Deciphering the molecular basis of memory failure in Alzheimer's disease.

By D. Walsh, D. Selkoe. Neuron, 2004

1,244 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Physiology

View Paper: https://www.semanticscholar.org/paper/5df17aebb163fa4dfe81d50afb0a658a62c638ff

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Citations in the corpus

Memantine: a NMDA receptor antagonist that improves memory by restoration of homeostasis in the glutamatergic system--too little activation is bad, too much is even worse. (2007, background): “4 and reviews by Greenamyre, 1991; Danysz et al., 2000; Danysz and Parsons, 2003; Walsh and Selkoe, 2004; Klein et al., 2004).”
Cortical Hubs Revealed by Intrinsic Functional Connectivity: Mapping, Assessment of Stability, and Relation to Alzheimer’s Disease (2009, background): “AD is associated with the pathological accumulation of misfolded proteins, including amyloid- (A ) (Mattson, 2004; Walsh and Selkoe, 2004).”
A network dysfunction perspective on neurodegenerative diseases (2006, background): “Notably, the abnormal proteins that are suspected of causing neurodegenerative disorders impair the integrity or function of presynaptic terminals and postsynaptic specialization”
Dendritic spine pathology in neuropsychiatric disorders (2011, background): “Dendritic spine loss is observed in the hippocampus and throughout the cortex, the principal areas affected by Alzheimer's disease–related patholog”
An epigenetic blockade of cognitive functions in the neurodegenerating brain (2012, background): “ppt"/> Cognitive decline is a debilitating feature of most neurodegenerative diseases of the central nervous system, including Alzheimer’s diseas”
Memory and executive function in aging and AD: multiple factors that cause decline and reserve factors that compensate. (2004, background): “Adapted from Rodrigue andwith build up of amyloid (extracellularly) and tau (intraRaz (2003).cellularly) in a pathological form (Golde et al., 2000; Matt- son, 2004; Walsh and Selkoe, 2004 [this issue of Neuron]).”
ApoE promotes the proteolytic degradation of Abeta. (2008, background): “These data demonstrate that the lipidation status of ApoE regulates its stability and influences extracellular soluble Ab proteolysis by IDE (and/or related proteinases).”
Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease. (2007, positive): “The excessive accumulation of pathogenic A b assemblies inthebrainappearstoplayacausalroleinAD(Glennerand Wong, 1984; Tanzi and Bertram, 2005; Walsh and Selkoe, 2004).”
Amyloid deposition is associated with impaired default network function in older persons without dementia (2009, neutral): “Despite compelling laboratory evidence that amyloidb exerts deleterious effects on synaptic activity associated with the formation of new memories (Walsh and Selkoe, 2004), the link between amyloid and the clinical syndrome of memory impairment in humans remains somewhat controversial.”
The Brain's Default Network (2008, background): “The leading hypothesis about the cause of AD proposes that toxic forms of the amyloid ß protein (Aß) initiate a cascade of events ending in synaptic dysfunction and cell death (Walsh & Selkoe 2004, Mattson 2004).”
Synaptic Targeting by Alzheimer's-Related Amyloid β Oligomers (2004, background): “The data provide a new molecular mechanism to support the emerging hypothesis that early AD memory loss is an oligomer-induced synapse failure, independent of neuron death and amyloid fibrils (Lambert et al., 1998; Klein et al., 2001; Hardy and Selkoe, 2002; Kirkitadze et al., 2002; Walsh and Selkoe”
Aβ Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease (2007, background): “…has been hypothesized that synapse dysfunction and degeneration are the early consequences of soluble A oligomers (Klein et al., 2001; Selkoe, 2002; Walsh and Selkoe, 2004; Klein, 2006; Standridge, 2006), which are potent CNS neurotoxins (Lambert et al., 1998) that accumulate in AD brain (Gong et…”
Inflammatory processes in Alzheimer's disease. (2007, positive): “Although Aβ has been considered to play a key role in AD pathogenesis (Walsh et al., 2002b; Walsh and Selkoe, 2004), it remains still uncertain whether Aβ plaques and neurofibrillary tangles are causative for AD.”