Circumventricular Organs

Oldfield, Brian J.

doi:10.1016/b978-0-12-374245-2.00015-2

Cited by 16 publications

(16 citation statements)

References 209 publications

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“…More recently, it has been found that the CVOs, including the choroid plexus (CP), act as brain-immune interfaces mediating the transfer of immune cells from blood to brain (Shimada and Hasegawa-Ishii, 2017 ). This is in line with recent attempts to systematize the CVOs while considering microglia to be an important component of these structures (Oldfield and McKinley, 2014 ; Miyata, 2015 ; Kaur and Ling, 2017 ).…”

Section: Introductionsupporting

confidence: 87%

Development of Circumventricular Organs in the Mirror of Zebrafish Enhancer-Trap Transgenics

et al. 2017

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The circumventricular organs (CVOs) are small structures lining the cavities of brain ventricular system. They are associated with the semitransparent regions of the blood-brain barrier (BBB). Hence it is thought that CVOs mediate biochemical signaling and cell exchange between the brain and systemic blood. Their classification is still controversial and development not fully understood largely due to an absence of tissue-specific molecular markers. In a search for molecular determinants of CVOs we studied the green fluorescent protein (GFP) expression pattern in several zebrafish enhancer trap transgenics including Gateways (ET33-E20) that has been instrumental in defining the development of choroid plexus. In Gateways the GFP is expressed in regions of the developing brain outside the choroid plexus, which remain to be characterized. The neuroanatomical and histological analysis suggested that some previously unassigned domains of GFP expression may correspond to at least six other CVOs–the organum vasculosum laminae terminalis (OVLT), subfornical organ (SFO), paraventricular organ (PVO), pineal (epiphysis), area postrema (AP) and median eminence (ME). Two other CVOs, parapineal and subcommissural organ (SCO) were detected in other enhancer-trap transgenics. Hence enhancer-trap transgenic lines could be instrumental for developmental studies of CVOs in zebrafish and understanding of the molecular mechanism of disease such a hydrocephalus in human. Their future analysis may shed light on general and specific molecular mechanisms that regulate development of CVOs.

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Section: Introductionsupporting

confidence: 87%

Development of Circumventricular Organs in the Mirror of Zebrafish Enhancer-Trap Transgenics

et al. 2017

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“…The extrinsic model accounts for communication of the glial cells with the immune challenges presented via the blood vascular system using the circumventricular organs and the choroid plexus that are devoid of the BBB ( 56 ). The cells from this region of the brain are fully equipped with the CD14 receptor and the toll-like receptor 4 (TLR 4) to recognize LPS from the peripheral blood circulation ( 27 , 28 ).…”

Section: The Inflammatory Hypothesismentioning

confidence: 99%

“…Circumventricular organs (permit polypeptide hypothalamic hormones to leave the brain without disrupting the BBB) are not dependent on the BBB ( 56 ) and may act as another entry portal to the brain for bacteria ( 157 ). Poole et al ( 8 ) postulated that bacteria and their products may also directly access the brain via the systemic circulation through the perivascular spaces.…”

Section: How Do Oral Microorganisms Reach the Brain?mentioning

confidence: 99%

Can oral infection be a risk factor for Alzheimer's disease?

Olsen

Singhrao

2015

Journal of Oral Microbiology

142

140

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Alzheimer's disease (AD) is a scourge of longevity that will drain enormous resources from public health budgets in the future. Currently, there is no diagnostic biomarker and/or treatment for this most common form of dementia in humans. AD can be of early familial-onset or sporadic with a late-onset. Apart from the two main hallmarks, amyloid-beta and neurofibrillary tangles, inflammation is a characteristic feature of AD neuropathology. Inflammation may be caused by a local central nervous system insult and/or by peripheral infections. Numerous microorganisms are suspected in AD brains ranging from bacteria (mainly oral and non-oral Treponema species), viruses (herpes simplex type I), and yeasts (Candida species). A causal relationship between periodontal pathogens and non-oral Treponema species of bacteria has been proposed via the amyloid-beta and inflammatory links. Periodontitis constitutes a peripheral oral infection that can provide the brain with intact bacteria and virulence factors and inflammatory mediators due to daily, transient bacteremias. If and when genetic risk factors meet environmental risk factors in the brain, disease is expressed, in which neurocognition may be impacted, leading to the development of dementia. To achieve the goal of finding a diagnostic biomarker and possible prophylactic treatment for AD, there is an initial need to solve the etiological puzzle contributing to its pathogenesis. This review therefore addresses oral infection as the plausible etiology of late-onset AD (LOAD).

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“…In the past the brain was considered as an "immunoprivileged organ," as elements of the immune system [such as neutrophils, naive T cells (adaptive immune system), plasma proteins, and extra-cerebral-toxins to prevent inappropriate glial cell activation] cannot cross the bloodbrain barrier (BBB). However, it is now understood that the circumventricular organs are not subject to the BBB [35], a region of the brain where infections (both systemic and direct via the trigeminal and olfactory nerve pathways (see Figure 1) and inflammatory mediators can access the brain [36][37][38].…”

Section: What Is Intra-cerebral Inflammation?mentioning

confidence: 99%

Oral Inflammation, Tooth Loss, Risk Factors, and Association with Progression of Alzheimer's Disease

Singhrao

Harding

Simmons

et al. 2014

JAD

101

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Periodontitis is a polymicrobial chronic inflammatory disease of tooth-supporting tissues with bacterial etiology affecting all age groups, becoming chronic in a subgroup of older individuals. Periodontal pathogens Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola are implicated in the development of a number of inflammatory pathologies at remote organ sites, including Alzheimer's disease (AD). The initial inflammatory hypothesis proposed that AD hallmark proteins were the main contributors of central nervous system (CNS) inflammation. This hypothesis is expanding to include the role of infections, lifestyle, and genetic and environmental factors in the pathogenesis of AD. Periodontal disease (PD) typifies a condition that encompasses all of the above factors including pathogenic bacteria. These bacteria not only are the source of low-grade, chronic infection and inflammation that follow daily episodes of bacteremia arising from everyday tasks such as brushing, flossing teeth, chewing food, and during dental procedures, but they also disseminate into the brain from closely related anatomical pathways. The long-term effect of inflammatory mediators, pathogens, and/or their virulence factors, reaching the brain systemically or otherwise would, over time, prime the brain's own microglia in individuals who have inherent susceptibility traits. Such susceptibilities contribute to inadequate neutralization of invading agents, upon reaching the brain. This has the capacity to create a vicious cycle of sustained local inflammatory milieu resulting in the loss of cytoarchitectural integrity and vital neurons with subsequent loss of function (deterioration in memory). The possible pathways between PD and AD development are considered here, as well as environmental factors that may modulate/exacerbate AD symptoms.

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Circumventricular Organs

Cited by 16 publications

References 209 publications

Development of Circumventricular Organs in the Mirror of Zebrafish Enhancer-Trap Transgenics

Development of Circumventricular Organs in the Mirror of Zebrafish Enhancer-Trap Transgenics

Can oral infection be a risk factor for Alzheimer's disease?

Oral Inflammation, Tooth Loss, Risk Factors, and Association with Progression of Alzheimer's Disease

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