Ccr2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer-like disease

By J. E. Khoury, M. Toft, S. Hickman, T. Means, K. Terada, C. Geula, A. Luster. Nature Medicine, 2007

912 citations recorded by the source corpus.

Subfields: Molecular Biology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/971098bc73cd4fcb007492bf5d6517b10cf21ad5

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In Molecular Biology

1. E. Latz
2. R. Bell
3. Katherine A. Fitzgerald
4. T. Wyss‐Coray
5. V. Hornung
6. Robin J. M. Franklin
7. K. Moore
8. Berislav Zlokovic

In Neurology

1. R. Ransohoff
2. Marco Prinz
3. Josef Priller
4. Berislav Zlokovic
5. R. Bell
6. T. Wyss‐Coray
7. Helmut Kettenmann
8. Kurt M. Lucin

In Physiology

1. R. Ransohoff
2. R. Bell
3. Berislav Zlokovic
4. T. Wyss‐Coray
5. Richard O'Brien
6. U. Hanisch
7. Helmut Kettenmann
8. Sangram S. Sisodia

Citations in the corpus

• Debris clearance by microglia: an essential link between degeneration and regeneration (2008, background): “Diseased mice deficient in CCR2 demonstrated increased perivascular Ab deposits and died prematurely possibly due to amyloid angiopathy, indicating that CCR2 function on circulating monocytes or microglia is required for prevention or clearance of perivascular Ab deposits (El Khoury et al., 2007).”
• Immune modulation of learning, memory, neural plasticity and neurogenesis. (2011, neutral): “Consistently, pharmacological or genetic inhibition of microglial functioning reduces Ab clearance and accelerated disease progression (Seabrook et al., 2006; El Khoury et al., 2007).”
• Dendritic function of tau mediates amyloid-beta toxicity in Alzheimer's disease mouse models. (2010, neutral): “Excitotoxicity has been linked to premature lethality in APP transgenic mice (Chis-hti et al., 2001; El Khoury et al., 2007; Leissring et al., 2003; Roberson et al., 2007).”
• Amyloid Precursor Protein Processing and Alzheimer’s Disease (2011, background): “Studies show loss of synaptic terminals (Irizarry et al. 1997, Spires et al. 2005), synaptic dysfunction (Kamenetz et al. 2003, Shankar et al. 2008), abnormalities on spatial memory tests (Chen et al. 2000), and inflammation (El Khoury et al. 2007).”
• Microglia and neurodegeneration: The role of systemic inflammation (2013, background): “…activation in AD models: CCL2 overexpression increased microglial number and exacerbated GLIA disease (Kiyota et al., 2009) while CCR22/2 mice crossed with Tg2576 (El Khoury et al., 2007) or APP/ PS1 (Naert and Rivest, 2012) showed impaired microglial accumulation and accelerated Ab deposition.”
• Heterogeneity of CNS myeloid cells and their roles in neurodegeneration (2011, background): “Subsequently accelerated CNS tissue pathology and early demise were reported in a mouse model of Alzheimer's disease that was unable to recruit monocytes to the CNS as a result of absence of CCR2, a receptor specific for the monocyte chemoattractant protein family of chemokine”
• Microglial Dysfunction and Defective β-Amyloid Clearance Pathways in Aging Alzheimer's Disease Mice (2008, methodology): “Indeed, early microglial accumulation appears to delay progression of AD-like pathology, and bone marrow-derived microglia may restrict plaque formation in transgenic mice (Simard et al., 2006; El Khoury et al., 2007).”
• The myeloid cells of the central nervous system parenchyma (2010, background): “We propose that the capacities of microglia are defined in part by their ontogeny and that monocyte-derived cells that enter the CNS during disease have properties that are distinct from those of microglia, as suggested by studies in animal model”