Plasma fibrinogen is associated with cognitive decline and risk for dementia in patients with mild cognitive impairment

Xu, Gelin; Zhang, H.; Zhang, S.; Fan, Xiaobing; Liu, Xiaojun

doi:10.1111/j.1742-1241.2007.01268.x

Cited by 69 publications

(51 citation statements)

References 39 publications

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“…High levels of fibrinogen in plasma increase the risk for dementia (van Oijen et al, 2005; Xu et al, 2008), and fibrinogen in cerebrospinal fluid (Craig-Schapiro et al, 2011; Vafadar-Isfahani et al, 2012) and plasma (Thambisetty et al, 2011; Yang et al, 2014) has been proposed as a useful biomarker to identify AD progression. Interestingly, fibrinogen has recently been found to be one of the few blood-based biomarkers specific for AD and not for other brain disorders (Chiam et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Fibrin deposited in the Alzheimer's disease brain promotes neuronal degeneration

Cortes‐Canteli¹,

Mattei²,

Richards³

et al. 2015

Neurobiology of Aging

143

146

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Alzheimer’s disease (AD) is the most common form of dementia and has no effective treatment. Besides the well-known pathological characteristics, this disease also has a vascular component, and substantial evidence shows increased thrombosis as well as a critical role for fibrin(ogen) in AD. This molecule has been implicated in neuroinflammation, neurovascular damage, blood brain barrier permeability, vascular amyloid deposition, and memory deficits that are observed in AD. Here we present evidence demonstrating that fibrin deposition increases in the AD brain and correlates with the degree of pathology. Moreover, we show that fibrin(ogen) is present in areas of dystrophic neurites and that a modest decrease in fibrinogen levels improves neuronal health and ameliorates amyloid pathology in the subiculum of AD mice. Our results further characterize the important role of fibrin(ogen) in this disease and support the design of therapeutic strategies aimed at blocking the interaction between fibrinogen and Aβ and/or normalizing the increased thrombosis present in AD.

show abstract

Section: Discussionmentioning

confidence: 99%

Fibrin deposited in the Alzheimer's disease brain promotes neuronal degeneration

Cortes‐Canteli¹,

Mattei²,

Richards³

et al. 2015

Neurobiology of Aging

143

146

View full text Add to dashboard Cite

show abstract

“…There is also a relationship between the neuro-and cardio-protective effects of wine, given that reducing the risk of atherosclerosis and coronary heart disease also lowers the risk of cognitive impairment [150,151]. Consistent with cardioprotection, an optimal amount of wine for neuro-protection appears to be up to 30 g alcohol daily [152].…”

Section: Discussionmentioning

confidence: 99%

Wine consumption, cognitive function and dementias – A relationship?

Stockley

2016

NUA

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Abstract. Healthy cognitive function is essential for quality of life, wellbeing and independent living, and is negatively associated with dementias. A series of longitudinal and neuro-imaging studies in the elderly have shown that light to moderate wine consumption is neuro-protective although heavy or abusive alcohol consumption is neuro-toxic. A J-shaped relationship between alcohol consumption, cognitive dysfunction and risk of dementias is also observed for younger and middle aged consumers. There is also no data to suggest that long-term light to moderate alcohol consumption exacerbates age-related cognitive decline and impairment. An optimal amount of wine for neuro-protection appears to be up to 30 g alcohol daily.There are multiple plausible biological mechanisms in various animal models, in vitro and in vivo for wine-derived phenolic compounds which go beyond their antioxidant activity and attenuation of oxidative stress.

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“…Interestingly, individuals with high serum fibrinogen have been shown at greater risk of AD (70,71).…”

Section: Page 17 Of 22mentioning

confidence: 99%

Blood-Brain Barrier Disruption Is an Early Event That May Persist for Many Years After Traumatic Brain Injury in Humans

Hay¹,

Johnson²,

Young³

et al. 2015

J Neuropathol Exp Neurol

115

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Traumatic brain injury (TBI) is a risk factor for dementia, with studies describing a mixed neurodegenerative pathology in late survivors. However, the mechanisms driving this post-TBI neurodegeneration remain elusive. Increasingly, blood brain barrier (BBB) disruption is recognized in a range of neurological disorders, including dementias; although little is known of the consequences of TBI on the BBB. From the Glasgow TBI Archive autopsy cases of single, moderate or severe TBI (n=70) were selected to include a range of survivals from acute (10h to 13days) to long-term (1 to 47years) survival, together with age-matched, uninjured controls (n=21). Multiple brain regions were examined for fibrinogen (FBG) and immunoglobulin G (IgG) immunohistochemistry. Following TBI, 40% of patients dying in the acute phase and 47% of those surviving a year or more from injury showed multi-focal, abnormal, perivascular and parenchymal FBG and IgG immunostaining localized to grey matter, with preferential distribution towards the crests of gyri and deep neocortical layers. In contrast, where present, controls showed only limited, localized immunostaining. These preliminary data demonstrate evidence of widespread BBB disruption in a proportion of TBI patients emerging in the acute phase and, intriguingly, persisting in a high proportion of late survivors.

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Plasma fibrinogen is associated with cognitive decline and risk for dementia in patients with mild cognitive impairment

Cited by 69 publications

References 39 publications

Fibrin deposited in the Alzheimer's disease brain promotes neuronal degeneration

Fibrin deposited in the Alzheimer's disease brain promotes neuronal degeneration

Wine consumption, cognitive function and dementias – A relationship?

Blood-Brain Barrier Disruption Is an Early Event That May Persist for Many Years After Traumatic Brain Injury in Humans

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