- 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
Neuroscientists, graduate students, post-docs, discovery scientists, clinicians, any biomedical/biological researchers interested in Alzheimer’s research.
Table of Contents
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
- No. of pages: 220
- Language: English
- Copyright: © Academic Press 2016
- Published: February 17, 2016
- Imprint: Academic Press
- eBook ISBN: 9780128043301
- Paperback ISBN: 9780128042564
About the Author
Michael R. D'Andrea
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 A42 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 death through an autoimmune mechanism in AD, suggesting that AD is an autoimmune disease. Most recently, he published a book entitled “Bursting Neurons and Fading Memories: An Alternative Hypothesis of the Neuropathology of Alzheimer’s Disease”. Furthermore, Michael has animated the “Inside-Out” hypothesis that is available on YouTube. Currently, he continues to post discussions on the matter.
Affiliations and Expertise
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