Current Hypotheses and Research Milestones in Alzheimer's Disease
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Almost four decades of innovative and intensive research on Alzheimer’s disease (AD) have brought major advances in our understanding of its pathogenesis, improved tools for diagnosis, and strategies for its treatment. This research has helped build a solid foundation of knowledge in the neurosciences and biological basis of AD and AD-related neurological disorders. Scientific background and insightful hypotheses are of major relevance in order to approach to an effective therapy for this devastating disease.
Current Hypotheses and Research Milestones in Alzheimer's Disease contains 20 seminal chapters by authors with varying views on the neuroanatomical, neuropathological, neuropsychological, neurological, and molecular aspects of AD. These chapters grew out of “Current Hypothesis on Alzheimer’s Disease”, held in Viña del Mar, Chile, in November of 2007. Participants included the world’s leading Alzheimer’s researchers, whose work has illuminated AD investigations during the past few decades.
Students, academics and medical professionals will find this text an invaluable addition to the study of this important subject.
occurring in concert with the second phase, is the differentiation of the newly born cells. In this phase, the majority of cells do become neurons, with a smaller percentage becoming astrocytes and oligodendrocytes. 4.The fourth phase involves migration of the neurons into the GCL, with most of the migration occurring around the first week . 5.Finally, the fifth phase involves the functional maturation of the neurons in the GCL which occurs around 4 weeks of age, but some cells may take
Although the correlative evidence amassed for a central position of Aβ in therapeutic concepts is intriguing, the advent of animal models based on human pathogenic mutations in key AD molecules has given further cause to believe that something must be amiss in a sequence of events termed the “Amyloid Cascade Hypothesis” . AβPP or AβPP/PS1 transgenic mice with human disease-causing mutations indeed produce massive amyloidoses, but no neurodegeneration [14, 15]. There are, however, functional
cause of dementia throughout the world, and the fourth cause of death in well-developed economies after cancer, cardiovascular diseases, and stroke. However, the set of disorders that causes cognitive impairment, which includes vascular brain disorders and head injury, is the largest cause of morbidity and mortality. More than 5 million people are affected by this disease in USA alone, and mortality is over 100,000 per year, with a cost to the economy that exceeds US$ 100 billion [33–36]. Thus,
adult hippocampal neurogenesis in the PDAPP mouse model of Alzheimer’s disease. J Comp Neurol 495:70–83PubMedCrossRef 38. Jin K, Galvan V, Xie L (2004) Enhanced neurogenesis in Alzheimer’s disease transgenic (PDGF-APPSw,Ind) mice. Proc Natl Acad Sci USA 101:13363–13367PubMedCrossRef 39. Dong H, Goico B, Martin M (2004) Modulation of hippocampal cell proliferation, memory, and amyloid plaque deposition in APPsw (Tg2576) mutant mice by isolation stress. Neuroscience 127:601–609PubMedCrossRef
microglia in the globus pallidus, an unaffected area of an AD case. In contrast, Fig. 1b shows activated microglia in the heavily affected entorhinal cortex of the same case. Figure 1c shows no staining in an unaffected area of the aorta in an elderly case. Figure 1d shows activated macrophages in a nearby atherosclerotic plaque. Figure 1e shows that no HLA-DR staining is detectable in the unaffected pancreas of an elderly case, while Fig. 1f shows activated phagocytes in a nearby inflamed area.