What is commonly referred to as Alzheimer's disease (AD) is really a syndrome, a common clinicopathologic entity that has multiple causes. Unusual forms of this syndrome are caused by highly penetrant autosomal-dominant mutations in one of three different genes: amyloid precursor protein (APP) gene, presenilin (PS) 1 gene, or PS 2 gene.1 Apparently, the same pathologic processes very commonly afflict adults with trisomy 21 or Down's syndrome. However, it is late onset AD (LOAD) that represents a significant and growing public health burden, a “silent epidemic,” currently affecting between 2.5 and 4 million people in the United States, and more than 10 million people worldwide.2,3 The causes of LOAD are not yet clarified, but several environmental and genetic risk factors have been identified, the most potent of these being inheritance of the e4 allele of the apolipoprotein (apo) E gene.4 It is estimated that LOAD will grow to staggering prevalence in the next generation with an estimated 8 to 12 million patients by the year 2050 in the United States alone. In addition to the untold suffering it causes patients and their families, AD is the third most costly medical condition in the United States.5-7 As the number of patients afflicted continues to mount, the need for safe and effective therapy to delay or avert LOAD will become imperative.8.
|Original language||English (US)|
|Title of host publication||Oxidative Stress and Age-Related Neurodegeneration|
|Number of pages||12|
|State||Published - Jan 1 2005|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)