Microvascular plasticity in aging

Riddle, David R.; Sonntag, William E.; Lichtenwalner, Robin J.

doi:10.1016/s1568-1637(02)00064-8

Cited by 205 publications

(163 citation statements)

References 138 publications

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“…This type of plasticity is reminiscent of the rapid microvascular response to diet in this study, as well as the restoration of normal Glut-1 expression levels following the alleviation of short-term hyperhomocysteinemia in rats (9). Clearly, the extent to which the adult brain retains such microvascular plasticity could affect brain and cognitive integrity during aging (44,45). In this context, our findings raise the intriguing possibility that impaired homocysteine metabolism might impair microvascular plasticity, thereby contributing to the accrual of age-or diseaserelated damage.…”

Section: Hippocampal Capillary Length (Micron)mentioning

confidence: 67%

B-vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice

Troen

Shea‐Budgell²,

Shukitt‐Hale³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

166

133

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In older adults, mildly elevated plasma total homocysteine (hyperhomocysteinemia) is associated with increased risk of cognitive impairment, cerebrovascular disease, and Alzheimer's disease, but it is uncertain whether this is due to underlying metabolic, neurotoxic, or vascular processes. We report here that feeding male C57BL6/J mice a B-vitamin-deficient diet for 10 weeks induced hyperhomocysteinemia, significantly impaired spatial learning and memory, and caused a significant rarefaction of hippocampal microvasculature without concomitant gliosis and neurodegeneration. Total hippocampal capillary length was inversely correlated with Morris water maze escape latencies (r ‫؍‬ ؊0.757, P < 0.001), and with plasma total homocysteine (r ‫؍‬ ؊0.631, P ‫؍‬ 0.007). Feeding mice a methionine-rich diet produced similar but less pronounced effects. Our findings suggest that cerebral microvascular rarefaction can cause cognitive dysfunction in the absence of or preceding neurodegeneration. Similar microvascular changes may mediate the association of hyperhomocysteinemia with human age-related cognitive decline. cerebrovascular ͉ homocysteine ͉ mouse ͉ nutrition

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Section: Hippocampal Capillary Length (Micron)mentioning

confidence: 67%

B-vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice

Troen

Shea‐Budgell²,

Shukitt‐Hale³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

166

133

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“…In order to account for differences in breathing and heart rate across age‐groups, and individuals, we collected both respiratory and cardiac pulse data for all participants and regressed these from participant's functional data. Nonetheless, the possibility of age‐related differences in other non‐neuronal factors, such as vasculature and cerebral blood flow (CBF) (Beason‐Held et al., 2012; Peters, 2006; Riddle, Sonntag, & Lichtenwalner, 2003), may have had an impact. However, a recent study revealed that, although older adults did exhibit reduced CBF in comparison with younger adults, the uptake of oxygen, lactate, and glucose did not differ between the two age‐groups, suggesting that reduced CBF in older adults does not affect the brain's ability to uptake nutrients (Fisher et al., 2013).…”

Section: Discussionmentioning

confidence: 99%

Thalamic functional connectivity and its association with behavioral performance in older age

et al. 2018

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IntroductionDespite the thalamus’ dense connectivity with both cortical and subcortical structures, few studies have specifically investigated how thalamic connectivity changes with age and how such changes are associated with behavior. This study investigated the effect of age on thalamo‐cortical and thalamo‐hippocampal functional connectivity (FC) and the association between thalamic FC and visual–spatial memory and reaction time (RT) performance in older adults.MethodsResting‐state functional magnetic resonance images were obtained from younger (n = 20) and older (n = 20) adults. A seed‐based approach was used to assess the FC between the thalamus and (1) sensory resting‐state networks; (2) the hippocampus. Participants also completed visual–spatial memory and RT tasks, from the Cambridge Neuropsychological Test Automated Battery (CANTAB).ResultsOlder adults exhibited a loss of specificity in the FC between sensory thalamic subregions and corresponding sensory cortex. Greater thalamo‐motor FC in older adults was associated with faster RTs. Furthermore, older adults exhibited greater thalamo‐hippocampal FC compared to younger adults, which was greatest for those with the poorest visual–spatial memory performance.ConclusionAlthough older adults exhibited poorer visual–spatial memory and slower reaction times compared to younger adults, “good” and “poorer” older performers exhibited different patterns of thalamo‐cortical and thalamo‐hippocampal FC. These results highlight the potential role of thalamic connectivity in supporting reaction times and memory in aging. Furthermore, these results highlight the importance of including the thalamus in studies of aging to fully understand how brain changes with age may be associated with behavior.

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“…It is generally considered that cerebromicrovascular rarefaction contributes to a decline in cerebral blood flow (CBF) that reduces metabolic support for neural signaling, thereby promoting neuronal dysfunction (Riddle et al 2003;Sonntag et al 1997;Khan et al 2002;Troen et al 2008). The hippocampus is a key brain region involved in learning and memory, one of the main regions affected in Alzheimer's disease and it is known to be particularly vulnerable to ischemia.…”

Section: Discussionmentioning

confidence: 99%

“…There is substantial evidence that the cerebral microcirculation is subject to continuous dynamic structural adaptation, a concept that implies a high plasticity of the cerebral microvascular network (Riddle et al 2003). Accordingly, there is a dynamic balance between capillary regression and growth, which is regulated by various paracrine factors produced by brain cells.…”

Section: Discussionmentioning

confidence: 99%

“…In the brain, the number of endothelial cells is very similar to that of neurons (GarciaAmado and Prensa 2012) and nearly every neuron is supplied by its own capillary, with an average distance of 8-20 μm between the neuron and the microvessels. Importantly, there is strong evidence that aging is associated with a decline in cerebral capillary density ("microvascular rarefaction") and that decreases in cerebromicrovascular density contribute to the agerelated decline in regional cerebral blood flow (Mitschelen et al 2009;Riddle et al 2003;Khan et al 2001;Lynch et al 1999;Sonntag et al 1997;Martin et al 1991;Moeller et al 1996;Farkas and Luiten 2001;Kawamura et al 1993;Krejza et al 1999;Schultz et al 1999;Bentourkia et al 2000;Hagstadius and Risberg 1989;Pagani et al 2002). The resulting mismatch between energy supply and demand has been causally linked to significant cognitive impairment (reviewed in Sonntag et al 1997;Ingraham et al 2008;Sonntag et al 2000;Warrington et al 2011;Warrington et al 2012).…”

Section: Introductionmentioning

confidence: 99%

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Circulating IGF-1 deficiency exacerbates hypertension-induced microvascular rarefaction in the mouse hippocampus and retrosplenial cortex: implications for cerebromicrovascular and brain aging

Tarantini

Tucsek

Valcarcel‐Ares

et al. 2016

AGE

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Strong epidemiological and experimental evidence indicate that both age and hypertension lead to significant functional and structural impairment of the cerebral microcirculation, predisposing to the development of vascular cognitive impairment (VCI) and Alzheimer's disease. Preclinical studies establish a causal link between cognitive decline and microvascular rarefaction in the hippocampus, an area of brain important for learning and memory. Age-related decline in circulating IGF-1 levels results in functional impairment of the cerebral microvessels; however, the mechanistic role of IGF-1 deficiency in impaired hippocampal microvascularization remains elusive. The present study was designed to characterize the additive/synergistic effects of IGF-1 deficiency and hypertension on microvascular density and expression of genes involved in angiogenesis and microvascular AGE (2016) 38:273-289

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Microvascular plasticity in aging

Cited by 205 publications

References 138 publications

B-vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice

B-vitamin deficiency causes hyperhomocysteinemia and vascular cognitive impairment in mice

Thalamic functional connectivity and its association with behavioral performance in older age

Circulating IGF-1 deficiency exacerbates hypertension-induced microvascular rarefaction in the mouse hippocampus and retrosplenial cortex: implications for cerebromicrovascular and brain aging

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