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A clinical look at the aging skin.

The aging Caucasian skin becomes yellow, dry, wrinkled and inelastic. Deterioration increases its susceptibility to malignant neoplasms, pruritus, and candidal infection. In addition, psychosomatic problems vascular disease, "little strokes," and chronic malnutrition may precipitate or exacerbate skin disorders in the elderly. Treatment with "strong" medications should be taboo because of the fragility of senile skin. The risk of toxic reactions or of allergic sensitization is great. Because healing is retarded in old tissue, time is an indispensable component of successful treatment.

Adolescent

[The aging skin (author's transl)].

Aging of the skin appears in circumscribed as well as in generalized forms. The localized alterations may be subdivided in such of inflammatory origin and in hyperplastic ones. The latter include benign and also precancerous tumors. The generalized and usually premature manifestations of cutaneous senescence are almost always part of some hereditary disease which frequently also affects the viscera, sense organs, skeleton, and the nervous system.

Aged

A Novel Moisturizer Formulated With Micronized Centella asiatica and Mandelic Acid Improves Mature, Crepey Skin.

BACKGROUND: Dermatoporosis is a condition of fragile, aging skin that manifests as altered pH, wrinkles, laxity, easy bruising, and hyperpigmentation. This study evaluated efficacy, safety, and subject perception after the use of a novel cream, GC (Galderma Laboratories, LP, Fort Worth, TX), on subjects with mature, aging skin. METHODS: A 12-week multicenter, randomized, blinded, in-use study enrolled female and male subjects aged 40 to 60 years of all races, ethnicities, and Fitzpatrick skin types. Subjects were required to have a history of fragile skin and dry, crepey skin on the knees and thighs. GC cream was applied to knee and upper thigh skin twice daily. Assessments included clinical grading, digital photography, bioinstrumentation (skin texture, pH, and heatmap hydration), standard safety assessments, and satisfaction. RESULTS: Use of GC cream for 12 weeks resulted in significant improvements in skin crepiness, photodamage, and firmness, as well as decreased skin pH and early improvements in skin roughness and smoothness from baseline. Corneometer heatmapping documented improved skin hydration over baseline. No adverse events were reported; the GC cream was well tolerated, and subjects reported high satisfaction. CONCLUSION: Twice-daily application of the novel GC skin cream significantly improved the overall skin quality of mature, aging skin, including crepiness, photodamage, firmness, texture, pH, and hydration. GC cream was well tolerated with high subject satisfaction. These data are intended to help guide healthcare providers and patients in choosing an effective moisturizer that was specifically designed for patients with fragile, mature skin.

Humans

Skin-innervating glutamatergic neurons modulate aging.

Peripheral nerves regulate skin homeostasis by secreting neurotransmitters, but their role during skin aging remains incompletely understood. Here, we report that cutaneous denervation accelerates skin aging, as evidenced by collagen reduction. Neurofilament heavy chain (Nefh) is decreased in aged skin and is predominantly expressed in vesicular glutamate transporter 2-positive (Vglut2+) skin-innervating glutamatergic neurons. Notably, dermal fibroblasts, the primary producers of collagen, frequently contact Nefh+ nerve fibers. Moreover, Nefh deletion in Vglut2+ glutamatergic neurons drives skin fibroblast senescence and collagen loss, whereas additional glutamate improves skin aging phenotypes. Mechanistically, cyclin-dependent kinase 5 (Cdk5) interacts with both Nefh and Vglut2 and maintains glutamate release and collagen homeostasis. Additionally, in skin fibroblasts, solute carrier family 1 member 3 (Slc1a3) governs the collagen-promoting and anti-senescence functions of glutamate. Together, these findings reveal Nefh-mediated glutamatergic neuromodulation of skin aging and provide therapeutic targets for aging-related skin disorders.

Animals

Structural changes in aging human skin.

In both exposed and protected areas of progressively older people the underside of the epidermis becomes increasingly flattened out. This flattening is accompanied by a comparable rarefaction of the superficial blood vessels. In this article we review the architecture of the elastic fiber framework in the papillary dermis of skin protected from the sun; aging changes that occur are similar to, but less severe than, those in sun-exposed areas. Most cutaneous sensory end organs are little affected by aging; those in the external genitalia, however, and particularly those underneath the vaginal epithelium become smaller and some disappear.

Adolescent

Intrinsic changes in cell differentiation and identity drive impaired wound healing in aged female murine skin.

Cellular and molecular mechanisms that drive a perturbed wound microenvironment and impaired healing in aged skin have not been fully delineated. To obtain a comprehensive understanding of cell-intrinsic changes acquired during ageing that impact early responses to injury, we performed single-cell RNA sequencing in young and aged intact female murine skin and wounds 3 days post-injury. We observed that substantial changes in the mean proportional distribution and transcriptomic state of skin resident subpopulations in aged, but not young, tissues accompany a global increase in basal inflammation. This is driven by an altered signalling environment leading to impaired keratinocyte differentiation, loss of fibroblast identity and defective macrophage function. Further, we show that ageing-induced changes in skin resident cells persist after injury, resulting in increased expression of senescence-related genes in wound fibroblasts and aberrant monocyte-to-macrophage transitioning coupled to an enhanced inflammatory signature and defective intercellular signalling in comparison to wounds in young mice. In summary, our data highlights a contribution of both cell-intrinsic changes and an altered tissue microenvironment to poor wound healing responses in aged mice.

Animals

Swimming and the skin.

Most skin diseases associated with swimming are relatively minor and either heal spontaneously or respond quickly to treatment. Exceptions are those diseases made worse by sunlight such as lupus erythematosus, skin cancer, or prematurely aged skin. With the use of better sunscreens in the future, that problem will be solved.

Chlorine