Amyloids and Are Generated Intracellularly in Cultured Human Neurons and Their Secretion Increases with Maturation

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High-Level Neuronal Expression of Aβ_1–42in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation

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Environmental Enrichment Reduces Aβ Levels and Amyloid Deposition in Transgenic Mice

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Increased Lipid Peroxidation Precedes Amyloid Plaque Formation in an Animal Model of Alzheimer Amyloidosis

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The Levels of Soluble versus Insoluble Brain Aβ Distinguish Alzheimer's Disease from Normal and Pathologic Aging

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Neuron loss in the 5XFAD mouse model of Alzheimer’s disease correlates with intraneuronal Aβ42 accumulation and Caspase-3 activation

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Evidence that neurones accumulating amyloid can undergo lysis to form amyloid plaques in Alzheimer’s disease

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Intraneuronal Aβ accumulation and origin of plaques in Alzheimer's disease

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The N-Terminal Region of Amyloid β Controls the Aggregation Rate and Fibril Stability at Low pH through a Gain of Function Mechanism

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A reducing and denaturing step maximizes the immunoprecipitations of m-calpain and I-2PP2A/SET: An approach toward antibodies that do not work well in immunoprecipitation

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Co-Immunoprecipitation from Transfected Cells

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Immunoprecipitation for Cell Culture

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Chapter 23 Immunoprecipitation Procedures

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Immunoprecipitation of cell lysates with RAP-5 does not specifically detect ras oncogene product p21

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