2010 - Fellow of American Physical Society (APS) Citation For seminal contributions in the physics of nucleation and phase transitions arising from fundamental advances in statistical fieldtheoretic techniques, and their application to general mean field systems
1989 - Fellow of the American Association for the Advancement of Science (AAAS)
1968 - Fellow of the American Association for the Advancement of Science (AAAS)
William L. Klein spends much of his time researching Alzheimer's disease, Neuroscience, Amyloid, Synapse and Biochemistry. His studies in Alzheimer's disease integrate themes in fields like Hippocampal formation and Immunology. His Neuroscience research incorporates elements of In vivo, Tau pathology and Pathogenesis.
He has included themes like Amyloid beta, Peptide, Antibody, Genetically modified mouse and Surface plasmon resonance in his Amyloid study. His Synapse research is multidisciplinary, incorporating perspectives in Neuropathology, Dementia, Disease and Insulin receptor. The study incorporates disciplines such as Immunofluorescence and Cell biology in addition to Biochemistry.
William L. Klein mainly investigates Cell biology, Biochemistry, Neuroscience, Alzheimer's disease and Amyloid. The various areas that William L. Klein examines in his Cell biology study include Endocrinology, Receptor, Internal medicine, Muscarinic acetylcholine receptor and Neurite. His Biochemistry study combines topics from a wide range of disciplines, such as Hippocampal formation, Amyloid β and Antibody.
His study looks at the relationship between Neuroscience and fields such as Long-term potentiation, as well as how they intersect with chemical problems. In his research on the topic of Alzheimer's disease, Amyloid precursor protein is strongly related with Genetically modified mouse. His Amyloid research is multidisciplinary, relying on both Biophysics and Human brain.
The scientist’s investigation covers issues in Neuroscience, Synapse, Alzheimer's disease, Cell biology and Amyloid. His Synapse research integrates issues from Liraglutide, Endocrinology, Amyloid beta, Insulin receptor and Internal medicine. His Alzheimer's disease research is under the purview of Pathology.
His research integrates issues of Biochemistry, Neuron, Single-Chain Variable Fragment Antibody and Aβ oligomers in his study of Cell biology. His biological study spans a wide range of topics, including Neurotoxicity and Amyloid β. His Amyloid study integrates concerns from other disciplines, such as Toxicity, Amyloid precursor protein and Pharmacology.
William L. Klein focuses on Alzheimer's disease, Pathology, Neuroscience, Synapse and Amyloid precursor protein. His work carried out in the field of Alzheimer's disease brings together such families of science as Hippocampus, Unfolded protein response, Genetically modified mouse, Pharmacology and Amyloid. William L. Klein works in the field of Neuroscience, focusing on Hippocampal formation in particular.
His work is dedicated to discovering how Hippocampal formation, Type 2 diabetes are connected with Neuroprotection and other disciplines. He interconnects Endocrinology, Insulin receptor and Internal medicine in the investigation of issues within Synapse. As a member of one scientific family, William L. Klein mostly works in the field of Long-term potentiation, focusing on Neurotoxicity and, on occasion, Cell biology.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
Diffusible, nonfibrillar ligands derived from Aβ1–42 are potent central nervous system neurotoxins
M. P. Lambert;A. K. Barlow;B. A. Chromy;C. Edwards.
Proceedings of the National Academy of Sciences of the United States of America (1998)
Alzheimer's disease-affected brain: Presence of oligomeric Aβ ligands (ADDLs) suggests a molecular basis for reversible memory loss
Yuesong Gong;Lei Chang;Kirsten L. Viola;Pascale N. Lacor.
Proceedings of the National Academy of Sciences of the United States of America (2003)
Targeting small Aβ oligomers: the solution to an Alzheimer's disease conundrum?
William L Klein;Grant A Krafft;Caleb E Finch.
Trends in Neurosciences (2001)
Aβ Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease
Pascale N. Lacor;Maria C. Buniel;Paul W. Furlow;Antonio Sanz Clemente.
The Journal of Neuroscience (2007)
Synaptic Targeting by Alzheimer's-Related Amyloid β Oligomers
Pascale N. Lacor;Maria C. Buniel;Lei Chang;Sara J. Fernandez.
The Journal of Neuroscience (2004)
Detection of a biomarker for Alzheimer's disease from synthetic and clinical samples using a nanoscale optical biosensor.
Amanda J Haes;Lei Chang;William L Klein;Richard P Van Duyne.
Journal of the American Chemical Society (2005)
Nanoparticle-based detection in cerebral spinal fluid of a soluble pathogenic biomarker for Alzheimer's disease
Dimitra G. Georganopoulou;Lei Chang;Jwa Min Nam;C. Shad Thaxton.
Proceedings of the National Academy of Sciences of the United States of America (2005)
Aβ Oligomers Induce Neuronal Oxidative Stress through an N-Methyl-D-aspartate Receptor-dependent Mechanism That Is Blocked by the Alzheimer Drug Memantine
Fernanda G. De Felice;Fernanda G. De Felice;Pauline T. Velasco;Mary P. Lambert;Kirsten L. Viola.
Journal of Biological Chemistry (2007)
A Localized Surface Plasmon Resonance Biosensor: First Steps toward an Assay for Alzheimer's Disease
Amanda J. Haes;W. Paige Hall;Lei Chang;William L. Klein.
Nano Letters (2004)
Aβ toxicity in Alzheimer's disease: Globular oligomers (ADDLs) as new vaccine and drug targets
William L Klein.
Neurochemistry International (2002)
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