Cerebral blood flow and vasoreactivity in aging: an arterial spin labeling study

Leoni, Renata Ferranti; Oliveira, Ícaro A.F.; Pontes-Neto, Octávio M.; Santos, Antônio Carlos dos; Leite, João Pereira

doi:10.1590/1414-431x20175670

Cited by 49 publications

(39 citation statements)

References 39 publications

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“…Decreases in phospho-eNOS (necessary for eNOS activation) and phospho-VASP (which undergoes phosphorylation when NO is increased) would impair collateral remodeling during this subacute period, but reduced eNOS could also impair vasodilation and could lead to reduced collateral diameter during acute stroke. This would agree with preclinical and clinical studies in the peripheral and cerebral circulation that suggest impaired vasodilation and vasoreactivity with aging [61][62][63].…”

Section: Discussionsupporting

confidence: 90%

Impaired Collateral Flow in Pial Arterioles of Aged Rats During Ischemic Stroke

Shuaib

et al. 2019

Transl. Stroke Res.

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Cerebral collateral circulation and age are critical factors in determining outcome from acute ischemic stroke. Aging may lead to rarefaction of cerebral collaterals, and thereby accelerate ischemic injury by reducing penumbral blood flow. Dynamic changes in pial collaterals after onset of cerebral ischemia may vary with age but have not been extensively studied. Here, laser speckle contrast imaging (LSCI) and two-photon laser scanning microscopy (TPLSM) were combined to monitor cerebral pial collaterals between the anterior cerebral artery (ACA) and the middle cerebral artery (MCA) in young adult and aged male Sprague Dawley rats during distal middle cerebral artery occlusion (dMCAo). Histological analysis showed that aged rats had significantly greater volumes of ischemic damage than young rats. LSCI showed that cerebral collateral perfusion declined over time after stroke in aged and young rats, and that this decline was significantly greater in aged rats. TPLSM demonstrated that pial arterioles narrowed faster after dMCAo in aged rats compared to young adult rats. Notably, while arteriole vessel narrowing was comparable 4.5 h after ischemic onset in aged and young adult rats, red blood cell velocity was stable in young adults but declined over time in aged rats. Overall, red blood cell flux through pial arterioles was significantly reduced at all time-points after 90 min post-dMCAo in aged rats relative to young adult rats. Thus, collateral failure is more severe in aged rats with significantly impaired pial collateral dynamics (reduced diameter, red blood cell velocity, and red blood cell flux) relative to young adult rats.

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Section: Discussionsupporting

confidence: 90%

Impaired Collateral Flow in Pial Arterioles of Aged Rats During Ischemic Stroke

Shuaib

et al. 2019

Transl. Stroke Res.

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“…Although we found that increasing fitness is related to decreased BOLD CVR in aging, it is difficult to attempt to interpret our results in comparison to other studies due to the high level of variability BOLD CVR in aging literature. For example, other studies report 0.19% BOLD/mmHg in line with our results 75 , yet others report higher levels at 0.28% 76 and lower levels at 0.13% 77 . This indicates that there is physiological variability within individuals and between studies, as well as technical variability (i.e.…”

Section: Limitationssupporting

confidence: 92%

Enhanced fitness relates to reduced cerebrovascular reactivity and perfusion in a sample of very healthy older adults

Intzandt

Sabra

Foster³

et al. 2018

Preprint

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Aging is accompanied by decreased grey matter volume (GMV), cerebral blood flow (CBF), and cerebrovascular reactivity (CVR), where the latter tends to decline the earliest in aging.Enhanced fitness in aging has been related to preservation of GMV and CBF, and in some cases CVR, although there are contradictory relationships reported between CVR and fitness.Therefore, to gain a better understanding of the complex interplay with fitness and GMV, CBF and CVR, it is necessary to study them concurrently. Here, we aimed to disentangle the interactions between these outcomes in healthy older adults. MRI acquisitions collected anatomical, CBF and CVR information in all participants, as well as VO 2 max. Results revealed decreased CVR was associated with increased fitness throughout large areas of the cerebral cortex. Within these regions it was found that lower fitness was associated with higher CBF and a slower hemodynamic response to hypercapnia. Overall, results indicate that the relationship between age, cerebral health and cerebral hemodynamics are complex. Future studies should collect other physiological outcomes in parallel with quantitative imaging, such as measures of carbon dioxide sensitivity and autoregulation, to further understand the intricacy of the effects fitness has on the aging brain, and how this may bias quantitative measures of cerebral health.

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“…For this study, those with the most severe cardiovascular disease (and CBVD) may have been more likely to be excluded due to attrition (e.g., premature death). In this sample, WMH are therefore more likely related to age-related microvascular changes (e.g., arteriosclerosis) [21,81,82] and/or MRI manifestations of ADNP (as discussed above) rather than large vessel pathologies associated with cardiovascular disease. Cause of death would shed further insight into the cardiovascular status, however, such data are not available from the NACC-NDS.…”

Section: Discussionmentioning

confidence: 99%

A Clinicopathological Investigation of White Matter Hyperintensities and Alzheimer’s Disease Neuropathology

Alosco

Sugarman

Besser

et al. 2018

JAD

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Background: White matter hyperintensities (WMH) on magnetic resonance imaging have been postulated to be a core feature of Alzheimer’s disease. Clinicopathological studies are needed to elucidate and confirm this possibility. Objective: This study examined: 1) the association between ante-mortem WMH and autopsy-confirmed Alzheimer’s disease neuropathology (ADNP), 2) the relationship between WMH and dementia in participants with ADNP, and 3) the relationships among cerebrovascular disease, WMH and ADNP. Methods: The sample included 82 participants from the National Alzheimer’s Coordinating Center’s Data Sets who had quantitated volume of WMH from ante-mortem FLAIR MRI and available neuropathological data. The Clinical Dementia Rating (CDR) scale (from MRI visit) operationalized dementia status. ADNP+ was defined by moderate to frequent neuritic plaques and Braak stage III-VI at autopsy. Cerebrovascular disease neuropathology included infarcts or lacunes, microinfarcts, arteriolosclerosis, atherosclerosis, and cerebral amyloid angiopathy. Results: 60/82 participants were ADNP+. Greater volume of WMH predicted increased odds for ADNP (p=0.037). In ADNP+ participants, greater WMH corresponded with increased odds for dementia (CDR≥1; p=0.038). WMH predicted cerebral amyloid angiopathy, microinfarcts, infarcts and lacunes (p’s<0.04). ADNP+ participants were more likely to have moderate-severe arteriolosclerosis and cerebral amyloid angiopathy compared to ADNP− participants (p’s<0.04). Conclusions: This study found a direct association between total volume of WMH and increased odds for having ADNP. In patients with Alzheimer’s disease, FLAIR MRI WMH may be able to provide key insight into disease severity and progression. The association between WMH and ADNP may be explained by underlying cerebrovascular disease.

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Cerebral blood flow and vasoreactivity in aging: an arterial spin labeling study

Cited by 49 publications

References 39 publications

Impaired Collateral Flow in Pial Arterioles of Aged Rats During Ischemic Stroke

Impaired Collateral Flow in Pial Arterioles of Aged Rats During Ischemic Stroke

Enhanced fitness relates to reduced cerebrovascular reactivity and perfusion in a sample of very healthy older adults

A Clinicopathological Investigation of White Matter Hyperintensities and Alzheimer’s Disease Neuropathology

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