It has been proposed that AD might reflect a continuum of the aging process (Brayne & Calloway, 1988). In other words, given the opportunity, every individual should eventually succumb to AD. This view can be supported by the undeniable fact that aging is the most important of the nongenetic risk factors as shown by the ever growing incidence of AD with aging. On the other hand, the prevalent notion is that the incidence of AD is influenced by a multitude of risks factors (as discussed below) in addition to aging, which might act in a cooperative manner. The extent of the life span could also be regulated by the genetic background interacting with environmental as well as lifestyle aspects (Finch & Tanzi, 1997). The role of genetics in determining the life span is complex and paradoxical. In short, the prevalent view is that for the sporadic form of AD, it is not necessarily all in the genes but rather an interplay with the life experience of that particular individual. The molecular mechanisms of brain aging remain elusive. Several molecular events are suspects in the age-related downfall of brain function, which might be linked to the earlier appearance of AD. Among these are the gradual increase in oxidative stress and inflammation, and decrease in the expression of sex hormones and growth factors, which maintain the neuronal phenotype. Some of these are discussed in subsequent chapters relating to possible therapies for AD. Some attention has also been paid to low levels of vitamin B complex and the plasma elevation of homocysteine, as being responsible for age-related cognitive deficits and unleashing the AD pathology (Seshadri, 2006; Smith, 2002). This issue remains unresolved, however, it is worth noting that epidemiological studies have shown elevations in plasma homocystein preceding the development of dementia and that the folate pathway is key to DNA methylation and therefore implicated in epigenetic mechanisms. As a result, the administration of complex B vitamins and homocysteine-lowering treatments have been recommended for the preservation of cognition in the early stages of MCI and AD (Seshadri, 2006). As aging is such a prominent AD risk factor, an obvious way to delay the aging process, such as low-calorie intake (Mattson, 2003), exercise, and sensory stimulation, can also delay the onset of AD.
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