Age Related Diseases

Regardless of the molecular mechanisms that underlie the aging process, a number of well-characterized changes to the structure and therefore the function of the major cellular biomolecules (lipids, proteins, carbohydrates, and nucleic acids) are known to occur with age (Table 2). The age-related alterations to the structure and therefore the function of cellular biomolecules have physiological consequences and may directly cause or lead to an increased susceptibility to the development of a number of diseases (Figure 2).

Cellular biomolecules are constantly exposed to a variety of extrinsic and intrinsic agents that have the potential to cause damage. A number of defense systems exist, e.g., antioxidant enzymes and DNA repair systems, which aim to reduce, remove, or repair damaged biomolecules. These defense systems are not perfect, however, and biomolecular damage may still occur. Such damage can result in the degradation of structural elements within the cells, tissues, and organs of the body, leading to a decline in biological function and eventually to disease and death.

Table 2 Major age-related alterations in biomolecule structure and the resultant physiological consequences of such structural changes Biomolecule Alteration Physiological consequence

Lipids Lipid peroxidation Oxidized membranes become rigid, lose selective permeability and integrity. Cell death may occur Peroxidation products can act as cross-linking agents and may play a role in protein aggregation, the generation of DNA damage and mutations, and the age-related pigment lipofuscin Proteins Racemization, deamination, Alterations to long-lived proteins may contribute to aging and/or oxidatation, and carbamylation pathologies. For example, modified crystallins may aggregate in the lens of the eye thus leading to the formation of cataracts Cross-linking and formation of advance glycosylation end-products (AGEs), which can severely affect protein structure and function Effects on the maintenance of cellular homeostasis Carbohydrates Fragmentation, depolymerization Alters physical properties of connective tissue. Such alteration may be Glucose auto-oxidation involved in the etiology and pathogenesis of osteoarthritis and other age-related joint disorders Glycosylation of proteins in vivo with subsequent alteration of biological function; for example, glycosylation of insulin in patients with diabetes may result in altered biological function of insulin and so contribute to the pathogenesis of the disease Nucleic acids Strand breaks Base adducts Damage could be expected to interfere with the processes of

Loss of 5-methyl cytosine transcription, translation, and DNA replication. Such interference may from DNA reduce a cell's capacity to synthesize vital polypeptides/proteins.

In such circumstances cell death may occur. The accumulation of a number of hits in critical cellular genes associated with the control of cell growth and division has been shown to result in the process of carcinogenesis

Dedifferentiation of cells (5-methylcytosine plays an important role in switching off genes as part of gene regulation) If viable, such dedifferentiated cells may have altered physiology and may contribute to altered tissue/organ function

The physiological alterations with age proceed at different rates in different individuals. Some of the common changes seen in humans are: the function of the immune system decreases by the age of 30 years of age, reducing defenses against infection or tumor establishment and increasing the likelihood of autoimmune disorders; metabolism starts to slow down at around 25 years of age; kidney and liver function decline; blood vessels lose their elasticity; bone mass peaks at age 30 years and drops about 1% per year thereafter; the senses fade; the epidermis becomes dry and the dermis thins; the quality of and need for sleep diminish; and the brain loses 20% of its weight, slowing recall and mental performance. A number of age-related diseases may develop as a consequence of the tissue, organ, and system deterioration (Table 3).

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