The Cellular Phase of Alzheimer's Disease.

By Bart de Strooper, E. Karran. Cell, 2016

1,734 citations recorded by the source corpus.

Subfields: Developmental Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/05bf53a5122d4cee0bb216e32e1db45106bdab4d

How researchers see this paper

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

In Developmental Neuroscience

1. M. Colonna
2. John Hardy
3. O. Butovsky

In Neurology

1. D. Selkoe
2. M. Colonna
3. John Hardy
4. O. Butovsky
5. D. Holtzman
6. J. Long

In Physiology

1. D. Selkoe
2. K. Viola
3. B. de Strooper
4. W. Klein
5. John Hardy
6. T. Saido
7. Jonathan M. Schott
8. C. Lane

Citations in the corpus

• Alzheimer's disease (2018, background): “A more nuanced model of the preclinical phase of AD, no longer viewing b-amyloid, tau and inflammation as steps along a sequential pathway but as part of a cellular phase of AD pathogenesis [71], will also lead to a more sophisticated approach to treatment and prevention.”
• APP mouse models for Alzheimer's disease preclinical studies (2017, positive): “…of improved AD model(s) by crossbreeding with appropriate mutant mice (Table 1), and (v) to study the cellular phase of Alzheimer’s disease (De Strooper & Karran, 2016), including the progressive response of vascular, astroglia, oligodendrocyte, and microglial cell populations upon amyloid…”
• The amyloid hypothesis of Alzheimer's disease at 25 years (2016, background): “As others have pointed out (Small & Duff, 2008; De Strooper & Karran, 2016) and we concur, after disease initiation, the complexity of the downstream pathogenic processes increases.”
• Inflammasomes in neuroinflammatory and neurodegenerative diseases (2019, background): “Although there is overwhelming evidence for a pathogenic role for Ab in AD, neuroinflammation is increasingly regarded as another key component that actively contributes to AD pathology (De Strooper & Karran, 2016; Sala Frigerio & De Strooper, 2016).”
• The Amyloid-β Oligomer Hypothesis: Beginning of the Third Decade (2018, background): “De Strooper and Karran propose that AD pathogenesis is not simply a neuron-centric, linear cascade initiated by A and leading to dementia, but rather a long, complex cellular phase consisting of feedback and feedforward responses of astrocytes, microglia, and vasculature [202].”
• Spatial Transcriptomics and In Situ Sequencing to Study Alzheimer's Disease. (2020, methodology): “…et al., 2015; Keren-Shaul et al., 2017; Krasemann et al., 2017; Sala Frigerio et al., 2019; Salih et al., 2018; Jansen et al., 2019; Sierksma et al., 2020), but astrocytes, neurons, and oligodendrocytes also display altered molecular responses to amyloid plaques (De Strooper and Karran, 2016).”
• Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017, background): “Moreover, progression of neurodegeneration is modified by cellular responses to biochemical alterations (95).”