Slow keratinocyte renewal leads to increased fragility of the epidermis and increased susceptibility to physical and chemical damage. Melanocytes, the cells responsible for pigmentation, decrease and regenerate more slowly, leading to dark age spots. Langerhans cells are responsible for the immune defence of the epidermis against carcinogenesis and infections. They also decrease with age, resulting in an increase in skin tumours and infections.98 Vitamin D production also takes place in the epidermis. Elderly people tend to avoid sun compared to young adults, and vitamin D precursors are reduced in their epidermis. Thus, the production rate of vitamin D decreases with age.
The skin dermis loses its thickness with age. A decrease in collagen production and loss of fat cells contribute to the lessening of the dermis. Clinically, while the dermis becomes thinner due to these mechanisms, the skin appears wrinkled and sagging. Collagen and fatty tissue are responsible for the skin’s endurance against physical damage. As these are lost in the dermis with age, the skin becomes more fragile and is easily damaged or torn as the result of even minor physical insults. Sebum production from the sebaceous glands decreases with age, along with dermis vascularization and the number of sweat glands. These mechanisms cause the skin to seem dry and rough. Dermis vascularization and sweating from sweat glands are major actors for balancing body temperature and losing heat from the skin.99 Since both mechanisms are impaired with age, elderly people tend to experience hyperthermia in hot weather. The opposite is also true: vasoconstriction of dermis arterioles and shivering are also impaired with age, resulting in undesired heat loss from the skin in cold weather.
Subcutaneous atrophy of fatty tissue changes the facial expression in the elderly. The cheeks become thinner, periorbital fatty tissue lessens, and cartilage such as that in the nose and ears seems to be enlarged. Subcutaneous fatty tissue increases in the abdomen.100 Hair loss and greying hair, which have a genetic basis inherited from previous generations, cause an undesired appearance. Hair in the ears and nostrils and near the lips grows with age, and nails become harder, thicker, and yellowish. Toenails may become hard to cut, causing irregular growth and infections.
Key points
The fundamental change in the nervous system that occurs with age is slowing, and it shows individual variations.
Ageing individuals exhibit slower sensory perception of information; slower transmission, processing, and interpretation of information; and slower responses to information.
Clinically, individuals become prone to coronary heart disease, hypertension, arrhythmia, and varicose veins.
A decrease in oestrogen is prominent after menopause, and it is responsible for postmenopausal symptoms. However, replacement therapy is not recommended after the age of 60 due to significant adverse effects.
Testosterone is the hormone most closely related to muscle size and strength. Replacement may be beneficial for sarcopenia, although adverse risks should be considered.
Loss of teeth is an important precipitating factor for digestive problems and loss of appetite.
Constipation prevalence increases with age because of slow peristalsis, changed muscular tone, trauma of the pelvic muscles (especially in women), and a fibre‐poor diet.
Liver‐mediated clearance of drugs slows with age, resulting in susceptibility to drug overdose.
Inflammageing is the presence of additional pathological mechanisms to immunosenescence.
Cigarette smoking, chemicals, and air pollutants contribute to the parenchymal destruction of alveoli. Cigarette smoking is responsible for 50% of larynx and lung cancers.
References
1 1. Lipsky MS, King M. Biological theories of aging. Disease‐a‐Month. 2015; 61(11):460–466.
2 2. Jin K. Modern biological theories of aging. Aging and Disease. 2010; 1(2):72.
3 3. Gems D, L. Partridge, Genetics of longevity in model organisms: debates and paradigm shifts. Annual Review of Physiology. 2013; 75:621–644.
4 4. Hayflick L, Moorhead PS. The serial cultivation of human diploid cell strains. Exp Cell Res. 1961; 25:585–621
5 5. Moskalev AA, Shaposhnikov MV, Plyusnina EN, Zhavoronkov A, Budovsky A, Yanai H, Fraifeld VE. The role of DNA damage and repair in aging through the prism of Koch‐like criteria. Ageing Res Rev. 2012. Published online.
6 6. Armanios M, Blackburn EH. The telomere syndromes. Nat Rev Genet. 2012; 13:693–704.
7 7. Fraga MF, Esteller M. Epigenetics and aging: the targets and the marks. Trends Genet. 2007; 23:413–418.
8 8. Lopez‐Otın C, A Blasco M, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell. 2013; 153:1194–1217.
9 9. Burke SN, Barnes CA. Neural plasticity in the ageing brain. Nature Reviews Neuroscience. 2006; 7:30–40.
10 10. Hendrickson SG. Nervous system. In: Lewis SL, Heitkemper MM, Dirksen SR, O’Brien PG, Bucher L, eds. Medical–Surgical Nursing. 7th ed. Mosby Elsevier; 2007:1441–1466.
11 11. Kaszniak AW, Menchola M. Behavioral neuroscience of emotion in aging. In: Pardon M, Bondi M, eds. Behavioral Neurobiology of Aging: Current Topics in Behavioral Neuroscience. Vol. 10. Springer; 2012:51–66.
12 12. Agnati L, Zolim F, Grlimadi R, et al. Cellular and synaptic alterations in the aging brain. Aging. 1990; 2:5–25.
13 13. Poirier J, Finch CE. Neurochemistry of the aging human brain. In: Hazzard WR, Bierman EL, Blass JP, Ettinger WH, Halter JB, eds. Principles of Geriatric Medicine and Gerontology. 3rd ed. McGraw‐Hill; 1994:1005–1012.
14 14. Kevorkian RT, Morley JE. The physiology of ageing. In: Sinclair AJ, Morley JE, Vellas B, eds. Pathy’s Principles and Practice of Geriatric Medicine. 5th ed. John Wiley and Sons, Ltd. Wiley‐Blackwell; 2012:38.
15 15. O’Brien M. Aids to Examination of the Peripheral Nervous System. Saunders; 2010.
16 16. Verrillo RT, Bolanowski SJ, Gescheider GA. Effect of aging on the subjective magnitude of vibration. Somatosens Mot Res. 2012; 19:238–244.
17 17. Folstein MF, Folstein SE, McHugh PR. Mini‐mental state. A practical method for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975; 12:189–198.
18 18. Borson S, Scanlan J, Brush M, et al. The mini‐cog: a cognitive ‘vital signs’ measure for dementia screening in multi‐lingual elderly. Int J Geriatr Psychiatry. 2000; 15:1021–1027.
19 19. Nasreddine ZS, Phillips NA, Bedirian V, et al. The Montreal cognitive assessment, MoCA: a brief screening tool for mild cognitive impairment. J Am Geriatr Soc. 2005; 53:695–699.
20 20. Olivetti G, Giordano G, Corradi D, et al. Gender differences and aging: effects on the human heart. J Am Coll Cardiol. 1995; 26:1068–1079.
21 21. Strait JB, Lakatta EG. Ageing‐associated cardiovascular changes and their relationship to heart failure. Heart Fail Clin. 2012; 8:143–164.
22 22. Marzetti E, Csiszar A, Dutta D. Role of mitochondrial dysfunction and altered autophagy in cardiovascular aging and disease: from mechanisms to therapeutics. Am J Physiol Heart Circ Physiol. 2013; 305:H459–H476.
23 23. Tanaka H, Seals DR. Endurance exercise performance in masters athletes: age‐associated changes and underlying physiological mechanisms. J Physiol. 2008; 586:55–63.
24 24. Ferrara N, Komici K, Corbi G, et al. β‐Adrenergic receptor responsiveness in aging heart and clinical implications. Front Physiol. 2014;4:396.
25 25. Goldspink DF. Ageing and activity: their effects on the functional reserve capacities of the heart and vascular smooth and skeletal muscles. Ergonomics. 2005; 48:1334–1351.
26 26. Fleg JL, Strait J. Age‐associated changes in cardiovascular structure and function: a fertile milieu for future disease. Heart Fail Rev. 2012;