Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory

By G. Shankar, Shaomin Li, Tapan H. Mehta, Amaya Garcia-Munoz, Nina E. Shepardson, Imelda M. Smith, F. Brett, Michael A. Farrell, M. Rowan, C. Lemere and 4 more. Nature Medicine, 2008

2,572 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/d08c819bbb60057ca0fda735f907c7cf2aadfc37

How researchers see this paper

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

In Cellular and Molecular Neuroscience

1. D. Holtzman
2. D. Selkoe
3. L. Mucke
4. G. Bu
5. C. Lüscher
6. J. Long
7. L. Ittner
8. J. Götz

In Neurology

1. D. Selkoe
2. C. Lüscher
3. D. Holtzman
4. John C. Morris
5. Dennis W. Dickson
6. J. Götz
7. E. Masliah
8. J. Long

In Physiology

1. D. Holtzman
2. D. Selkoe
3. L. Mucke
4. John C. Morris
5. J. Long
6. G. Bu
7. J. Herz
8. L. Ittner

Citations in the corpus

• NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD). (2012, background): “…well before this stage, and there is growing evidence that one of the toxic protein species believed to be etiologically related to AD, soluble Ab oligomers, causes early memory problems by disrupting LTP and LTD mechanisms (Walsh et al. 2002; Tanzi 2005; Shankar et al. 2008; Cisse et al. 2011).”
• Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020, background): “Abbreviations AD: Alzheimer’s disease; APOE: Apolipoprotein E; Aβ: β-Amyloid; APP: Amyloid precursor protein; KCC2: K-Cl cotransporter 2; GABA : γaminobutyric acid; sAPP: Soluble amyloid precursor proteins; CNS: Central nervous system; PS1/2: Presenilins 1/2; CSF: Cerebral spinal fluid; LRP1: Lowden”
• Critical role of soluble amyloid-β for early hippocampal hyperactivity in a mouse model of Alzheimer’s disease (2012, methodology): “Therefore, we used previously characterized cross-linked dimers (26, 31) to test whether they can directly mediate neuronal hyperactivity.”
• Apolipoprotein E and apolipoprotein E receptors: normal biology and roles in Alzheimer disease. (2012, background): “…Snyder et al. 2005; Lesne et al. 2006; Townsend et al. 2006; Haass and Selkoe 2007; Shankar et al. 2007; Berman et al. 2008; Puzzo et al. 2008; Shankar et al. 2008; Nygaard and Strittmatter 2009; Gimbel et al. 2010; Palop and Mucke 2010; Renner et al. 2010; Ronicke et al. 2010) (see Mucke and…”
• Cellular Prion Protein Mediates Impairment of Synaptic Plasticity by Amyloid-β Oligomers (2009, neutral): “While this formulation of A β 42-oligomer is not chromatographically identical to A β 42-oligomer from brain2,3,9, it affords detection of high affinity binding sites likely to share pathological actions with sites for other A β 42-oligomer preparations5,6,11.”
• Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019, positive): “They also cause impairment in cognitive tasks when injected into the lateral ventricles of rodent models (Shankar et al., 2008).”
• The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics (2011, background): “A modification of the amyloid cascade hypothesis is supported by increasing evidence from the literature that smaller, soluble oligomeric species of amyloid-β mediate either neuronal death or affect synaptic neurotransmissio”
• Emerging roles of Wnts in the adult nervous system (2010, background): “Aβ oligomers have also been shown to reduce the surface expression of glutamate receptors in hippocampal neuron”