代写thesis

代写assignment:阿尔茨海默病病理

代写assignment:阿尔茨海默病病理

Meyer, Harlrarl和Schellack(2016)将阿尔茨海默病(AD)描述为一种退化性脑病,它是由神经细胞的破坏和大脑皮层的中性连接造成的,这一疾病导致了80%的痴呆症病例。因此,随着时间的推移,这将导致一个人的记忆和认知功能的逐渐和永久的恶化。虽然失忆是最大的临床特征之一,但语言问题、个人卫生状况不佳、情绪的极端变化以及家人和朋友的认知度下降也是广告发展的警示信号。风险因素包括年龄、高血压、CVA、脑瘤和糖尿病(Meyer et al., 2016)。

代写assignment:阿尔茨海默病病理
细胞内的淀粉样斑块和神经纤维缠结的形成是AD发展的标志特征。这导致了神经元的死亡和大脑内突触的丢失。这种病理过程导致一个人的记忆和认知功能的逐渐丧失(Kocahan & Dogan 2017)。NMDA受体内的谷氨酸神经元的失调也得到了临床证据的支持,以减少AD患者的学习和记忆功能。这是由于高浓度的谷氨酸神经元引起的NMDA受体的慢性激活,导致神经退化的过度激活。各种各样的假设已经发表在AD的发病机制上,而当他们得出相同的神经毒性和突触破坏的结论时,他们的大脑(Kocahan & Dogan 2017)的病理改变也会有轻微的不同。

代写assignment:阿尔茨海默病病理

Meyer, Harlrarl, and Schellack (2016) describe Alzheimer’s disease (AD) as a degenerative brain disease caused by the destruction of nerve cells and neutral connections in the cerebral cortex that is responsible for up to 80% of dementia cases. Consequently, over time, this causes a gradual and permanent deterioration of one’s memory and cognitive functions. Although memory loss is one of the biggest clinical features, language problems, poor personal hygiene, extreme changes in mood and decreased recognition of family and friends are also warning signs of the development of AD. Risk factors include age, hypertension, CVA, brain tumors and diabetes (Meyer et al., 2016).

代写assignment:阿尔茨海默病病理
The formation of amyloid-beta plaque and neurofibrillary tangles within the intracellular space are the hallmark characteristics in the development of AD. This leads to the death of neurons and loss of synapses within the brain. This pathological process causes the progressive loss of a person’s memory and cognitive function (Kocahan & Dogan 2017). Dysregulation of glutamatergic neurons within the NMDA receptors is also well supported by clinical evidence to decrease learning and memory functions in people with AD. This is due to higher concentrations of glutamatergic neurons causing chronic activation of the NMDA receptors resulting in neurodegeneration due to excessive activation. Various other hypothesizes have been published on the pathogenesis of AD and whilst all differ slightly when they come to the same conclusion of neurotoxicity and synaptic destruction that results in pathological changes in the brain (Kocahan & Dogan 2017).