Journal of Patient Care is a peer-reviewed Nursing journal that focuses on a wide range of topics in this field such as patient health, patient safety, patient education, and so on. It provides a platform for authors to contribute to the journal and the editorial office promises a peer review process for submitted manuscripts to ensure the quality of publication.

This journal, which ranks among the best open access journals, aims to publish the most thorough and trustworthy source of information on discoveries and current developments in the form of original articles, review articles, case reports, short communications, etc.

Atopic dermatitis (AD), commonly known as atopic eczema, is a chronic skin disease (dermatitis). It causes itchy, red, puffy, cracked skin. Clear fluid may leak from the damaged locations and thicken with time. While the disorder can develop at any age, it usually begins in infancy and progresses in severity over time. In children under the age of one year, most of the body may be affected. The insides of the knees and elbows are the most typically afflicted sites in youngsters as they get older. The hands and feet are the most typically afflicted in adults. Scratching the afflicted regions increases the symptoms, and people who are affected are more likely to get skin infections. Many people who suffer from atopic dermatitis develop hay fever or asthma. The disorder causes severe morbidity and has a negative impact on quality of life. Patients are not only affected by the social shame of having a visible skin ailment, but the disease's extreme itching frequently causes skin injuries and significant sleep disruptions. The aetiology is unknown, however it is thought to entail genetics, immune system malfunction, environmental exposures, and skin permeability issues. If one identical twin has the disease, the other has an 85% probability of having it as well. Those who live in cities or in arid climates are more likely to be harmed. Certain chemicals, as well as regular hand washing, aggravate symptoms. While emotional stress might exacerbate symptoms, it is not a cause. The condition is not communicable.  Typically, a diagnosis is made based on the indications and symptoms.

Contact dermatitis, psoriasis, and seborrheic dermatitis are some of the other disorders that must be ruled out before establishing a diagnosis. People with Alzheimer's disease frequently have dry and scaly skin that covers the whole body, with the exception of the diaper region, and very itchy red, splotchy, raised lesions that grow in the bends of the arms or legs, face, and neck. AD often affects the eyelids, causing Dennie-Morgan infraorbital folds, infra-auricular fissures, and periorbital pigmentation.  The traditional "dirty neck" image is caused by postinflammatory hyperpigmentation on the neck. Secondary infection may be indicated by lichenification, excoriation, and trunk erosion or crusting. Flexural distribution with ill-defined margins, with or without hyperlinearity, is also prevalent on the wrist, finger knuckles, ankle, foot, and hands. Although the pathophysiology of Alzheimer's disease is not fully understood, the disorder appears to be the result of a complex interplay between impairments in epidermal barrier function, immunological dysregulation, and environmental and viral agents.

Skin barrier dysfunction appears to be linked to mutations in the filaggrin gene, which produces a structural protein required for skin barrier development. The skin of people with Alzheimer's disease is also deficient in ceramides (lipid molecules) and antimicrobial peptides like cathelicidins, which are the first line of defence against many pathogenic pathogens. These skin barrier anomalies cause transepidermal water loss (the flow of water from within the body through the epidermal layer of the skin to the surrounding environment) and higher allergen and microbial penetration into the skin. Staphylococcus aureus (S. aureus) is the most common infectious agent in Alzheimer's disease (AD), colonising nearly 90% of patients. Defective innate immune responses appear to lead to an increase in bacterial and viral infections in Alzheimer's disease patients. This interaction of factors causes T cell responses in the skin (initially a predominantly T helper-2  response and later a predominantly 1 response), resulting in the release of chemokines and proinflammatory cytokines (e.g., interleukin [IL]-4, IL-5, and tumour necrosis factor) that promote immunoglobulin E (IgE) production and systemic inflammatory responses, resulting in pruritic inflammation of the skin.

The therapy of Alzheimer's disease should focus on rebuilding the skin barrier, which includes moisturising and healing the skin, reducing itching, and decreasing inflammation as needed. As a result, successful management of Alzheimer's disease (AD) necessitates a multifaceted approach that includes patient and carer education, optimal skin care practises, anti-inflammatory treatment with topical corticosteroids (first-line) and/or topical calcineurin inhibitors (TCIs), and treatment of skin infections. In severe instances that cannot be managed with adequate skin care and topical treatment, systemic immunosuppressive drugs may be tried. Although first-generation antihistamines are not routinely recommended for the management of Alzheimer's disease due to their sedative and impairing side effects, short-term use of these agents may be beneficial in individuals experiencing severe flares of Alzheimer's disease, particularly if these flares are associated with significant sleep disturbances. A simplified, sequential procedure for the treatment of Alzheimer's disease Physicians should periodically examine patient progress and disease progression, as well as evaluate the efficacy and tolerability of medication. Follow-up assessments should include a review of medication use (e.g., kind, quantity used, refills made, etc.), allowing the physician to assess compliance and drug risks.