Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disease in which the skin barrier is disrupted and the immune system is dysregulated. Patients with Alzheimer's disease are vulnerable to cutaneous infections, which can lead to consequences such as staphylococcal septicemia. Although the majority of research has focused on filaggrin mutations, the physical barrier and antimicrobial barrier are equally important in the aetiology of Alzheimer's disease. The stratum corneum and tight connections are the most significant components of the physical barrier. Tight connections not only compromise the physical barrier, but they also cause immunological problems. Antimicrobial peptides (AMPs) are the innate immune system's initial line of defence against microbial infections. Antimicrobial peptides such LL-37, human -defensins, and S100A7 also help to improve tight junction barrier function. Recent research into the pathophysiology of Alzheimer's disease has led to the creation of a skin barrier repair therapy for people with the disease. This chapter investigates the link between skin barrier disruption and antimicrobial peptides in Alzheimer's disease patients in order to determine the effect of these peptides on skin barrier repair and to consider using antimicrobial peptides in barrier repair strategies as a supplement to standard AD treatment.
Author (s) DetailsHai Le Thanh Nguyen
Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan and Department of Dermatology and Allergology, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Juan Valentin Trujillo-Paez
Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Yoshie Umehara
Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Hainan Yue
Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan and Department of Dermatology and Allergology, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Ge Peng
Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan and Department of Dermatology and Allergology, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Chanisa Kiatsurayanon
Institute of Dermatology, Department of Medical Services, Ministry of Public Health, Bangkok 10400, Thailand.
Panjit Chieosilapatham
Department of Microbiology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
Pu Song
Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, China.
Ko Okumura
Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Hideoki Ogawa
Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
Shigaku Ikeda
Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan and Department of Dermatology and Allergology, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan.
François Niyonsaba
Atopy (Allergy) Research Center, Juntendo University Graduate School of Medicine, Tokyo 113-8421, Japan and Faculty of International Liberal Arts, Juntendo University, Tokyo 113-8421, Japan.
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