Journal of Clinical and Aesthetic Dermatology

APR 2018

An evidence-based, peer-reviewed journal for practicing clinicians in the field of dermatology

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27 JCAD JOURNAL OF CLINICAL AND AESTHETIC DERMATOLOGY April 2018 • Volume 11 • Number 4 C A S E R E P O R T (Figure 4) are involved in amyloidogenesis in the skin and brain. Presenilin-1 is an amyloid precursor that is involved in epidermal growth factor receptor turnover, and its loss is associated with cutaneous inflammatory diseases. Physiological changes in the skin of patients with Alzheimer's disease have been reported. These alterations include lower oxidant defenses, dysfunctional bradykinin receptor signaling in fibroblasts, and the expression of b-amyloid and tau proteins by mastocytes. Amyloid beta-protein precursor (AbPP) can be detected in the skin of Alzheimer's disease patients, which acts as an autocrine growth stimulus in the epidermis and is released by keratinocytes. These findings support the close connection between skin and brain amyloidopathies. Other evidence supporting this skin-brain connection is the presence of psycho-emotional stress-induced neurogenic inflammation and pruritus. Pruritus can cause scratching, which can lead to inflammation. This inflammation can induce conformational changes in proteins, which can lead to amyloid deposition. 3 Mediators that cause inflammation include corticotropin-releasing hormone (CRH), neurotensin, and substance P (Figure 4). Therefore, inflammatory cutaneous diseases might lead to amyloid deposition in the brain, while neurogenic inflammation might lead to skin amyloidosis. Amyloid deposition in the skin and brain is closely connected because of similar pathogenic mechanisms. CONCLUSION There is a paucity of data regarding the concurrent occurrence of skin and brain amyloidopathies. The correlation between the two organs is not well explored in the literature, and further study is necessary. The establishment of a link between the skin-brain axis will improve understanding of the role that anti-amyloid antibodies play in the treatment of cutaneous and neurodegenerative amyloidoses. REFERENCES 1. Tillement JP, Lecanu L, Papadopoulos V. Amyloidosis and neurodegenerative diseases: current treatments and new pharmacological options. Pharmacology. 2010;85(1):1–17. 2. Clos AL, Kayed R, Lasagna- Reeves CA. Association of skin with the pathogenesis and treatment of neurodegenerative amyloidosis. Front Neurol. 2012;20;3:5 3. Schreml S, Kaiser E, Landthaler M, et al. Amyloid in skin and brain: What's the link?. Exp Dermatol. 2010;19(11):953–957. 4. Bandhlish A, Aggarwal A, Koranne RV. A clinico- epidemiological study of macular amyloidosis from north India. Indian J Dermatol. 2012;57(4):269– 274. 5. Joachim CL, Mori H, Selkoe DJ. Amyloid beta- protein deposition in tissues other than brain in Alzheimer's disease. Nature. 1989; 341(6239):226– 230. 6. Merlini G, Seldin DC, Gertz MA. Amyloidosis: pathogenesis and new therapeutic options. J Clin Oncol. 2011;29(14):1924–1933. 7. Murphy MP, Levine H 3rd. Alzheimer's disease and beta-amyloid peptide. J Alzheimers Dis. 2010;19(1):311–323. 8. Krishna A, Nath B, Dhir GG, et al. Study on epidemiology of cutaneous amyloidosis in northern India and effectiveness of dimethylsulphoxide in cutaneous amyloidosis. Indian Dermatol Online J. 2012;3(3):182–186. 9. Jayabhanu AA, Bubna AK, Rangarajan S, et al. A clinicopathologic study of cutaneous amyloidosis at a tertiary health care center in South India. Pigment Int. 2016;3:17–23. JCAD FIGURE 3. Amorphous deposits of amyloid and melanophages in the dermal papillae FIGURE 4. Various genes and neurotransmitters showing the link between the skin and brain

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