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| http://dx.doi.org/10.1136/bmjgh-2022-008652 | DOI Listing |
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Cancer neuroscience and glioma: clinical implications.
Acta Neurochir (Wien)
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Department of Neurosurgery, University Hospital Eppendorf, Hamburg, Germany.
In recent years, it has been increasingly recognized that tumor growth relies not only on support from the surrounding microenvironment but also on the tumors capacity to adapt to - and actively manipulate - its niche. While targeting angiogenesis and modulating the local immune environment have been explored as therapeutic approaches, these strategies have yet to yield effective treatments for brain tumors and remain under refinement. More recently, the nervous system itself has been explored as a critical environmental support for cancer, with extensive neuro-tumoral interactions observed both intracranially and in extracranial sites containing neural components.
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Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Background: Angiotensin-converting enzyme (ACE) is a validated risk locus for developing late-onset Alzheimer's disease (LOAD). ACE1 controls blood pressure through the renin-angiotensin system (RAS), but it is also present and acts locally in the brain. Hypertension is associated with an increased risk for developing AD, and people taking select RAS-targeting therapeutics have reduced incidence of AD.
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Department of Medicine, University of Wisconsin-Madison School of Medicine and Public Health, Madison, WI, USA.
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Indiana University School of Medicine, Indianapolis, IN, USA.
Background: Dysfunctional microglial activity has recently been identified as a potential mechanism leading to accumulation of amyloid beta and pTau and subsequent neurodegeneration in Alzheimer's Disease. The CX3CR1/fractalkine axis serves as a mechanism for bi-directional communication between microglia and neurons, respectively, to promote a resting, anti-inflammatory state in microglia. Previous studies have demonstrated that deficiency in CX3CR1 signaling leads microglia to a more pro-inflammatory phenotype, phagocytic deficits, and increased susceptibility of neurons to cell death.
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