肥胖与阿尔茨海默病

阿尔茨海默病(AD)是老年人常见的神经系统变性疾病,是痴呆最常见的病因。病理特征为老年斑、神经元纤维缠结、海马锥体细胞变性和神经元缺失。临床起病隐袭、进行性智能衰退伴人格改变。至今引起该疾病的病因不详,但多种危险因素与AD的发生相关。减少β-淀粉样蛋白(Aβ)在脑中的聚积,是治疗和预防AD的措施之一。多项研究证明肥胖与AD的发生密切相关,控制肥胖、缓解认知功能的损害,为AD的预防和治疗提供了新的方向。     

Pathogenesis of Alzheimer's disease

The 160 and 200 Kd phosphorylated and non-phosphorylated neurofilament monoclonal antibodies were used as the probe to study the cytoskeletal protein distribution inside cerebral neurons of 2 normal adults and 2 patients with Alzheimer's disease (AD). Immunocytochemical technique was applied in this study. Non-phosphorylated neurofilament was located in the perikarua, whereas, the phosphorylated neurofilament was rich in the peripheral of the neuron's cell body and axons in the normal adult brain. In AD, no significant difference was seen when non-phosphorylated neurofilament was compared with normal adult brain; but phosphorylated neurofilament was seen accumulated inside the neuron's cell bodies. We did not find any immunoreactivity of the above cytoskeletal proteins in the senile plaques. These results indicate that the accumulation of high molecular weight phosphorylated neurofilament inside the neuron's cell bodies is the early pathogenetic change of AD.     

阿尔茨海默病的治疗

阿尔茨海默病(AD)是一种以进行性认知功能减退为特征的神经变性疾病,虽然已有多种药物被批准用于AD的治疗,但疗效有限.目前,一些针对AD发病机制的药物正在研究之中,主要是针对β-淀粉样蛋白致病性及易损神经元变性,还有一些针对载脂蛋白E和Tau蛋白致病性的不太成熟的治疗措施.文章就AD的治疗前景及存在的问题作一综述.     

胰岛素与阿尔茨海默病

近年来,阿尔茨海默病(AD)的发病率呈明显增加的趋势,但其发病机制仍不明确.胰岛素及其受体被认为可能与AD的发病有关.文章就胰岛素与脑内葡萄糖代谢的关系以及胰岛素、胰岛素受体和胰岛素抵抗与AD发病的关系及其可能机制进行综述,并介绍AD的治疗进展.     

阿尔茨海默病的药物治疗新进展

近年来,随着以β淀粉样蛋白（β-Amyloid,Aβ）单抗为代表的疾病修饰治疗（disease-modifying therapies,DMT）药物的出现,阿尔茨海默病（Alzheimer''s disease,AD）的药物治疗进入了一个全新的阶段,目前已经有2种靶向淀粉样蛋白的抗体-阿杜卡单抗和伦卡纳单抗相继上市,在全世界引起了广泛关注;同时非Aβ非tau蛋白治疗靶点的药物研发也取得明显进展。本文拟对AD新型药物的研发和应用,包括临床试验阶段和已获批上市的药物治疗进展进行一全面分析和阐述。     

Probable efficacy of high-dose salicylates in reducing coronary involvement in Kawasaki disease

The efficacy of high-dose salicylates in reducing the coronary artery involvement of Kawasaki disease was compared in 36 children who received acetylsalicylic acid, 80 to 180 mg/kg/day, and in 18 who did not receive high-dose salicylates during the febrile phase of the disease and whose fever was controlled mainly with acetaminophen. The two groups were comparable with respect to age and body weight. In the acetylsalicylic acid-treated group, the dose was adjusted to meet the therapeutic serum concentration range (greater than or equal to 20 mg/dL). There were significantly more cases of coronary involvement in the nontreated group (50%) than in the salicylate-treated group (16.6%) and of coronary aneurysms (39% vs 3%). During the febrile phase of the disease, salicylate serum concentrations achieved with a given dose were on the average twofold lower than during the nonfebrile phase, owing to impaired absorption of acetylsalicylic acid. It is suggested that despite the difficulty in achieving therapeutic serum concentrations of salicylate during the febrile phase of Kawasaki disease with a dose as high as 100 mg/kg/day, this dose is potentially capable of preventing the associated coronary disease.     

Screening mammograms in Alzheimer's disease patients

Very little guidance exists to help clinicians and families decide whether mammograms are useful in elderly women with Alzheimer's Disease (AD). We present a case of a patient with moderate AD who had a positive mammogram and discuss the dilemma faced by the family and clinician in deciding what was best to do for the patient. In this case, the family opted for breast conserving surgery (BCS) followed by palliative care which brought up the question of whether screening was appropriate with this treatment goal in mind. We reviewed the literature on AD and breast cancer screening and summarize these findings in our discussion.