Cerebral hypoperfusion yields capillary damage in the hippocampal CA1 area that correlates with spatial memory impairment

Jong, G.I. de; Farkas, Eszter; Stienstra, C.M.; Plass, Jacqueline R. M.; Keijser, Johannes; Torre, Jack C. de la; Luiten, P.G.M.

doi:10.1016/s0306-4522(98)00659-9

Cited by 168 publications

(144 citation statements)

References 30 publications

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“…This interpretation is consistent with data from a study of rats showing a similar correlation between the severity of ultrastructural damage to hippocampus capillaries and performance on the Morris water maze after microvascular damage was induced by chronic occlusion of the common carotid artery (32). Nevertheless, this correlation alone cannot prove that that the observed microvascular changes in hippocampus mediate the cognitive impairment.…”

Section: Hippocampal Capillary Length (Micron)supporting

confidence: 89%

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

140

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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)supporting

confidence: 89%

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

140

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“…In a previous study with rhesus monkeys from the same colony as in the present study, we showed that aging is associated with an increase in aberrations of capillary walls in the CA1 and CA3 regions of the hippocampus [25]. These microvascular aberrations had previously been shown in rats to correlate with cognitive impairments [11], and may deteriorate the passage of oxygen and nutrients to the neuropil, eventually leading to decreased memory performance in rhesus monkeys.…”

Section: Discussionsupporting

confidence: 72%

Preservation of hippocampal neuron numbers in aged rhesus monkeys

Keuker

Luiten

Fuchs

2003

Neurobiology of Aging

122

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Preservation of hippocampal neuron numbers in aged rhesus monkeys Keuker, J.I.H.; Luiten, P.G.M.; Fuchs, E. Take-down policy If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately and investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the number of authors shown on this cover page is limited to 10 maximum. AbstractTo investigate whether or not aging of nonhuman primates is accompanied by a region-specific neuron loss in the hippocampal formation, we used the optical fractionator technique to obtain stereological estimates of unilateral neuron numbers of the hippocampi of eight young (0-4 years) and five aged (18-31 years) male rhesus monkeys (Macaca mulatta). Our results show a preservation of neurons (mean × 10 3 ± S.D. × 10 3 ) in the subiculum (young = 588 ± 124, aged = 612 ± 207), CA1 (young = 1051 ± 249, aged = 1318 ± 311), CA2 (young = 100 ± 18, aged = 113 ± 12), CA3 (young = 478 ± 125, aged = 509 ± 139), hilus (young = 337 ± 115, aged = 394 ± 90), and dentate gyrus (young = 5550 ± 1725, aged = 7799 ± 2087) of the hippocampal formation. These results confirm a previous stereological study in rhesus monkeys, but are in conflict with data for humans, showing age-dependent region-specific alterations in the hippocampal formation.

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“…The CA1 region of the hippocampus results particularly vulnerable to decreased blood flow and glucose supply caused by 2VO occlusion, that cause failure of neuronal signaling, and impairments in hippocampally-based forms of memory (De Jong et al 1999;Liu et al 2005;Farkas et al 2006;Melani et al 2010;Lana et al 2013). It is well known that CA3 and CA1 hippocampal areas, although well interconnected, respond differently to ischemic/hypoxic insults (Kirino 2000).…”

Section: Discussionmentioning

confidence: 99%

The neuron-astrocyte-microglia triad in CA3 after chronic cerebral hypoperfusion in the rat: Protective effect of dipyridamole

Lana

Ugolini

Melani

et al. 2017

Experimental Gerontology

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Cerebral hypoperfusion yields capillary damage in the hippocampal CA1 area that correlates with spatial memory impairment

Cited by 168 publications

References 30 publications

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

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

Preservation of hippocampal neuron numbers in aged rhesus monkeys

The neuron-astrocyte-microglia triad in CA3 after chronic cerebral hypoperfusion in the rat: Protective effect of dipyridamole

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