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lüll Amyloid-independent mechanisms in Alzheimer s disease pathogenesis Pimplikar SW; Nixon RA; Robakis NK; Shen J; Tsai LHJ Neurosci 2010[Nov]; 30 (45): 14946-54Despite the progress of the past two decades, the cause of Alzheimer's disease (AD) and effective treatments against it remain elusive. The hypothesis that amyloid-beta (Abeta) peptides are the primary causative agents of AD retains significant support among researchers. Nonetheless, a growing body of evidence shows that Abeta peptides are unlikely to be the sole factor in AD etiology. Evidence that Abeta/amyloid-independent factors, including the actions of AD-related genes, also contribute significantly to AD pathogenesis was presented in a symposium at the 2010 Annual Meeting of the Society for Neuroscience. Here we summarize the studies showing how amyloid-independent mechanisms cause defective endo-lysosomal trafficking, altered intracellular signaling cascades, or impaired neurotransmitter release and contribute to synaptic dysfunction and/or neurodegeneration, leading to dementia in AD. A view of AD pathogenesis that encompasses both the amyloid-dependent and -independent mechanisms will help fill the gaps in our knowledge and reconcile the findings that cannot be explained solely by the amyloid hypothesis.|Alzheimer Disease/*etiology/pathology[MESH]|Amyloid beta-Peptides[MESH]|Humans[MESH]|Lysosomes/*pathology[MESH]|Neurons/*pathology[MESH]|Protein Transport[MESH]|Signal Transduction[MESH] |