Abstract
Background and PurposeBoth cerebral hypoperfusion and vascular risk factors have been implicated in early aging of the brain and the development of neurodegenerative disease. However, the current knowledge of the importance of cardiovascular health on resting brain perfusion is limited. The aim of the present study was to elucidate the relation between brain perfusion variability and risk factors of endothelial dysfunction and atherosclerosis in healthy aged subjects.MethodsThirty-eight healthy subjects aged 50–75 years old were included. Mean global brain perfusion was measured using magnetic resonance phase contrast mapping and regional brain perfusion by use of arterial spin labeling.ResultsMean global brain perfusion was inversely correlated with caffeine and hematocrit, and positively with end-tidal PCO2. Furthermore, the mean global brain perfusion was inversely correlated with circulating homocysteine, but not with asymmetric dimethylarginine, dyslipidemia or the carotid intima-media thickness. The relative regional brain perfusion was associated with circulating homocysteine, with a relative parietal hypoperfusion and a frontal hyperperfusion. No effect on regional brain perfusion was observed for any of the other risk factors. A multiple regression model including homocysteine, caffeine, hematocrit and end-tidal PCO2, explained nearly half of the observed variability.ConclusionBoth intrinsic and extrinsic factors influenced global cerebral perfusion variation between subjects. Further, the results suggest that the inverse relation between homocysteine and brain perfusion is owing to other mechanisms, than reflected by asymmetric dimethylarginine, and that homocysteine may be a marker of cerebral perfusion in aging brains.
Highlights
Mounting evidence has suggested an association of vascular and brain health
[3] Among several humoral factors associated with endothelial dysfunction, homocysteine is a well-established risk factor for stroke and dementia and has been associated with structural signs of brain aging. [7,8,9] The effects of homocysteine and of other risk factors have been suggested to be mediated by the endogenous nitric oxide (NO) synthase inhibitor asymmetric dimethylarginine (ADMA), which has been demonstrated as an independent risk factor for vascular disease [10] and structural signs of brain aging.[11]
The effect remained significant after adjustment for age and sex (Table 2), and when adjusted for hematocrit too (21.96 [95% CI: 23.79, 20.14] mL/100 g/min per MMSE score Total cholesterol (mmol/L), p = 0.036)
Summary
Mounting evidence has suggested an association of vascular and brain health. Alzheimer’s disease too shares many risk factors with cerebrovascular disease, an observation that has led to the suggestion that cerebrovascular dysfunction and hypoperfusion may play a role in the pathogenesis of neurodegenerative disorders.[1]. Increased carotid intima-media thickness (IMT), a measure of subclinical atherosclerosis, is associated with impaired endothelial function and has been reported to correlate with structural brain aging, cognitive decline [3,12] and with regional brain perfusion changes.[13] both prior and very recent studies have shown that severe hyperlipidemia may influence cerebrovascular tone by mechanisms unrelated to the proatherogenic properties of hyperlipidemia.[14,15] Both cerebral hypoperfusion and vascular risk factors have been implicated in early aging of the brain and the development of neurodegenerative disease. The aim of the present study was to elucidate the relation between brain perfusion variability and risk factors of endothelial dysfunction and atherosclerosis in healthy aged subjects
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
