This paper appears in the following: News Paper Alert: Patient Aβ Dimers Impair Plasticity, Memory 26 Jun 2008 San Francisco: Tau—Time to Shine as Therapeutic Target? 17 May 2011 The Toxic Fold? Aβ Dodecamers, Tetramers Show Their Conformations 16 Jun 2009 Bad Guys—Aβ Oligomers Live Up to Reputation in Human Studies 7 May 2010 Aβ Sufficient for Seeding—But Is It a Prion? 23 Jun 2012 Aβ Oligomers: A Fatal Attraction for Glutamate Receptors? 21 Jun 2010 Model Shows Oligomers Impair Memory, Questions Role of Prion Protein 25 Jan 2010 Neuronal Glutamate Fuels Aβ-induced LTD 27 Jun 2009 Soluble Aβ—Bane or Boon? Real-time Data in Humans Yield New Insight 2 Sep 2008 San Diego: Aβ Oligomers Seen, With ApoE, at Synapses of Human Brain 6 Dec 2010 Research Brief: Assessing Aβ Oligomers Toxicity in Live Mice 9 Jun 2012 Aβ Neurotoxicity—Is it the Dimer? No, and Yes 2 Nov 2010 Patient Aβ Dimers Sufficient for Tau, Neuritic Changes 14 Mar 2011 ADNI: Mission Creep From Alzheimer Disease to Healthy Senior? 23 May 2009 Aβ*56 Found in Human CSF, Correlates With Tau? 15 Mar 2013 Microglia Need Scara1 Receptor to Clear Soluble Amyloid 28 Jun 2013 Glutamate Receptor Links Aβ-Prion Complex with Fyn, Synaptic Damage 11 Sep 2013 Sylvain Lesné, Who Found Aβ*56, Accused of Image Manipulation 22 Jul 2022
Comments
Inserm
After plaques, protofibrils, Aβ42, it is suggested that the killer is the dimer. How can we reconcile this in vitro finding with neuropathological observations of non-demented patients with widespread and huge Aβ aggregates (not plaque cores) in the neocortex?
Make a Comment
To make a comment you must login or register.