Nature Neuroscience7, 1181 - 1183 (2004)
Published online: 10 October 2004; | doi:10.1038/nn1335
Fibrillar amyloid deposition leads to local synaptic abnormalities and breakage of neuronal branches
Julia Tsai1, Jaime Grutzendler1, 3, Karen Duff2
& Wen-Biao Gan1
1
Molecular Neurobiology Program, Skirball Institute and Department of Neuroscience and Physiology, New York University School of Medicine, New York, New York 10016, USA.
2
Center for Dementia Research, Nathan Kline Institute and New York University School of Medicine, Orangeburg, New York 10962, USA.
3
Present address: Department of Neurology, Northwestern University, Chicago, Illinois 60611, USA.
Amyloid plaques are a hallmark of Alzheimer disease, but their importance in its pathogenesis is controversial. By neuronal labeling and transcranial two-photon imaging, we show in a transgenic mouse model of Alzheimer disease that dendrites passing through or near fibrillar amyloid deposits undergo spine loss and shaft atrophy, and nearby axons develop large varicosities, together leading to neurite breakage and large-scale, permanent disruption of neuronal connections. Thus, fibrillar amyloid deposition is more detrimental to neuronal circuitry than previously thought, underscoring the importance of prevention and early clearance of plaques.
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