Intracellular Consequences of Amyloid in Alzheimer's Disease

Consequences of Intracellular Amyloid in Alzheimer?s Disease addresses one of the more currently unresolved aspects confounding Alzheimer?s research, the significance of intraneuronal amyloid. It seeks to explain some of the unresolved questions concerning intracellular amyloid and its origin, entry, and toxicity.

Following up on Dr. D?Andrea?s first book, Bursting Neurons and Fading Memories: An Alternative Hypothesis for the Pathogenesis of Alzheimer?s Disease, this book further examines the Inside-Out or Bursting alternative hypothesis of how amyloid escapes the circulatory system to ultimately enter neurons, also examining whether there is a relationship between intracellular amyloid, amyloid plaques, and cognitive impairment. Through a comprehensive explanation of the currently relevant scientific research on intracellular amyloid compiled in this handy reference, readers will better understand the mechanisms that lead to neuron death.

1. Amyloid basis of Alzheimer’s disease

2. Origin(s) of Intraneuronal Amyloid

3. Natural Intracellular Consequences of amyloid

4. Pathological consequences of Abeta from extracellular to intraneuronal

5. Intraneuronal Amyloid and Plaque Formation

6. Intraneuronal Amyloid and Cognitive Impairment

7. Intraneuronal Amyloid and Inflammation

8. Consequences of Intracellular Amyloid in the Vascular System

9. Implications of Intraneuronal Amyloid

Appendix: Glossary

Neuroscientists, graduate students, post-docs, discovery scientists, clinicians, any biomedical/biological researchers interested in Alzheimer’s research.

Dr. D’Andrea has a PhD in Cell and Developmental Biology and an MS in Molecular Biology. He has authored over 100 scientific publications, including invited review papers on Alzheimer’s disease, and co-invented 11 patents. His technical expertise is in the areas of histopathology/neuropathology, immunohistochemistry, and image analysis. Since 1996, he was Team Leader and Principal Scientist of Target Validation Team at Johnson & Johnson Pharmaceutical Research & Development. There he discovered and validated novel targets, biomarkers, and compounds to treat cancer, inflammatory diseases, and Alzheimer’s disease, and accepted numerous awards for these endeavors. Currently, he is president and histopathologist at Slidomics, LLC.

He has presented is Alzheimer’s research at the following sponsored international, national and regional meetings: Society of Neuroscience; International Conference on Alzheimer’s Disease and Related Disorders; The Alzheimer’s Imaging Consortium; and International Neurodegeneration in Alzheimer’s Disease, Parkinson’s Disease & Related Disorders. In addition, he spoke at various meetings at the Annual Biological Staining Commission, The National Disease Research Institute, University of Pennsylvania, and was invited to lead the AlzForum’s WebCast International discussion for the Alzheimer’s Disease Forum on the evidence that neuronal cell death in AD is due to an autoimmune mechanism. He was also invited to the Challenging Views Of Alzheimer’s Disease: Round II meeting to debate the inflammatory aspects of AD. In addition, he has reviewed international AD grants (Spain, Israel) and is on several scientific editorial boards.

He was one of the first to publish the presence of intracellular A?42 in normal and AD neurons in 1999, first to hypothesize that plaques originate from neuronal lysis, first to report the presence of various plaques types in the AD brain, and first to provide morphological evidence of apoptotic neuronal deat

• Presents the latest research on the significance of intracellular amyloid as it relates to Alzheimer’s
• Addresses crucial questions about intracellular amyloid, including how if forms and enters neurons, its toxicity, if it triggers cell death, and how amyloid plaques are formed
• Examines the potential relationship between intracellular amyloid, plaques, and cognitive impairment in an effort to answer whether Alzheimer’s is initially a problem of amyloid, the neuron, or of the blood-brain barrier
• Seeks to help researchers generate additional alternative therapeutic opportunities to cure Alzheimer’s