Preface

Alzheimer’s disease (AD) is the most common cause of dementia. The term “dementia” is derived from the Latin word demens, meaning “being out of one’s mind,” and has been used since the 13th century. AD has been recognized as a distinct entity since the publication of Alzheimer’s description of a patient with presenile dementia in 1906. The first biochemical identification of amyloid beta (Aβ) as the major component of amyloid plaques, a key neuropathological lesion in AD, was published in 1984 with the seminal work of Dr. George Glenner. The latter discovery led to the amyloid cascade hypothesis of AD, with a focus on developing amyloid directed therapeutic approaches. The latter have all failed in clinical trials thus far. More recently, there is growing body of genetic, transcriptomic, and proteomic data pointing to the complexity of AD pathogenesis. This has resulted in a greater diversity of therapeutic approaches being attempted—in effect, resulting in “more shots on goal,” with the prospect that at least some of these approaches will be efficacious. Hence, despite the many failures of AD therapeutic clinical trials, this is a hopeful time in AD research. There is a growing anticipation that our greater understanding of the underlying multifactorial pathogenesis of AD will result in effective therapeutic interventions in the near future. CONTINUE READING…..