A network dysfunction perspective on neurodegenerative diseases

By J. Palop, Jeannie Chin, L. Mucke. Nature, 2006

682 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/f5bc18651d65932c99b100ee0c9ce47bcfe52552

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. H. Ko
2. Peter W. Kalivas
3. Valina L. Dawson
4. L. Mucke
5. T. Dawson
6. J. Palop
7. Michael W. Weiner
8. Ashish Raj

In Pharmacology

1. L. Mucke
2. H. Ko
3. Valina L. Dawson
4. T. Dawson
5. Michael W. Weiner
6. Ashish Raj
7. Amy Kuceyeski
8. J. Palop

In Physiology

1. L. Mucke
2. J. Palop
3. Michael W. Weiner
4. Ashish Raj
5. Amy Kuceyeski
6. H. Ko
7. Valina L. Dawson
8. T. Dawson

Citations in the corpus

• A Network Diffusion Model of Disease Progression in Dementia (2012, positive): “It could be that the starting configuration is dictated by selective vulnerability due to various stressors (Saxena and Caroni, 2011; Palop et al., 2006; Braak et al., 2000; Seeley et al., 2009), but the subsequent patterns are determined by macroscopic network dynamics.”
• Abnormal Cortical Networks in Mild Cognitive Impairment and Alzheimer's Disease (2010, background): “Reports on the characteristics of the structural cortical network in MCI have been rare [26].”
• Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease. (2007, positive): “…was not found in any of the 135 NTG controls and likely reflects a recent episode of abnormal overexcitation (Link et al., 1995; Lyford et al., 1995; Palop et al., 2006). hAPP-J20 mice with increased Arc expression had even higher NPY levels and lower calbindin levels than hAPP-J20 mice with…”
• Epilepsy and Cognitive Impairments in Alzheimer Disease (2009, background): “Many patients with AD experience fluctuations in cognitive functions such as transient episodes of amnestic wandering and disorientation.(22,40) The intermittent inability to retrieve memories cannot be easily explained by relatively protracted processes such as neuronal loss, plaque deposition, or ”
• Amyloid-β Induced Neuronal Dysfunction in Alzheimer’s Disease: From Synapses toward Neural Networks (2010, background): “Pathologically elevated Aβ may also affect cognitive performance by inducing abnormal patterns of neuronal activity and compensatory responses at the level of neuronal circuits and network”
• PARIS (ZNF746) Repression of PGC-1α Contributes to Neurodegeneration in Parkinson’s Disease (2011, neutral): “Similar compensatory mechanisms are likely to occur in PD (Bezard et al., 2003; Palop et al., 2006), and compensation accounts, in part, for the age-dependence of PD.”
• Neurodegenerative diseases target large-scale human brain networks (2009, background): “, 2007), some authors have suggested that neurodegeneration may relate to neural network dysfunction (Buckner et al., 2005; Palop et al., 2006).”
• Genetic Animal Models of Parkinson’s Disease (2010, positive): “Identifying, understanding , and potentially harnessing these compensatory mechanisms is important, as they may provide potential biomarkers and novel therapeutic opportunities (Palop et al., 2006).”
• Harnessing neuroplasticity for clinical applications (2011, positive): “Another perspective on neuroplasticity with degenerative diseases is that, with increasing pathology over time, compensatory mechanisms may fail or perhaps even become pathogenic via their effects on vulnerable neuronal populations, thereby destabilizing networks (Palop et al., 2006).”
• Levetiracetam suppresses neuronal network dysfunction and reverses synaptic and cognitive deficits in an Alzheimer’s disease model (2012, background): “However, as previously suggested, some of the compensatory changes may themselves interfere with normal synaptic functions (12, 28, 29).”