diet and healthy ageing
In their paper in the Ageing Research Reviews journal, Michael Heinrich and José Prieto look back 100 years, and assess how our diets will change in the next 100 years in relation to ‘healthier ageing’. Their argument centres around a series of dichotomies used to explain the changes in dietary habits — the continuous move from local dietary traditions, low in technological input and based on empiricism, to diets which are global, requiring high technological input and are more science-based.
Below is Table 1 showing key developments in human diet:
Ageing Research Reviews
Volume 7, Issue 3, October 2008, Pages 249-274
cytokeratin-related loss of cellular integrity is not a major driving force of human intrinsic skin ageing
Kamil Oender and colleagues published a paper recently about cytoskeletal keratins on the journal Mechanisms of Ageing and Development ( Volume 129, Issue 10, October 2008, Pages 563-571, doi:10.1016/j.mad.2008.05.008). Below is the introduction:
Aging is the progressive decline in cellular metabolic capacity accompanied by a loss of gene expression potential, accumulation of somatic mutations, and diminished structural integrity of the cell that ultimately is incompatible with life. Aging is acknowledged to be both under genetic control (which contributes to intrinsic aging) and cumulative environmental wear and tear (extrinsic aging). In sunlight-exposed skin, the primary exogenous cause of aging is ultraviolet irradiation, hence the term “photoaging”.
The causes and mechanisms of intrinsic aging are far less well understood than for photoaging. Sun-protected, aged skin appears thin, lax, finely lined, has a transparent quality, and shows the clinical signs of increased fragility and loss of elasticity. Histologically, the stratum corneum remains relatively unchanged, but the epidermis and dermis both become thinner and there is a flattening of the dermo-epidermal junction (Gilchrest, 1982). At the ultrastructural level, the collagen fibrils of the dermis of sun-protected, aged skin become fragmented and disorganized as compared to the skin of a child. In addition to a reduction of type I procollagen synthesis, the increased activity of matrix metalloproteinases (MMP) degrades the collagenous matrix in aged skin ([Chung et al., 2000] and [Varani et al., 2000]). At the molecular level, aging is hypothesized to be caused by the effects of oxidative damage associated with cellular metabolism; by genome instabilities such as telomere shortening, mitochondrial DNA mutations, and chromosomal pathologies; by accumulation of lipofuscin; and by protein cross linking ([Fisher et al., 2002] and [Jenkins, 2002]).
PDF (96 K)Cytoskeletal filaments function in the maintenance of cell morphology and polarity, in endocytosis and intracellular trafficking, and in contractility, motility and cell division (Gourlay and Ayscough, 2005). Cytokeratins, a family of fibrous intermediate-filament protein polymers, are involved in epithelial structural maintenance, protection from mechanical trauma, and possibly communication between adjacent cells or cytoplasm components. These structural proteins of epithelial cells that can be divided into two subgroups, type 1 and type 2 keratins, based on biochemical properties such as molecular weight and isoelectric point ([Koch and Roop, 2004] and [Jacques et al., 2005]).
Based on the clinical appearance of intrinsically aged skin, mechanical strength and renewability of the cytoskeleton are expected to become reduced with age. Recent work has indicated that during skin aging, some cytoskeletal genes are regulated at the transcriptional level (Lener et al., 2006). Given the importance of the keratins to the overall function of epithelial cells we focused our study on genes encoding the cytoskeletal keratins, K1-K23 (intermediate filaments) as well as ACTB (microfilament), JUP (junctional component), and TUBA (microtubuli), the latter constituting so-called house-keeping genes. We show that the expression of house-keeping genes at both the RNA and protein levels becomes reduced with age, whereas some of the keratins are up- and some are down-regulated.
Fig. 4. Immunofluorescence staining of K19, K16 and K5 in young versus aged skin tissue samples. K19 staining in the basal layer of the epidermis of a (A) young (1 year) patient compared to an (B) aged (59 years) patient, where K19 seems to be absent. Immunofluorescence staining of K5 showed an equal protein expressin in the stratum basale in both (C) young (1 year) and (D) aged (44 years) patient. (E) K16 staining in young (6 years) is less dominant than K16 staining in (F) aged (44 years). Prominent F-actin staining in (G) young skin (7 years) shown by phalloidin-conjugated with Texas red fluorescence, compared to (H) aged (76 years) tissue. (A, B, G, H) magnification factor 200× (C, D, E, F) magnification factor 400×, D = dermis; ED = epidermis.
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