What Is Ad

Of the various dementing illnesses our understanding of AD has progressed the farthest at the molecular level. That is not to say that our molecular understanding of AD is good, but rather that we have at least a few clues as to what is happening. As we will discuss later, a number of specific genes involved with AD have been identified. These genes, when mutated, essentially invariably lead to an individual developing AD. We will discuss these genes and gene products in more detail later, but for now I raise the issue to make two points. First, even considering the already-identified genes for AD, we can still only account mechanistically for factors contributing to about 30% of AD cases. Second, among the known genes, there are heterogeneous mechanisms by which they lead one to arrive in the AD state. Thus, it appears certain that AD is, in fact, more than one disease. As our understanding of the molecular bases of

AD increases, it is likely that AD subtypes will be diagnosable and perhaps differentially treatable. For our purposes in this chapter, because of the present limited state of understanding, I will refer to AD monolithically.

Despite the clear molecular heterogeneity of AD, there are commonalities to AD that are defined clinically. A number of different schema have emerged for describing the progression of AD (see Table 1). The one that I will follow here is based on the system promulgated by Heiko and Eva Braak (6-9) that is based on histopatho-logical criteria, specifically the development of neurofibrillary tangles in various brain regions and associated clinical symptomology.

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