AbstractMultiple forms of the chronic skin disease psoriasis can manifest over a person's lifetime, including plaque, flexural, guttate, pustular, and erythrodermic. Multiple factors, including immunology, genetics, and the environment, contribute to the development of psoriasis. As an important societal concern, psoriasis can negatively impact patients' quality of life by causing physical impairment, making it impossible for them to work, and so on. An inflammatory skin condition known as psoriasis triggers immune pathways that involve dendritic cells, NK cells, macrophage cells, and an inflammatory mediator. The pathophysiology of Alzheimer's disease (AD) dementia is characterized by two proteins aggregations: beta-amyloid into plaques and phosphorylated tau into neurofibrillary tangles. According to popular belief, the abnormal buildup of amyloid protein is seen as an early initiating event in the AD cascade, and the spread of Tau into the neocortex and medial temporal lobe happens later on, closer to the onset of clinical symptoms of dementia, in contrast to this. The renowned genetic risk factor for Alzheimer's disease, apolipoprotein E4 (APOE4), may have an effect on the cognitive impairment linked to Parkinson's disease (PD).
This review article aims to determine the link between serum beta-amyloid and serum Apolipoprotein E4 in psoriasis and cognitive impairment.
