Introduction: Alzheimer’s disease (AD) is characterized by progressive loss of cognitive ability, with deposits of extraneuronal beta-amyloid peptides and neurofibrillary tangles derived from intracellular TAU proteins in the central nervous system (CNS). This disease, due to the aging population, has been increasing significantly, being, some studies, related to obesity. Objective: To associate the relationship of obesity with the onset of AD. Methodology: Researches carried out in the SciELO, CAPES Periodical Portal, PubMED and BVS databases between 2014 and 2017. The descriptors were “Alzheimer” and “obesity”, being the inclusion criteria of complete articles in humans, addressing neurology, medicine and metabolism. Results and Discussion: We found 16 related articles, of which five included the theme addressed, being read in the whole. AD increases chronic inflammation, oxidative stress, and vascular changes. These effects are enhanced by obesity, which is considered a systemic inflammation. Adipose tissue is responsible for the release of inflammatory molecules, such as interleukin-6, tumor necrosis factor-alpha and adiponectins, which affect different organs and can influence the CNS, impairing brain functions. One of the experiments reported involved the high fat diet, showing the significant increase of phosphorylated TAU proteins and beta-amyloid proteins in the brain, being considered indicative of induction of the disease. As aging and metabolic diseases alter the metabolism of the whole organism, the brain is an affected organ, contributing to the onset of AD. Conclusion: Changes of adipose tissue can influence characteristics of aging, as a cognitive fragility, favoring its progress towards diseases that lead to dementia. In spite of the malignant evidence of some adipose tissues, they are still scarce in the studies related to the subject, being necessary more investments in the area for tests and, possibly, future studies of treatments in this field.
Introduction: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by signs of dementia and cognitive loss. This disease affects ≈38 million individuals worldwide. In Mediterranean countries, it is believed that because of the influence of dietary factors, the prevalence of this disease is lower. Objective: To investigate the dietary habits of the Mediterranean population related to AD. Methodology: Researches were carried out in the databases SciELO, BVS and CAPES Periodical Portal between 2013 and 2017. The keywords used were “Alzheimer”, “diet” and “Mediterranean”. Results and Discussion: 25 articles were included in English, Spanish and Portuguese, of which five were selected, using as an inclusion criterion the direct relationship with the disease and the Mediterranean diet. In AD there is the formation of neuritic plaques and neurofibrillary tangles, as well as increased inflammation, oxidative stress and cardiovascular disorders. The studies indicate that the Mediterranean diet decreases the risk factors for the development of AD. Food rich in fish, olive oil, wine, some fruits and vegetables avoids mild cognitive impairment. Dietary adherence decreases levels of inflammatory markers, such as C-reactive protein and interleukin-6. The diet has several nutrients, such as omega-3, which contribute to reducing the damage from increased oxidative stress in AD. The omega-3 present in this diet increases eicosapentaenoic acid and docosahexaenoic acid, decreasing inflammation. Another benefit described involves the reduction of thrombolytic factors, reducing cerebral vascular damage, and consequently neuronal damage. Conclusion: The consumption of foods present in the Mediterranean diet has an anti-inflammatory effect, antioxidative action and cardiovascular protection. Thus, it may contribute to primary prevention as well as to the prevention of AD progression.
Introduction: Parkinson’s disease (PD) is a neurodegenerative disease that installs progressively and usually manifests itself in individuals around 60 years of age. Identifying the presence of olfactory dysfunction may enable early treatment and delay the onset of motor symptoms. Objective: To relate the diagnosis of olfaction dysfunction with the delay of the appearance of other symptoms of Parkinson’s Disease. Methodology: Review the BVL and SciELO databases using the descriptors “Parkinson” and “Smell” and applying the inclusion criteria: articles available on human studies in the period between 2012 and 2017. Results and Discussion: The main symptoms associated with PD are motor (tremors, stiffness, postural instability). However, PD is a multifactorial pathology, and there may even be olfactory dysfunction. This situation is worrying because it can reduce the patient’s quality of life. Through the smell it is possible to avoid the ingestion of toxic foods, besides the fact that the olfaction is always associated with the sense of taste, the palate. Olfactory dysfunction does not always occur in PD patients, but, when present, it is one of the initial symptoms, and may occur even a few years before motor manifestations. Therefore, it would be possible to initiate an early treatment to delay the appearance of other symptoms, considering that PD is still incurable. Conclusion: The use of olfaction tests is essential to identify risk groups for PD and is economically viable. Thus, the routine implementation of these tests is of great relevance as a way to delay the onset of motor symptoms of PD and to promote the improvement patients’s quality of life.
Introduction: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that compromises memory, concentration and reasoning of individuals. Due to the aging population, it is estimated that in the year 2050, 1 in every 85 people will be affected by AD in the world. B vitamins are essential for the proper functioning of the neurological system. Objective: To relate the use of vitamin B6, B9 and B12 with delayed onset of Alzheimer’s disease. Methodology: Review of PubMed, BVS and SciELO databases using the descriptors “Alzheimer’s disease”, “B vitamins” and “Homocysteine”. The inclusion criteria were: articles available in humans between 2012 and 2017. Results and Discussion: 3 articles fit the inclusion criteria proposed. The role of vitamins B6, B9 and B12 is critical to avoid accumulation of the amino acid homocysteine. Pyridoxine acts on the conversion of homocysteine to cysteine, while folic acid and cobalamin act to produce methionine from homocysteine. This amino acid originates from the metabolism of methionine and may have a neurotoxic effect. Its presence at high levels in the organism is related to neurological diseases. The increase of this compound is responsible for the worsening in the cases of patients with AD by raising the rates of β-amyloid, thus provoking hyperphosphorylation of the Tau proteins. Although B vitamins have not been confirmed in all studies to improve secondary prevention of patients, such substances appear to reduce the risk of developing AD. Conclusion: Adequate nutrition is essential throughout life, but during the aging process, the use of foods rich in complex B vitamins such as deep-sea fish, whole grains, legumes and dark green leaves is emphasized in order to avoid or delay this disease.
Introduction: Alzheimer’s disease (ad) is characterized by being a progressive neurological disorder that involves the accumulation of the protein Amyloid Beta (Aβ) and Tau in neurons, leading to degeneration and death of these. Causing changes in memory, brain and behavior, is a slow and installation syndrome that often goes unnoticed in the early stages. Objectives: Analyze the main gene involved in the and identify a genetic interaction network, correlating to the changes in the functions of this gene. Methodology: We used the ALZGene database to know the main gene involved in the. After identifying the gene APOE, bioinformatics, GeneMANIA, was accessed to establish relations of APOE with other genes involved in the. Results and Discussion: It was found that the APOE gene is more predominant in the mutations, and that genes that exhibit physical interaction with APOE are: APP, LCK, APOC2, VLDLR, LDLR, LRP1, PLTP, APOA2, LIPC, CNTF, APOB, SCARB1. The results showed that one of the isoforms of APOE ε4 is causing increased risk of triggering, stimulating the Aβ deposition, affecting cognitive and functional decline in patients with mild cognitive decline and triggering inflammatory Cascades that cause neurovascular dysfunction allowing the entry of toxic proteins derived from blood in the brain. High education, leisure activities and exercise can reduce the risk of and cognitive decline. The diagnosis is made based on the signs of cognitive impairment being important to the exclusion of other potential causes, such as dementia and cerebal vascular disease. Conclusion: The presence of APOE ε4 does not require the development of the disease, however, the effects of this on the brain network connectivity, memory and cognitive decline are present in the patients and cognitively normal individuals.