Intraneuronal Alzheimer abeta42 accumulates in multivesicular bodies and is associated with synaptic pathology.

By R. Takahashi, T. Milner, Feng Li, E. E. Nam, M. Edgar, H. Yamaguchi, M. Beal, Huaxi Xu, Paul Greengard, Gunnar K. Gouras. American Journal of Pathology, 2002

767 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/85ed974c7569b317c791ec826eb1d405f333b3cc

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. A. Cuervo
2. C. Duyckaerts
3. K. Duff
4. Ralph A. Nixon
5. Y. Uchiyama

In Physiology

1. Ralph A. Nixon
2. A. Cuervo
3. C. Duyckaerts
4. Marie-Claude Potier
5. Benoit Delatour
6. M. Mercken
7. N. Mizushima

In Psychiatry and Mental health

1. C. Duyckaerts
2. Marie-Claude Potier
3. Benoit Delatour

Citations in the corpus

• Docosahexaenoic acid protects from dendritic pathology in an Alzheimer's disease mouse model. (2004, unknown): “The selective accumulation of Aβ42 in dendritic compartments in Tg2576 and AD (Takahashi et al., 2002) and toxic Aβ oligomer binding at punctate PSD-95-positive sites (Gong et al., 2003) could drive this compartmentalized postsynaptic pathology, which was revealed at the ultrastructural level by…”
• Classification and basic pathology of Alzheimer disease (2009, background): “Moreover, Ab 42 was found to accumulate in multivesicular bodies in preand post-synaptic compartment [306].”
• Autophagy, amyloidogenesis and Alzheimer disease (2007, unknown): “MVBs and late endosomes are relatively rich in APP and APP secretases, and those in AD brain and mouse models of AD contain A peptide (Gouras et al., 2000; Takahashi et al., 2002).”
• Macroautophagy—a novel β-amyloid peptide-generating pathway activated in Alzheimer's disease (2005, background): “Previous studies have identified intracellular A accumulation in endosomes (Cataldo et al., 2004a) and multivesicular bodies (Takahashi et al., 2002) in AD and Down syndrome (Gyure et al., 2001).”
• Intraneuronal β-Amyloid Aggregates, Neurodegeneration, and Neuron Loss in Transgenic Mice with Five Familial Alzheimer's Disease Mutations: Potential Factors in Amyloid Plaque Formation (2006, background): “4D), consistent with the hypothesis that A accumulation within neurites may contribute to degeneration and deposit formation (Takahashi et al., 2002).”