Cognition and Hemodynamics

Abstract

The relationship between cerebral hemodynamics and cognitive performance has increasingly become recognized as a major challenge in clinical practice for older adults. Both diabetes and hypertension worsen brain perfusion and are major risk factors for cerebrovascular disease, stroke and dementia. Cerebrovascular reserve has emerged as a potential biomarker for monitoring pressure–perfusion–cognition relationships. Endothelial dysfunction and inflammation, microvascular disease, and mascrovascular disease affect cerebral hemodynamics and play an important role in pathohysiology and severity of multiple medical conditions, presenting as cognitive decline in the old age. Therefore, the identification of cerebrovascular vascular reactivity as a new therapeutic target is needed for prevention of cognitive decline late in life.

Vascular risk factors, cerebrovascular reactivity, and the default-mode brain network

“…Given evidence of the association of mid-life VRF and dementia in late-life (Launer et al, 1995; Launer et al, 2000; Kivipelto et al, 2001; Roberts et al, 2014), potential neurovascular mechanisms of AD (Benarroch, 2007; Novak, 2012), as well as studies suggesting reduced cerebrovascular function in brain regions overlapping the DMN (Claus et al, 1998; Johnson et al, 2005; Dai et al, 2009; Jagust and D'Esposito, 2009), we hypothesized that mean CVR would be lower for regions underlying the DMN, relative to reference brain regions, in those subjects with VRF as opposed to those without. Mean CVR was reduced significantly in different regions of the DMN in subjects with prehypertension/ hypertension when compared with normotensive subjects.…”

“…In addition, cerebrovascular disorders -- e.g., cerebral small vessel disease, white matter lesions, and reduced white matter integrity-- have been linked to reduced brain network functioning that include the default-mode network (DMN) and other networks involved in cognitive control (Damoiseaux and Greicius, 2009; Mayda et al, 2011; Papma et al, 2013). Evidence from epidemiologic studies of VRF in mid-life and risk of dementia in late-life (Launer et al, 1995; Launer et al, 2000; Kivipelto et al, 2001; Roberts et al, 2014), as well as cumulating evidence of neurovascular mechanisms of Alzheimer's disease (AD) (Benarroch, 2007; Novak, 2012) warrants investigation of VRF and brain changes that could represent vascular contributions to AD.…”

“…Typically, CVR has been used to evaluate global brain response (Last et al, 2007; Jagust and D'Esposito, 2009) as well as to measure effects on hemodynamic response in specific vascular territories (Vernieri et al, 1999; Silvestrini et al, 2000; Sorond et al, 2010). However, regional differences in CVR have been observed (Kastrup et al, 1999) and, additionally, CVR has been shown to vary regionally with respect to VRF (Novak, 2012). It is possible that reduced CVR —i.e., representative of lower cerebrovascular function associated with different VRF—may occur in brain regions that underlie the DMN and may affect DMN function.…”

Neuroimaging and its Relevance to Understanding Pathways Linking Diabetes and Cognitive Dysfunction

“…With respect to cerebrovascular physiology, MRI with arterial spin labelling (ASL) (Fig. 1) enables the study of cerebral perfusion [68], which is becoming increasingly recognized as a potential pathway linking vascular risk factors such as diabetes with neurodegeneration [69]. Finally, more recently, direct visualization of cerebral microinfarcts and small deep cerebral vessels with high field imaging (7Tesla MRI) [70] and the measurement of blood-brain barrier permeability (BBB) with dynamic contrast enhancing MRI are becoming possible [71].…”

Metabolic syndrome and cerebrovascular impairment in Alzheimer's disease

“…Hyperglycemia and insulin resistance play a central role in the mechanism of direct and indirect vascular damage, and they are probably among the main causes of reduced CVR in MeS (Novak, 2012;Yates et al, 2012). Hypertension, another MeS element, is characterized by low-grade inflammation and vessel infiltration by macrophages.…”