Correlation between elevated levels of amyloid beta-peptide in the brain and cognitive decline.

By J. Näslund, V. Haroutunian, R. Mohs, K. Davis, P. Davies, Paul Greengard, Joseph D. Buxbaum. Journal of the American Medical Association (JAMA), 2000

1,358 citations recorded by the source corpus.

Subfields: Neurology, Physiology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/d7dca5e10d81d000a3833887fa57c73824f3b7c3

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Citations in the corpus

The Relationship between Aβ and Memory in the Tg2576 Mouse Model of Alzheimer's Disease (2002, positive): “More recently, when more sensitive antibody-based methods were used to measure A deposits and subject pools that represented a broad range of cognitive impairment were examined, highly significant and robust correlations were found (Cummings et al., 1996; Bartoo et al., 1997; Naslund et al., 2000).”
Folding proteins in fatal ways (2003, background): “This animal work fits nicely with growing evidence that memory and cognitive deficits in Alzheimer's disease and in its harbinger, minimal cognitive impairment, correlate better with cerebral Aβ concentrations than with amyloid plaque number”
Natural Oligomers of the Alzheimer Amyloid-β Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway (2007, background): “Conversely, although rises in cortical levels of soluble A appear to correlate with disease progression in animal models and AD subjects (Kuo et al., 1996; McLean et al., 1999; Mucke et al., 2000; Naslund et al., 2000; Moolman et al., 2004; Spires et al., 2005), no specific soluble form of A that in”
Autophagy, amyloidogenesis and Alzheimer disease (2007, neutral): “Before A is deposited extracellularly, the intracellular pool of soluble A rises substantially in endosomal-lysosomal compartments (Cataldo et al., 2004a; Takahashi et al., 2004) and remains substantial even in the heavily plaque-laden AD brain (Naslund et al., 2000).”
Natural oligomers of the amyloid-β protein specifically disrupt cognitive function (2005, background): “β-amyloid(1-40) effects on behavior and memory.”
Aβ peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease (2000, background): “Either might explain the divergent effects on levels of dense-cored plaques and Aβ measured biochemically (although high levels of cerebral Aβ in the presence of relatively few plaques are seen in human”
Paradigm shifts in Alzheimer's disease and other neurodegenerative disorders: The emerging role of oligomeric assemblies (2002, positive): “Not surprisingly, an important paradigm guiding efforts over the last century toward therapeutic intervention in AD has been that ﬁbril formation by A (cid:1) leads to neuro-degeneration and death (Hardy and Higgins, 1992).”