Abstract：
Alzheimer\'s disease (AD) is the most common form of dementia, generally affecting elderly people in the age group of above 60-65 years. Amyloid deposition has been found to be a possible cause and a characteristic feature of Alzheimer\'s disease. Mutations, variant genotypes, or downregulation that reduce amyloid clearance or accelerate amyloid accumulation can lead to Alzheimer\'s disease. This study involved clinically confirmed AD patients, age matched controls of similar ethnicity, and patients who had no history of cancer or any other chronic disease. DNA and RNA extractions of samples were done as per Saguna et al. [45] and TRIzol method, respectively. Frequencies of variant genotypes were observed using the RFLP technique, whereas, for expression analysis, qPCR was performed. The association between diet, smoking status, family history, and co-morbidities was calculated using statistical tools. Expression analysis showed downregulation in more than 65% of AD cases. Hypertension and diabetes also had a significant association with AD. Allelic isoforms ε2:ε2 and ε2:ε3 tend to be less frequent among AD cases compared to controls (2.85% vs 26.15% and 11.42% vs 21.43%, respectively). Among individuals (AD cases) with ε2:ε3 and ε2:ε4, 37.5% of the patients were having severe dementia and 62.5% were having mild to moderate dementia, whereas, among individuals with ε3:ε4 and ε4:ε4, 57% were having severe dementia and 43% were having mild to moderate dementia. Besides this, all early-onset Alzheimer\'s patients were found to have at least one ε4 allele. The percentage of individuals with family history (cases vs controls) was 34.17% vs 3.75%, without family history 64.55% vs 95%. On comparing AD cases against controls for smoking status, the results observed are the following: chain smokers, 12.65% vs 18.75%; moderate smokers, 16.45% vs 6.25%; ex-smokers, 36.70% vs 22.50%; non-smokers, 34.17% vs 52.50%. On comparing dietary habits in AD cases against controls, the results were as follows: individuals with generally fatty diet 26.58% vs 11.25%, with mixed diet 36.70% vs 78.75%, with generally vegetarian diet 34.17% vs 10.00%, data not available 2.53% among AD cases. Family history, dietary habits, genetics, and socioeconomic status are strongly associated with the development of Alzheimer disease. Although family history or genetic makeup cannot be changed, eating habits can be changed quite easily. We simply need to go from a high-fat diet to one that is lower in fat. Regarding socioeconomic status, which includes stress of both kinds, including economic stress, stress brought on by the loss of loved ones through death or separation, and co-morbidities (hypertension and diabetes), all are manageable and even modifiable through counseling, positive behavior, and physical activity like exercise, walking, cycling, and playing games.
摘要：
阿尔茨海默病(AD)是最常见的痴呆,通常影响60-65岁以上年龄组的老年人。已经发现淀粉样蛋白沉积是阿尔茨海默病的可能原因和特征。突变,变异基因型，或降低淀粉样蛋白清除或加速淀粉样蛋白积累的下调可导致阿尔茨海默病。这项研究涉及临床证实的AD患者，相似种族的年龄匹配对照，以及没有癌症或任何其他慢性病史的患者。根据Saguna等人进行样品的DNA和RNA提取。[45]和TRIzol方法，分别。使用RFLP技术观察到变异基因型的频率，然而,对于表达式分析，进行qPCR。饮食之间的联系，吸烟状况,家族史,并使用统计工具计算合并症。表达分析显示在超过65%的AD病例中下调。高血压和糖尿病也与AD有显著关联。与对照组相比，AD病例中等位基因亚型ε2：ε2和ε2：ε3的频率较低（2.85％vs26.15％和11.42％vs21.43％，分别)。在患有ε2：ε3和ε2：ε4的个体（AD病例）中，37.5％的患者患有重度痴呆，62.5％的患者患有轻度至中度痴呆，然而,在ε3:ε4和ε4:ε4的个体中，57%患有重度痴呆，43%患有轻度至中度痴呆。除此之外,发现所有早发性阿尔茨海默病患者至少有一个ε4等位基因。有家族史的个体百分比（病例与对照组）为34.17％vs3.75％，无家族史64.55%vs95%。在将AD病例与吸烟状况对照进行比较时，观察到的结果如下：连锁吸烟者，12.65%vs18.75%；中度吸烟者，16.45%vs6.25%；戒烟者，36.70％对22.50％；不吸烟者，34.17%比52.50%。在比较AD病例与对照组的饮食习惯时，结果如下:一般高脂肪饮食的个体26.58%和11.25%，混合饮食36.70%和78.75%，一般素食为34.17%和10.00%，AD病例中无数据2.53%。家族史,饮食习惯，遗传学,和社会经济地位与阿尔茨海默病的发展密切相关。虽然家族史或基因组成不能改变，饮食习惯可以很容易地改变。我们只需要从高脂肪饮食转向低脂肪饮食。关于社会经济地位，其中包括两种压力，包括经济压力，因死亡或分离而失去亲人带来的压力，和合并症（高血压和糖尿病），所有这些都是可管理的，甚至可以通过咨询进行修改，积极的行为，和运动等身体活动，走路,骑自行车,和玩游戏。
