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The Clinical Spectrum of Alzheimer’s Disease, 362 Pages
- The Clinical Spectrum of Alzheimer’s Disease: The Charge Toward Comprehensive Diagnostic and Therapeutic Strategies is highly informative and current. Acknowledged experts in the field critically review both standard and under-appreciated clinical, behavioral, epidemiological, genetic, and neuroimaging attributes of Alzheimer’s disease. The collection covers diverse topics of interest to clinicians and researchers alike. Experienced professionals and newcomers to the field will benefit from the read. The strengths and weaknesses of current clinical, non-invasive, neuro-imaging, and biomarker diagnostic approaches are explained. The perspectives give fresh insights into the process of neurodegeneration. Readers will be enlightened by the evidence that the neural circuits damaged by neurodegeneration are much broader than conventionally taught, suggesting that Alzheimer’s could be detected at earlier stages of disease by utilizing multi-pronged diagnostic approaches. This book inspires renewed hope that more effective treatments could be developed based upon the expanding list of potential therapeutic targets.- The most common form of dementia is Alzheimer’s disease (AD) (Blennow et al., 2006). Due to worldwide demographic aging, its incidence and socioeconomic impact is going to be growing noticeably within the next fifty years (Sloane et al., 2002). Typically the disease progresses slowly with a mean decline of about 3 MMSE (Mini Mental Status Examination) pts/yr (Morris et al., 1993). On average, patients survive 8 years after the diagnosis has been established (Goldberg, 2007). But sometimes fast progressive AD forms with distinct clinical features are observed (Caselli et al., 1998; Josephs et al., 2009; Mann et al., 1989; Schmidt et al., 2010; van Everbroeck et al., 2004). During the past few years AD has increasingly being understood as a disease that appears in rather heterogeneous variants (Blennow et al., 2006; Wilkosz et al., 2010; van der Vlies et al., 2009a; Iqbal et al., 2005; Querfurth & LaFerla, 2010). This accounts for its clinical profile, biomarker patterns or neuropathological features. Still, studies sufficiently interrelating symptomatology to neuropathology, pathophysiology and biopathochemistry are lacking. Factors, which might cause heterogeneity, appear to be diverse. For instance, different deterioration speeds may occur in different disease stages (Wilkosz et al., 2010; Brooks et al., 1993; Storandt et al., 2002). Also differences in the so-called cognitive reserve (Stern, 2006; Mortimer et al., 2005; Paradise et al., 2009) could account for phenotypical disparities. But furthermore, different biological causes or processes that converge on a common final pathophysiological pathway might evoke heterogeneity (Ritchie & Touchon, 1992). With ever growing evidence of AD heterogeneity, rapidly progressive AD forms (rpAD) might very well be one representative of such AD subentities. In this book chapter, we review clinical evidence regarding AD heterogeneity in general and rapidly progressive AD (rpAD) in particular. Questions arising regard the epidemiological evidence for rpAD, its predictability, the biological / pathophysiological basis and the impact on therapeutic decision-making (subtype adapted therapy).
| Nguồn | : Internet |
| Tác giả | : Suzanne De La Monte, |
| Kiểu tập tin | |
| Độ lớn tập tin | : 11MB |
| Đăng bởi | : Thanh Thao |
| Cập nhật | : 02.01.2012 |
| Số lượt xem | : 150 |
| Số lượt tải | : 5 |
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