Microglial VEGF Receptor Response Is an Integral Chemotactic Component in Alzheimer's Disease Pathology

Ryu, Jae K.; Cho, Taesup; Choi, Hyun B.; Wang, Yu Tian; McLarnon, James G.

doi:10.1523/jneurosci.2888-08.2009

Cited by 100 publications

(98 citation statements)

References 44 publications

(51 reference statements)

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“…We did not detect convincing VEGFR1 immunopositivity within microglia in either AD or control brains, in contrast to the findings of Ryu et al [2009]. The reason for the disparity is not clear but could include their use of a different VEGFR1 antibody whose specificity was not confirmed, and differing fixation protocols [41]. VEGFR1, like VEGF, is upregulated by hypoxia [61,62,67] and our expectation was therefore that VEGFR1 production would increase in AD.…”

Section: Discussioncontrasting

confidence: 99%

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VEGFR1 and VEGFR2 in Alzheimer’s Disease

Harris

Miners

Allen

et al. 2017

JAD

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Section: Discussioncontrasting

confidence: 99%

“…VEGFR1 transduces signals for cellular proliferation and permeability, and is important in postnatal angiogenesis [37], neuroprotection [38,39], neurogenesis [40] and microglial migration [41,42]. VEGFR1 has a high affinity for VEGF, although its kinase activity is only around one tenth of that of VEGFR2 [43].…”

Section: Introductionmentioning

confidence: 99%

VEGFR1 and VEGFR2 in Alzheimer’s Disease

Harris

Miners

Allen

et al. 2017

JAD

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“…In our study we focused on the changes in neuronal levels of IRβ and did not measure glial alterations. Still since it is documented in the literature that in AD there is an increase in glial cells (Ryu et al 2009;Vehmas et al 2003;Venneti et al 2009), it is rather less likely that our findings might occur due to changes in glial cells. However we cannot exclude the possibility whether there can be a "selective" neuronal cell lost of only IRβ positive neurons in AD.…”

Section: Discussionmentioning

confidence: 70%

Alzheimer's disease and type 2 diabetes: Two diseases, one common link?

Bartl

Monoranu

Wagner

et al. 2012

The World Journal of Biological Psychiatry

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OBJECTIVES: Although Alzheimer's disease (AD) is the most common form of dementia in the elderly, its aetiology remains mostly unknown. A potential pathophysiological mechanism for AD arises from the knowledge that insulin is also synthesized independently in the central nervous system and is involved in the regulation of memory formation. AD may represent a brain-specific form of insulin resistance. METHODS: We used immunohistochemistry to investigate the numbers of cells expressing insulin receptor -subunit (IR) and phosphorylated PPAR (PPAR(p)) in human post-mortem tissue from patients with AD; AD combined with type 2 diabetes mellitus (T2DM); just T2DM , and from aged-matched controls. These numbers were evaluated in frontal cortex and in dorsal/ventral parts of the hippocampus. RESULTS: We observed significantly lower numbers of IR positive cells in AD cases compared to all other groups in all investigated brain regions. Also significantly more PPAR(p) positive cells occurred in each patient group compared to control. CONCLUSIONS: T2DM and AD may not be directly linked, but may share common histological features including lower numbers of IR positive cells and higher numbers of PPAR(p) positive cells in all investigated brain regions. These observations may at least partially explain the increased frequency of AD in elderly diabetic patients. Objectives: Although Alzheimer's disease (AD) is the most common form of dementia in the elderly, its aetiology remains mostly unknown. A potential pathophysiological mechanism for AD arises from the knowledge that insulin is also synthesized independently in the central nervous system and is involved in the regulation of memory formation. AD may represent a brain-specific form of insulin resistance.

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“…High VEGF levels around neovascular tufts can potentially support migration and growth of microglial cells that express VEGF receptors 1 and 2 (65). Although it is unlikely that microglia significantly contribute to the overall VEGF production, their tropism to neovessels could locally affect vessel sprouts and thereby substantially influence neovascular tuft formation (66). Of particular interest is the improved vascular recovery (i.e.…”

Section: Discussionmentioning

confidence: 99%

Single and Compound Knock-outs of MicroRNA (miRNA)-155 and Its Angiogenic Gene Target CCN1 in Mice Alter Vascular and Neovascular Growth in the Retina via Resident Microglia

Yan

Lee

Lazzaro

et al. 2015

Journal of Biological Chemistry

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Background: MicroRNA-155 is a proinflammatory small RNA, but its function in pathological angiogenesis is unknown. Results: MicroRNA-155 deficiency increases angiogenic protein CCN1 expression, which harnesses retinal neovascularization by reducing both microglia activation and inflammation. Conclusion: The microRNA-155/CCN1 regulatory axis regulates angiogenic and inflammatory responses in the retina. Significance: Modulation of microRNA-155 and CCN1 interaction is potentially beneficial in retinal neovascularization therapy.

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Microglial VEGF Receptor Response Is an Integral Chemotactic Component in Alzheimer's Disease Pathology

Cited by 100 publications

References 44 publications

VEGFR1 and VEGFR2 in Alzheimer’s Disease

VEGFR1 and VEGFR2 in Alzheimer’s Disease

Alzheimer's disease and type 2 diabetes: Two diseases, one common link?

Single and Compound Knock-outs of MicroRNA (miRNA)-155 and Its Angiogenic Gene Target CCN1 in Mice Alter Vascular and Neovascular Growth in the Retina via Resident Microglia

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