins is due to differences in phosphorylation. Untangling tau hyperphosphorylation in drug design for neurodegenerative diseases.