Articles de revues : « Brain chronic hypoperfusion »

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Quintana, Dominic, Xuefang Ren, Heng Hu, Deborah Corbin, Elizabeth Engler-Chiurazzi, Muhammad Alvi et James Simpkins. « IL-1β Antibody Protects Brain from Neuropathology of Hypoperfusion ». Cells 10, n^o 4 (9 avril 2021) : 855. http://dx.doi.org/10.3390/cells10040855.

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Chronic brain hypoperfusion is the primary cause of vascular dementia and has been implicated in the development of white matter disease and lacunar infarcts. Cerebral hypoperfusion leads to a chronic state of brain inflammation with immune cell activation and production of pro-inflammatory cytokines, including IL-1β. In the present study, we induced chronic, progressive brain hypoperfusion in mice using ameroid constrictor, arterial stenosis (ACAS) surgery and tested the efficacy of an IL-1β antibody on the resulting brain damage. We observed that ACAS surgery causes a reduction in cerebral blood flow (CBF) of about 30% and grey and white matter damage in and around the hippocampus. The IL-1β antibody treatment did not significantly affect CBF but largely eliminated grey matter damage and reduced white matter damage caused by ACAS surgery. Over the course of hypoperfusion/injury, grip strength, coordination, and memory-related behavior were not significantly affected by ACAS surgery or antibody treatment. We conclude that antibody neutralization of IL-1β is protective from the brain damage caused by chronic, progressive brain hypoperfusion.

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Abbott, Noelle T., Carolyn J. Baker, Conan Chen, Thomas T. Liu et Tracy E. Love. « Defining Hypoperfusion in Chronic Aphasia : An Individualized Thresholding Approach ». Brain Sciences 11, n^o 4 (13 avril 2021) : 491. http://dx.doi.org/10.3390/brainsci11040491.

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Within the aphasia literature, it is common to link location of lesioned brain tissue to specific patterns of language impairment. This has provided valuable insight into the relationship between brain structure and function, but it does not capture important underlying alterations in function of regions that remain structurally intact. Research has demonstrated that in the chronic stage of aphasia, variable patterns of reduced cerebral blood flow (CBF; hypoperfusion) in structurally intact regions of the brain contribute to persisting language impairments. However, one consistent issue in this literature is a lack of clear consensus on how to define hypoperfusion, which may lead to over- or underestimation of tissue functionality. In the current study, we conducted an exploratory analysis in six individuals with chronic aphasia (>1 year post-onset) using perfusion imaging to (1) suggest a new, individualized metric for defining hypoperfusion; (2) identify the extent of hypoperfused tissue in perilesional bands; and (3) explore the relationship between hypoperfusion and language impairment. Results indicated that our individualized metric for defining hypoperfusion provided greater precision when identifying functionally impaired tissue and its effects on language function in chronic aphasia. These results have important implications for intervention approaches that target intact (or impaired) brain tissue.

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Ueno, Yuji, Masato Koike, Yoshiaki Shimada, Hideki Shimura, Kenichiro Hira, Ryota Tanaka, Yasuo Uchiyama, Nobutaka Hattori et Takao Urabe. « L-Carnitine Enhances Axonal Plasticity and Improves White-Matter Lesions after Chronic Hypoperfusion in Rat Brain ». Journal of Cerebral Blood Flow & ; Metabolism 35, n^o 3 (mars 2015) : 382–91. http://dx.doi.org/10.1038/jcbfm.2014.210.

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Chronic cerebral hypoperfusion causes white-matter lesions (WMLs) with oxidative stress and cognitive impairment. However, the biologic mechanisms that regulate axonal plasticity under chronic cerebral hypoperfusion have not been fully investigated. Here, we investigated whether L-carnitine, an antioxidant agent, enhances axonal plasticity and oligodendrocyte expression, and explored the signaling pathways that mediate axonal plasticity in a rat chronic hypoperfusion model. Adult male Wistar rats subjected to ligation of the bilateral common carotid arteries (LBCCA) were treated with or without L-carnitine. L-carnitine-treated rats exhibited significantly reduced escape latency in the Morris water maze task at 28 days after chronic hypoperfusion. Western blot analysis indicated that L-carnitine increased levels of phosphorylated high-molecular weight neurofilament (pNFH), concurrent with a reduction in phosphorylated phosphatase tensin homolog deleted on chromosome 10 (PTEN), and increased phosphorylated Akt and mammalian target of rapamycin (mTOR) at 28 days after chronic hypoperfusion. L-carnitine reduced lipid peroxidation and oxidative DNA damage, and enhanced oligodendrocyte marker expression and myelin sheath thickness after chronic hypoperfusion. L-carnitine regulates the PTEN/Akt/mTOR signaling pathway, and enhances axonal plasticity while concurrently ameliorating oxidative stress and increasing oligodendrocyte myelination of axons, thereby improving WMLs and cognitive impairment in a rat chronic hypoperfusion model.

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Miyamoto, Nobukazu, Ryota Tanaka, Hideki Shimura, Terubumi Watanabe, Hideo Mori, Masafumi Onodera, Hideki Mochizuki, Nobutaka Hattori et Takao Urabe. « Phosphodiesterase III Inhibition Promotes Differentiation and Survival of Oligodendrocyte Progenitors and Enhances Regeneration of Ischemic White Matter Lesions in the Adult Mammalian Brain ». Journal of Cerebral Blood Flow & ; Metabolism 30, n^o 2 (14 octobre 2009) : 299–310. http://dx.doi.org/10.1038/jcbfm.2009.210.

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Vascular dementia is caused by blockage of blood supply to the brain, which causes ischemia and subsequent lesions primarily in the white matter, a key characteristic of the disease. In this study, we used a chronic cerebral hypoperfusion rat model to show that the regeneration of white matter damaged by hypoperfusion is enhanced by inhibiting phosphodiesterase III. A rat model of chronic cerebral hypoperfusion was prepared by bilateral common carotid artery ligation. Performance at the Morris water-maze task, immunohistochemistry for bromodeoxyuridine, as well as serial neuronal and glial markers were analyzed until 28 days after hypoperfusion. There was a significant increase in the number of oligodendrocyte progenitor cells in the brains of patients with vascular dementia as well as in rats with cerebral hypoperfusion. The oligodendrocyte progenitor cells subsequently underwent cell death and the number of oligodendrocytes decreased. In the rat model, treatment with a phosphodiesterase III inhibitor prevented cell death, markedly increased the mature oligodendrocytes, and promoted restoration of white matter and recovery of cognitive decline. These effects were cancelled by using protein kinase A/C inhibitor in the phosphodiesterase III inhibitor group. The results of our study indicate that the mammalian brain white matter tissue has the capacity to regenerate after ischemic injury.

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Kusaka, Noboru, Kenji Sugiu, Koji Tokunaga, Atsushi Katsumata, Ayumi Nishida, Katsunari Namba, Hirofumi Hamada, Hiroyuki Nakashima et Isao Date. « Enhanced brain angiogenesis in chronic cerebral hypoperfusion after administration of plasmid human vascular endothelial growth factor in combination with indirect vasoreconstructive surgery ». Journal of Neurosurgery 103, n^o 5 (novembre 2005) : 882–90. http://dx.doi.org/10.3171/jns.2005.103.5.0882.

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Object. Vascular endothelial growth factor (VEGF) is a secreted mitogen associated with angiogenesis. The conceptual basis for therapeutic angiogenesis after plasmid human VEGF gene (phVEGF) transfer has been established in patients presenting with limb ischemia and myocardial infarction. The authors hypothesized that overexpression of VEGF using a gene transfer method combined with indirect vasoreconstruction might induce effective brain angiogenesis in chronic cerebral hypoperfusion, leading to prevention of ischemic attacks. Methods. A chronic cerebral hypoperfusion model induced by permanent ligation of both common carotid arteries in rats was used in this investigation. Seven days after induction of cerebral hypoperfusion, encephalomyosynangiosis (EMS) and phVEGF administration in the temporal muscle were performed. Fourteen days after treatment, the VEGF gene therapy group displayed numbers and areas of capillary vessels in temporal muscles that were 2.2 and 2.5 times greater, respectively, in comparison with the control group. In the brain, the number and area of capillary vessels in the group treated with the VEGF gene were 1.5 and 1.8 times greater, respectively, relative to the control group. Conclusions. In rat models of chronic cerebral hypoperfusion, administration of phVEGF combined with indirect vasoreconstructive surgery significantly increased capillary density in the brain. The authors' results indicate that administration of phVEGF may be an effective therapy in patients with chronic cerebral hypoperfusion, such as those with moyamoya disease.

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Sweet, Julie G., Siu-Lung Chan et Marilyn J. Cipolla. « Effect of hypertension and carotid occlusion on brain parenchymal arteriole structure and reactivity ». Journal of Applied Physiology 119, n^o 7 (1 octobre 2015) : 817–23. http://dx.doi.org/10.1152/japplphysiol.00467.2015.

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We studied the effect of hypertension and chronic hypoperfusion on brain parenchymal arteriole (PA) structure and function. PAs were studied isolated and pressurized from 18-wk-old Wistar-Kyoto (WKY18; n = 8) and spontaneously hypertensive stroke prone (SHRSP18; n = 8) and 5-wk-old prehypertensive (SHRSP5; n = 8) rats. In separate groups, unilateral common carotid artery occlusion (UCCAo) was performed for 4 wk to cause chronic hypoperfusion in 18-wk-old WKY (WKY18-CH; n = 8) and SHRSP (SHRSP18-CH; n = 8). UCCAo caused PAs to have significantly diminished myogenic tone (31 ± 3 vs. 14 ± 6% at 60 mmHg; P < 0.05) and reactivity to pressure from WKY18-CH vs. WKY18 animals. The effect of UCCAo was limited to normotensive animals, as there was little effect of chronic hypoperfusion on vascular reactivity or percent tone in PAs from SHRSP18 vs. SHRSP18-CH animals (53 ± 4 vs. 41 ± 3%; P > 0.05). However, PAs from SHRSP18 and SHRSP5 animals had significantly greater tone compared with WKY18, suggesting an effect of strain and not hypertension per se on PA vasoconstriction. Structurally, PAs from SHRSP18 and SHRSP5 animals had similar sized lumen diameters, but increased wall thickness and distensibility compared with WKY18. Interestingly, chronic hypoperfusion did not affect the structure of PAs from either WKY18-CH or SHRSP18-CH animals. Thus PAs responded to UCCAo with active vasodilation, but not structural remodeling, an effect that was absent in SHRSP. The increased tone of PAs from SHRSP animals, combined with lack of response to chronic hypoperfusion, may contribute to the propensity for ischemic lesions and increased perfusion deficit during hypertension.

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Aliev, Gjumrakch, Joséph Charles Lamanna, Ludis Morales Álvarez, Mark Eric Obrenovich, Gerardo Jesús Pacheco, Hector Palacios, Eldar Qasimov et Brianna Walrafen. « Oxidative stress-induced mitochondrial failure and vasoactive substances as key initiators of pathology favor the reclassification of Alzheimer Disease as a vasocognopathy ». Nova 6, n^o 10 (15 décembre 2008) : 170. http://dx.doi.org/10.22490/24629448.408.

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Alzheimer disease and cerebrovascular accident are two leading causes of age-related dementia. Increasing evidence supports the idea that chronic hypoperfusion is primarily responsible for the pathogenesis that underlies both disease processes. Hypoperfusion is associated with oxidative imbalance, largely due to reactive oxygen species, which is associated with other age-related degenerative disorders. Recent evidence indicates that a chronic injury stimulus induces the hypoperfusion seen in the microcirculation of vulnerable regions of the brain. This leads to energy failure, manifested by damaged mitochondrial ultrastructure. Mitochondrial derangements lead to the formation of a large number of electron-dense, ¿hypoxic¿ mitochondria and cause the overproduction of mitochondrial DNA (mtDNA) deletions, which is most likely due to double stranded breaks. Additionally, these mitochondrial abnormalities coexist with increased redox metal activity, lipid peroxidation, and RNA oxidation, all of which are well established features of Alzheimer disease pathology, prior to the appearance of amyloid b deposition. Alzheimer disease, oxidative stress occurs within various cellular compartments and within certain cell types more than others, namely the vascular endothelium, which is associated with atherosclerotic damage, as well as in pyramidal neurons and glia. Interestingly, these vulnerable cells show mtDNA deletions and oxidative stress markers only in the regions that are closely associated with damaged vessels. This evidence strongly suggests that chronic hypoperfusion induces the accumulation of the oxidative stress products. Furthermore, brain vascular wall lesions linearly correlate with the degree of neuronal and glial cell damage. We, therefore, conclude that chronic hypoperfusion is a key initiator of oxidative stress in various brain parenchymal cells, and the mitochondria appear to be primary targets for brain damage in Alzheimer disease. In this manuscript, we outline a role for the continuous accumulation of oxidative stress products, such as an abundance of nitric oxide products (via the overexpression of inducible and/or neuronal NO synthase (iNOS and nNOS respectively) and peroxynitrite accumulation, as secondary but accelerating factors compromising the blood brain barrier (BBB). If this turns out to be the case, pharmacological interventions that target chronic hypoperfusion might ameliorate the key features of dementing neurodegeneration.

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Kudo, T., M. Takeda, S. Tanimukai et T. Nishimura. « Neuropathologic changes in the gerbil brain after chronic hypoperfusion. » Stroke 24, n^o 2 (février 1993) : 259–64. http://dx.doi.org/10.1161/01.str.24.2.259.

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Shin, Jin Seon, Seung Ye Hyun, Dong Hyun Kim, Seungjoo Lee, Ji Wook Jung, Ji Woong Choi, Kwang Ho Ko, Jong Moon Kim et Jong Hoon Ryu. « Chronic hypoperfusion increases claudin-3 immunoreactivity in rat brain ». Neuroscience Letters 445, n^o 2 (novembre 2008) : 144–48. http://dx.doi.org/10.1016/j.neulet.2008.08.082.

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Kawaguchi, Chikako, Shunya Takizawa, Kiyoshi Niwa, Tokuzen Iwamoto, Ichiro Kuwahira, Hirotaka Kato et Yukito Shinohara. « Regional vulnerability to chronic hypoxia and chronic hypoperfusion in the rat brain ». Pathophysiology 8, n^o 4 (août 2002) : 249–53. http://dx.doi.org/10.1016/s0928-4680(02)00014-7.

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Chuang, Chin-Min, Ching-Liang Hsieh, Tsai-Chung Li et Jaung-Geng Lin. « Acupuncture Stimulation at Baihui Acupoint Reduced Cerebral Infarct and Increased Dopamine Levels in Chronic Cerebral Hypoperfusion and Ischemia-Reperfusion Injured Sprague-Dawley Rats ». American Journal of Chinese Medicine 35, n^o 05 (janvier 2007) : 779–91. http://dx.doi.org/10.1142/s0192415x07005260.

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The Baihui acupoint has three Yang and five convergences; it is needled in order to activate spirit and resuscitate the brain in traditional Chinese medicine. Therefore, the purpose of the present study is to investigate the effect of acupuncture stimulation at the Baihui acupoint on cerebral infarct and dopamine levels. A chronic cerebral hypoperfusion animal model was established by permanent ligation of both common carotid arteries; a cerebral infarct animal model was established by blocking the blood flow of both common carotid arteries and the right middle cerebral artery for 90 min followed by reperfusion in Sprague-Dawly (SD) rats. The Baihui acupoint was stimulated for 20 min 3 days per week for 4 weeks. The cognitive and memory functions were evaluated by measuring the successful rates for rats to negotiate an 8-arm radial maze test; the test was performed after operation once a week for 4 weeks. Finally, the rats were sacrificed and their brains were removed; the dopamine levels in brain tissue were measured and the percentage of right to left hemisphere area was calculated. The results indicated that acupuncture stimulation (AS) did not increase the success rate of performing the 8-arm radial maze in chronic cerebral hypoperfusion and cerebral ischemia-reperfusion injured rat models. AS increased dopamine levels in the right cerebral cortex and hippocampus in the chronic cerebral hypoperfusion rats, and increased dopamine levels of the cerebral cortex in the cerebral ischemia-reperfusion injured rat's models. The neurological deficit score was similar between control and AS groups 24 hours after reperfusion, whereas the AS group comprised of ischemia-reperfusion injured rats had a greater percentage of right to left hemisphere area than the control group. In conclusion, AS at the Baihui acupoint for 4 weeks increased dopamine levels in the brain tissue of chronic cerebral hypoperfusion rats and of cerebral ischemia-reperfusion injured rats. The AS also reduced brain atrophy after cerebral infarct, suggesting that AS at the Baihui acupoint acts as neuroprotector. However, regular stimulation at the Baihui acupoint enhances cognition and memory functions need further study.

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Washida, Kazuo, Yorito Hattori et Masafumi Ihara. « Animal Models of Chronic Cerebral Hypoperfusion : From Mouse to Primate ». International Journal of Molecular Sciences 20, n^o 24 (7 décembre 2019) : 6176. http://dx.doi.org/10.3390/ijms20246176.

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Vascular cognitive impairment (VCI) or vascular dementia occurs as a result of brain ischemia and represents the second most common type of dementia after Alzheimer’s disease. To explore the underlying mechanisms of VCI, several animal models of chronic cerebral hypoperfusion have been developed in rats, mice, and primates. We established a mouse model of chronic cerebral hypoperfusion by narrowing the bilateral common carotid arteries with microcoils, eventually resulting in hippocampal atrophy. In addition, a mouse model of white matter infarct-related damage with cognitive and motor dysfunction has also been established by asymmetric common carotid artery surgery. Although most experiments studying chronic cerebral hypoperfusion have been performed in rodents because of the ease of handling and greater ethical acceptability, non-human primates appear to represent the best model for the study of VCI, due to their similarities in much larger white matter volume and amyloid β depositions like humans. Therefore, we also recently developed a baboon model of VCI through three-vessel occlusion (both the internal carotid arteries and the left vertebral artery). In this review, several animal models of chronic cerebral hypoperfusion, from mouse to primate, are extensively discussed to aid in better understanding of pathophysiology of VCI.

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Wang, Qing-Guang, Xiao Xue, Yang Yang, Peng-Yu Gong, Teng Jiang et Ying-Dong Zhang. « Angiotensin IV suppresses inflammation in the brains of rats with chronic cerebral hypoperfusion ». Journal of the Renin-Angiotensin-Aldosterone System 19, n^o 3 (juillet 2018) : 147032031879958. http://dx.doi.org/10.1177/1470320318799587.

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Introduction: This study aimed to evaluate the influence of central angiotensin IV (Ang IV) infusion on chronic cerebral hypoperfusion (CCH)-related neuropathological changes including amyloid-β (Aβ), hyperphosphorylated tau (p-tau) and the inflammatory response. Materials and methods: Rats with CCH received central infusion of Ang IV, its receptor AT4R antagonist divalinal-Ang IV or artificial cerebrospinal fluid for six weeks. During this procedure, the systolic blood pressure (SBP) was monitored, and the levels of Aβ42, p-tau and pro-inflammatory cytokines in the brain were detected. Results: Rats with CCH exhibited higher levels of Aβ42, p-tau and pro-inflammatory cytokines in the brain when compared with controls. Infusion of Ang IV significantly reduced the expression of pro-inflammatory cytokines in the brains of rats with CCH. Meanwhile, the reduction of pro-inflammatory cytokines levels caused by Ang IV was reversed by divalinal-Ang IV. During the treatment, the SBP in rats was not significantly altered. Conclusion: This study demonstrates for the first time that Ang IV dose-dependently suppresses inflammation through AT4R in the brains of rats with CCH, which is independent from SBP. These findings suggest that Ang IV/AT4R may represent a potential therapeutic target for CCH-related neurological diseases.

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Shcherbak, N. S., M. A. Popovetskiy, G. Yu Yukina et M. M. Galagudza. « Effect of curcumin in the acute phase of ischemia in chronic cerebral hypoperfusion in rats ». Regional blood circulation and microcirculation 17, n^o 1 (30 mars 2018) : 69–73. http://dx.doi.org/10.24884/1682-6655-2018-17-1-69-73.

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Curcumin presents antioxidant and anti-inflammatory properties and can be considered as a neuroprotector. Data on doses and duration of application of curcumin to achieve protective effects in various types of ischemic brain injury is controversial. The purpose was to study the neuroprotective properties of curcumin in the acute phase of ischemia in chronic cerebral hypoperfusion in rats. It is shown that a single application of curcumin (300 mg/kg, i.p.) is not has neuroprotective effect in the acute phase of ischemia in chronic hypoperfusion in Wistar rats. The results allow to conclude that the neuroprotective effect of a single application of curcumin.

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Wang, Xiaodong, Xudong Yang, Fang Han, Ling Gao et Yi Zhou. « Propofol improves brain injury induced by chronic cerebral hypoperfusion in rats ». Food Science & ; Nutrition 9, n^o 6 (5 mai 2021) : 2801–9. http://dx.doi.org/10.1002/fsn3.1915.

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Kurumatani, Takahiro, Takashi Kudo, Yasumitsu Ikura et Masatoshi Takeda. « White Matter Changes in the Gerbil Brain Under Chronic Cerebral Hypoperfusion ». Stroke 29, n^o 5 (mai 1998) : 1058–62. http://dx.doi.org/10.1161/01.str.29.5.1058.

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Zhao, Yang, et Cheng-Xin Gong. « From Chronic Cerebral Hypoperfusion to Alzheimer-Like Brain Pathology and Neurodegeneration ». Cellular and Molecular Neurobiology 35, n^o 1 (29 octobre 2014) : 101–10. http://dx.doi.org/10.1007/s10571-014-0127-9.

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Horsburgh, Karen, Michell M. Reimer, Philip Holland, Guiquan Chen, Gillian Scullion et Jill H. Fowler. « Axon–glial disruption : the link between vascular disease and Alzheimer's disease ? » Biochemical Society Transactions 39, n^o 4 (20 juillet 2011) : 881–85. http://dx.doi.org/10.1042/bst0390881.

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Vascular risk factors play a critical role in the development of cognitive decline and AD (Alzheimer's disease), during aging, and often result in chronic cerebral hypoperfusion. The neurobiological link between hypoperfusion and cognitive decline is not yet defined, but is proposed to involve damage to the brain's white matter. In a newly developed mouse model, hypoperfusion, in isolation, produces a slowly developing and diffuse damage to myelinated axons, which is widespread in the brain, and is associated with a selective impairment in working memory. Cerebral hypoperfusion, an early event in AD, has also been shown to be associated with white matter damage and notably an accumulation of amyloid. The present review highlights some of the published data linking white matter disruption to aging and AD as a result of vascular dysfunction. A model is proposed by which chronic cerebral hypoperfusion, as a result of vascular factors, results in both the generation and accumulation of amyloid and injury to white matter integrity, resulting in cognitive impairment. The generation of amyloid and accumulation in the vasculature may act to perpetuate further vascular dysfunction and accelerate white matter pathology, and as a consequence grey matter pathology and cognitive decline.

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Bi, Xiaochen, Yanfei Feng, Zemin Wu et Jianqiao Fang. « Electroacupuncture Attenuates Cognitive Impairment in Rat Model of Chronic Cerebral Hypoperfusion via miR-137/NOX4 Axis ». Evidence-Based Complementary and Alternative Medicine 2021 (19 avril 2021) : 1–10. http://dx.doi.org/10.1155/2021/8842022.

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Electroacupuncture has shown protective effects on cognitive decline. However, the underlying molecular mechanisms are not clear. The present study was conducted to determine whether the cognitive function was ameliorated in cerebral hypoperfusion rats following electroacupuncture and to investigate the role of miR-137/NOX4 axis. In this study, chronic cerebral hypoperfusion (CCH) model was established by bilateral common carotid artery occlusion. Electroacupuncture treatment attenuated brain injury in CCH model group via regulating miR-137/NOX4 axis. Furthermore, the data of neuronal apoptosis and oxidative stress were observed. Our findings indicated that (1) neuronal apoptosis and oxidative stress in CCH rats were significantly increased compared with control group; (2) the animal cognitive performance was evaluated using the Morris water maze (MWM). The results showed that electroacupuncture therapy ameliorated spatial learning and memory impairment in cerebral hypoperfusion rats; and (3) electroacupuncture therapy reduces neuronal apoptosis and oxidative stress by activating miR-137/NOX4 axis. These results suggest that electroacupuncture therapy for CCH may be mediated by miR-137/NOX4 axis. Electroacupuncture therapy may act as a potential therapeutic approach for chronic cerebral hypoperfusion.

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Tian, Zhengming, Xunming Ji et Jia Liu. « Neuroinflammation in Vascular Cognitive Impairment and Dementia : Current Evidence, Advances, and Prospects ». International Journal of Molecular Sciences 23, n^o 11 (2 juin 2022) : 6224. http://dx.doi.org/10.3390/ijms23116224.

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Vascular cognitive impairment and dementia (VCID) is a major heterogeneous brain disease caused by multiple factors, and it is the second most common type of dementia in the world. It is caused by long-term chronic low perfusion in the whole brain or local brain area, and it eventually develops into severe cognitive dysfunction syndrome. Because of the disease’s ambiguous classification and diagnostic criteria, there is no clear treatment strategy for VCID, and the association between cerebrovascular pathology and cognitive impairment is controversial. Neuroinflammation is an immunological cascade reaction mediated by glial cells in the central nervous system where innate immunity resides. Inflammatory reactions could be triggered by various damaging events, including hypoxia, ischemia, and infection. Long-term chronic hypoperfusion-induced ischemia and hypoxia can overactivate neuroinflammation, causing apoptosis, blood–brain barrier damage and other pathological changes, triggering or aggravating the occurrence and development of VCID. In this review, we will explore the mechanisms of neuroinflammation induced by ischemia and hypoxia caused by chronic hypoperfusion and emphasize the important role of neuroinflammation in the development of VCID from the perspective of immune cells, immune mediators and immune signaling pathways, so as to provide valuable ideas for the prevention and treatment of the disease.

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Salvadores, Natalia, James L. Searcy, Philip R. Holland et Karen Horsburgh. « Chronic cerebral hypoperfusion alters amyloid-β peptide pools leading to cerebral amyloid angiopathy, microinfarcts and haemorrhages in Tg-SwDI mice ». Clinical Science 131, n^o 16 (24 juillet 2017) : 2109–23. http://dx.doi.org/10.1042/cs20170962.

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Cerebral hypoperfusion is an early feature of Alzheimer’s disease (AD) that influences the progression from mild cognitive impairment to dementia. Understanding the mechanism is of critical importance in the search for new effective therapies. We hypothesized that cerebral hypoperfusion promotes the accumulation of amyloid-β (Aβ) and degenerative changes in the brain and is a potential mechanism contributing to development of dementia. To address this, we studied the effects of chronic cerebral hypoperfusion induced by bilateral carotid artery stenosis on Aβ peptide pools in a transgenic mouse model of AD (transgenic mice with Swedish, Dutch and Iowa mutations in human amyloid precursor protein (APP) (Tg-SwDI)). Cerebrovascular integrity was characterized by quantifying the occurrence of microinfarcts and haemorrhages and compared with wild-type mice without Aβ. A significant increase in soluble Aβ peptides (Aβ40/42) was detected after 1 month of hypoperfusion in the parenchyma in parallel with elevated APP and APP proteolytic products. Following 3 months, a significant increase in insoluble Aβ40/42 was determined in the parenchyma and vasculature. Microinfarct load was significantly increased in the Tg-SwDI as compared with wild-type mice and further exacerbated by hypoperfusion at 1 and 3 months. In addition, the number of Tg-SwDI hypoperfused mice with haemorrhages was increased compared with hypoperfused wild-type mice. Soluble parenchymal Aβ was associated with elevated NADPH oxidase-2 (NOX2) which was exacerbated by 1-month hypoperfusion. We suggest that in response to hypoperfusion, increased Aβ production/deposition may contribute to degenerative processes by triggering oxidative stress promoting cerebrovascular disruption and the development of microinfarcts.

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Pinçon, Anthony, Olivia De Montgolfier, Nilay Akkoyunlu, Caroline Daneault, Philippe Pouliot, Louis Villeneuve, Frédéric Lesage et al. « Non-Alcoholic Fatty Liver Disease, and the Underlying Altered Fatty Acid Metabolism, Reveals Brain Hypoperfusion and Contributes to the Cognitive Decline in APP/PS1 Mice ». Metabolites 9, n^o 5 (25 mai 2019) : 104. http://dx.doi.org/10.3390/metabo9050104.

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Non-alcoholic fatty liver disease (NAFLD), the leading cause of chronic liver disease, is associated with cognitive decline in middle-aged adults, but the mechanisms underlying this association are not clear. We hypothesized that NAFLD would unveil the appearance of brain hypoperfusion in association with altered plasma and brain lipid metabolism. To test our hypothesis, amyloid precursor protein/presenilin-1 (APP/PS1) transgenic mice were fed a standard diet or a high-fat, cholesterol and cholate diet, inducing NAFLD without obesity and hyperglycemia. The diet-induced NAFLD disturbed monounsaturated and polyunsaturated fatty acid (MUFAs, PUFAs) metabolism in the plasma, liver, and brain, and particularly reduced n-3 PUFAs levels. These alterations in lipid homeostasis were associated in the brain with an increased expression of Tnfα, Cox2, p21, and Nox2, reminiscent of brain inflammation, senescence, and oxidative stress. In addition, compared to wild-type (WT) mice, while brain perfusion was similar in APP/PS1 mice fed with a chow diet, NAFLD in APP/PS1 mice reveals cerebral hypoperfusion and furthered cognitive decline. NAFLD reduced plasma β40- and β42-amyloid levels and altered hepatic but not brain expression of genes involved in β-amyloid peptide production and clearance. Altogether, our results suggest that in a mouse model of Alzheimer disease (AD) diet-induced NAFLD contributes to the development and progression of brain abnormalities through unbalanced brain MUFAs and PUFAs metabolism and cerebral hypoperfusion, irrespective of brain amyloid pathology that may ultimately contribute to the pathogenesis of AD.

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Morgan, Michael K., et Thoralf M. Sundt. « The Case Against Staged Operative Resection of Cerebral Arteriovenous Malformations ». Neurosurgery 25, n^o 3 (1 septembre 1989) : 429–36. http://dx.doi.org/10.1227/00006123-198909000-00018.

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Abstract Three cases of large cerebral arteriovenous fistulae are presented in which surgical ablation was complicated by brain swelling from hyperperfusion breakthrough believed to be caused by acute intraoperative hypoperfusion superimposed on chronic preoperative hypoperfusion. On the basis of these cases, experimental data, and theoretical considerations, we seriously question the wisdom of using staged surgical resection of cerebral arteriovenous malformation to prevent complications related to alterations in cerebral hemodynamics. The reasons for this concern are: the repeated occurrence of acute-on-chronic hypoperfusion during staged resection; a lack of understanding of the time course for the correction of a disordered autoregulation; risk of hemorrhage between the initial and final resection; difficulty in assessing and substantiating flow reduction after subtotal resection; the rapidity of collateralization; the divergence of flow from large, readily accessible feeding arteries to deep penetrating vessels; and attenuation of the wall thickness in collateral vessels as a consequence of increased flow.

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Márquez-Martín, Ana, Francesc Jiménez-Altayó, Ana P. Dantas, Laura Caracuel, Anna M. Planas et Elisabet Vila. « Middle cerebral artery alterations in a rat chronic hypoperfusion model ». Journal of Applied Physiology 112, n^o 3 (1 février 2012) : 511–18. http://dx.doi.org/10.1152/japplphysiol.00998.2011.

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Chronic cerebral hypoperfusion (CHP) induces microvascular changes that could contribute to the progression of vascular cognitive impairment and dementia in the aging brain. This study aimed to analyze the effects of CHP on structural, mechanical, and myogenic properties of the middle cerebral artery (MCA) after bilateral common carotid artery occlusion (BCCAO) in adult male Wistar rats. Sham animals underwent a similar surgical procedure without carotid artery (CA) ligation. After 15 days of occlusion, MCA and CA were dissected and MCA structural, mechanical, and myogenic properties were assessed by pressure myography. Collagen I/III expression was determined by immunofluorescence in MCA and CA and by Western blot in CA. mRNA levels for 1A1, 1A2, and 3A1 collagen subunits were quantified by quantitative real-time PCR in CA. Matrix metalloproteinase (MMP-1, MMP-2, MMP-9, and MMP-13) and hypoxia-inducible factor-1α (HIF-1α) protein expression were determined in CA by Western blot. BCCAO diminished cross-sectional area, wall thickness, and wall-to-lumen ratio. Nevertheless, whereas wall stress was increased, stiffness was not modified and myogenic response was diminished. Hypoperfusion triggered HIF-1α expression. Collagen I/III protein expression diminished in MCA and CA after BCCAO, despite increased mRNA levels for 1A1 and 3A1 collagen subunits. Therefore, the reduced collagen expression might be due to proteolytic degradation, since the expression of MMP-1 and MMP-9 increased in the CA. These data suggest that BCCAO induces hypotrophic remodeling by a mechanism that involves a reduction of collagen I/III in association with increased MMP-1 and MMP-9 and that decreases myogenic tone in major arteries supplying the brain.

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He, Xiao-Li, Yue-Hua Wang, Mei Gao, Xiao-Xiu Li, Tian-Tai Zhang et Guan-Hua Du. « Baicalein protects rat brain mitochondria against chronic cerebral hypoperfusion-induced oxidative damage ». Brain Research 1249 (janvier 2009) : 212–21. http://dx.doi.org/10.1016/j.brainres.2008.10.005.

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Chen, Xingyong, Nannan Yao, Zejing Lin et Yinzhou Wang. « Inhibition of the Immunoproteasome Subunit LMP7 Ameliorates Cerebral White Matter Demyelination Possibly via TGFβ/Smad Signaling ». Evidence-Based Complementary and Alternative Medicine 2021 (12 octobre 2021) : 1–12. http://dx.doi.org/10.1155/2021/6426225.

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Objectives. Chronic cerebral hypoperfusion induces white matter ischemic injury and cognitive impairment, whereas the mechanism remains unclear. Immunoproteasomes have been implicated in the pathogenesis of acute ischemia stroke and multiple sclerosis. However, the expression and role of immunoproteasomes in the brain of chronic cerebral hypoperfusion remain to be clarified. Methods. Chronic white matter ischemic injury mice models were induced by bilateral carotid artery stenosis (BCAS). A selective immunoproteasome subunit low-molecular-mass peptide-7 (LMP7) inhibitor PR957 was administered to mice. Cognitive function, white matter integrity, and potential pathways were assessed after BCAS. Results. The present study found that chronic cerebral hypoperfusion following BCAS induced cerebral white matter demyelination and cognitive impairment, accompanied with elevated expression of the immunoproteasomes LMP2 and LMP7, activation of astrocytes and microglia, and increased production of inflammatory cytokines (e.g., interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), IL-10, transforming growth factor-β1 (TGFβ1), and insulin-like growth factor-1 (IGF-1)). However, inhibition of LMP7 with the specific proteasome inhibitor PR957 significantly mitigated the histological damage of the white matter, suppressed inflammatory response, and paralleled by an improvement of cognitive function. Furthermore, treatment of PR957 significantly upregulated the level of TGFβ1, the total expression level, and the phosphorylation level of Smad2/3 and promoted brain remyelination. Surprisingly, PR957 alone had no effects on the neuroinflammation response and the activation of TGFβ/Smad signaling in the sham-operated (BCAS-nonoperated) mice. Conclusions. The possible mechanism underlying this was attributed to that the immunoproteasome regulates TGFβ/Smad signaling-mediated neuroinflammation and oligodendrocyte remyelination.

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Kihira, Shingo, Clara Koo, Kambiz Nael et Puneet Belani. « Regional Parieto-occipital Hypoperfusion on Arterial Spin Labeling Associates with Major Depressive Disorder ». Open Neuroimaging Journal 13, n^o 1 (25 novembre 2020) : 30–36. http://dx.doi.org/10.2174/1874440002013010030.

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Background: Reduced cerebral blood flow in parieto-occipital regions has been reported in neurodegenerative disorders using ASL. We aimed to investigate neuropsychiatric and neurodegenerative comorbidities that may associate with parieto-occipital region hypoperfusion. Methods: This was a retrospective single-center study. Between March 2017 to May 2018, adult patients who underwent brain MRI with the inclusion of ASL perfusion and who had bilateral reductions of CBF in the parieto-occipital regions were included. ASL was performed using a pseudo-continuous arterial spin labeling (pCASL) technique on 1.5T MR system. Age and gender-matched patients with no perfusion defect were concurrently collected. Comorbidity data was collected from EMR, including major depressive disorder, Alzheimer’s disease, Parkinson’s disease, Schizophrenia, anxiety disorder, hypertension, diabetes mellitus type II, coronary artery disease, and chronic kidney disease. A Pearson’s Chi-Square test was performed to assess for comorbidities associated with hypoperfusion of the parieto-occipital lobes. Results: Our patient cohort consisted of 93 patients with bilateral hypoperfusion in the parieto-occipital lobes and 93 age and gender-matched patients without corresponding perfusion defects based on ASL-CBF. Among the comorbidities assessed, there was a statistically significant association between hypoperfusion of the parieto-occipital lobes and major depressive disorder (p=0.004) and Parkinson’s disease (p=0.044). There was no statistically significant association for Alzheimer’s disease, generalized anxiety disorder, diabetes mellitus type II, hypertension, coronary artery disease, or chronic kidney disease. Conclusion: Major depressive disorder may be linked to regional parieto-occipital hypoperfusion on ASL.

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Shin, Jung-Won, Ki-Jung Kweon, Dong-Kyu Kim, Pyungsoo Kim, Tae-Dong Jeon, Sungho Maeng et Nak-Won Sohn. « Scutellarin Ameliorates Learning and Memory Deficit via Suppressing β-Amyloid Formation and Microglial Activation in Rats with Chronic Cerebral Hypoperfusion ». American Journal of Chinese Medicine 46, n^o 06 (janvier 2018) : 1203–23. http://dx.doi.org/10.1142/s0192415x18500635.

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Chronic cerebral hypoperfusion is considered as a pivotal factor of cognitive impairment that occurs in cerebrovascular diseases. This study investigated the ameliorating effect of scutellarin (SCT) on spatial cognitive impairment and [Formula: see text]-amyloid (A[Formula: see text]) formation in rats with chronic cerebral hypoperfusion induced by permanent bilateral common carotid artery occlusion (pBCAO). SCT is a flavonoid in medicinal herb of Erigeron breviscapus (vant.) Hand. Mazz. known to have neuroprotective, antioxidative and anti-inflammatory effects. However, the beneficial effect and pivotal mechanism of SCT on cognitive impairment are still unclear. SCT was treated orally with two doses (10 or 30[Formula: see text]mg/kg) for 4 weeks. Results of Morris water maze test performed on the ninth week after pBCAO revealed that SCT (30[Formula: see text]mg/kg)-treated rats had significantly shortened escape latencies in acquisition training trials, significantly prolonged swimming time at the platform and its surrounding zone, significant increase in memory score, significant reduction in the number of target heading, and significant reduction in the time required for the first target heading during the retention trial compared to rats in the sham-control group. SCT significantly inhibited the production of A[Formula: see text] and A[Formula: see text] in brain tissues. However, SCT significantly upregulated the expression levels of amyloid precursor protein and [Formula: see text]-site APP-converting enzyme-1 in the hippocampus. In addition, SCT significantly inhibited the activation of Iba1-expressing microglia in brain tissues. The results suggest that SCT can exert ameliorating effect on spatial cognitive impairment caused by chronic cerebral hypoperfusion through suppressing A[Formula: see text] formation and microglial activation in brain tissues. Therefore, SCT can be used as a beneficial drug for vascular dementia and Alzheimer’s disease.

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Kašparová, Svatava, Vlasta Brezová, Marián Valko, Jaromír Horecký, Vladimír Mlynárik, Tibor Liptaj, Ol’ga Vančová, Ol’ga Uličná et Dušan Dobrota. « Study of the oxidative stress in a rat model of chronic brain hypoperfusion ». Neurochemistry International 46, n^o 8 (juin 2005) : 601–11. http://dx.doi.org/10.1016/j.neuint.2005.02.006.

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Wu, Xiangmei, Jing Sun et Liang Li. « Chronic cerebrovascular hypoperfusion affects global DNA methylation and histone acetylation in rat brain ». Neuroscience Bulletin 29, n^o 6 (28 mai 2013) : 685–92. http://dx.doi.org/10.1007/s12264-013-1345-8.

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Liu, Jing, Dao-Zhong Jin, Liang Xiao et Xing-Zu Zhu. « Paeoniflorin attenuates chronic cerebral hypoperfusion-induced learning dysfunction and brain damage in rats ». Brain Research 1089, n^o 1 (mai 2006) : 162–70. http://dx.doi.org/10.1016/j.brainres.2006.02.115.

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Ihara, Masafumi, Hidekazu Tomimoto, Makoto Kinoshita, Junseo Oh, Makoto Noda, Hideaki Wakita, Ichiro Akiguchi et Hiroshi Shibasaki. « Chronic Cerebral Hypoperfusion Induces MMP-2 but Not MMP-9 Expression in the Microglia and Vascular Endothelium of White Matter ». Journal of Cerebral Blood Flow & ; Metabolism 21, n^o 7 (juillet 2001) : 828–34. http://dx.doi.org/10.1097/00004647-200107000-00008.

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White matter lesions are closely associated with cognitive impairment and motor dysfunction in the aged. To explore the pathophysiology of these lesions, the authors examined the expression of matrix metalloproteinase-2 (MMP-2) and MMP-9 in the white matter in a rat model of chronic cerebral hypoperfusion. After bilateral clipping of the common carotid arteries, myelin staining revealed demyelinating changes in the optic tract and the corpus callosum on day 7. Zymographic analyses indicated an increase in the level of MMP-2, but not MMP-9, after the hypoperfusion. Immunohistochemical analyses revealed the presence (most abundantly on day 3) of MMP-2–expressing activated microglia in the optic tract and corpus callosum. In contrast, the capillary endothelial cells expressed MMP-2 later. IgM-immunoreactive glial cells were absent in the sham-operated animals, but were present in the hypoperfused animals by day 3, reflecting the disrupted blood–brain barrier. These findings suggest that the main sources of the elevated MMP-2 were the microglia and the endothelium, and that these cells may contribute to the remodeling of the white matter myelin and microvascular beds in chronic cerebral hypoperfusion.

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Hai, Jian, Meixiu Ding, Zhilin Guo et Bingyu Wang. « A new rat model of chronic cerebral hypoperfusion associated with arteriovenous malformations ». Journal of Neurosurgery 97, n^o 5 (novembre 2002) : 1198–202. http://dx.doi.org/10.3171/jns.2002.97.5.1198.

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Object. A new experimental model of chronic cerebral hypoperfusion was developed to study the effects of systemic arterial shunting and obstruction of the primary vessel that drains intracranial venous blood on cerebral perfusion pressure (CPP), as well as cerebral pathological changes during restoration of normal perfusion pressure. Methods. Twenty-four Sprague—Dawley rats were randomly assigned to either a sham-operated group, an arteriovenous fistula (AVF) group, or a model group (eight rats each). The animal model was readied by creating a fistula through an end-to-side anastomosis between the right distal external jugular vein (EJV) and the ispilateral common carotid artery (CCA), followed by ligation of the left vein draining the transverse sinus and bilateral external carotid arteries. Systemic mean arterial pressure (MAP), draining vein pressure (DVP), and CPP were monitored and compared among the three groups preoperatively, immediately postoperatively, and again 90 days later. Following occlusion of the fistula after a 90-day interval, blood—brain barrier (BBB) disruption and water content in the right cortical tissues of the middle cerebral artery territory were confirmed and also quantified with transmission electron microscopy. Formation of a fistula resulted in significant decreases in MAP and CPP, and a significant increase in DVP in the AVF and model groups. Ninety days later, there were still significant increases in DVP and decreases in CPP in the model group compared with the other groups (p < 0.05). Damage to the BBB and brain edema were noted in animals in the model group during restoration of normal perfusion pressure by occlusion of the fistula. Electron microscopy studies revealed cerebral vasogenic edema and/or hemorrhage in various amounts, which correlated with absent astrocytic foot processes surrounding some cerebral capillaries. Conclusions. The results demonstrated that an end-to-side anastomosis between the distal EJV and CCA can induce a decrease in CPP, whereas a further chronic state of cerebral hypoperfusion may be caused by venous outflow restriction, which is associated with perfusion pressure breakthrough. This animal model conforms to the basic hemodynamic characteristics of human cerebral arteriovenous malformations.

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Rajeev, Vismitha, David Y. Fann, Quynh Nhu Dinh, Hyun Ah Kim, T. Michael De Silva, Mitchell K. P. Lai, Christopher Li-Hsian Chen, Grant R. Drummond, Christopher G. Sobey et Thiruma V. Arumugam. « Pathophysiology of blood brain barrier dysfunction during chronic cerebral hypoperfusion in vascular cognitive impairment ». Theranostics 12, n^o 4 (2022) : 1639–58. http://dx.doi.org/10.7150/thno.68304.

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Chen, Xin, Xue-Mei Jiang, Lin-Jing Zhao, Lin-Lin Sun, Mei-Ling Yan, You Tian, Shuai Zhang et al. « MicroRNA-195 prevents dendritic degeneration and neuron death in rats following chronic brain hypoperfusion ». Cell Death & ; Disease 8, n^o 6 (juin 2017) : e2850-e2850. http://dx.doi.org/10.1038/cddis.2017.243.

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Takahashi, Y., H. Wakita, K. Mizutani, S. Sonoda et H. Tomimoto. « Spatial and temporal distribution of adiponectin in the rat brain under chronic cerebral hypoperfusion ». Journal of the Neurological Sciences 381 (octobre 2017) : 1102. http://dx.doi.org/10.1016/j.jns.2017.08.3112.

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Feng, Zhanbo, Yapeng Lu, Xiaomei Wu, Peng Zhao, Jiejia Li, Bin Peng, Zhongming Qian et Li Zhu. « Ligustilide alleviates brain damage and improves cognitive function in rats of chronic cerebral hypoperfusion ». Journal of Ethnopharmacology 144, n^o 2 (novembre 2012) : 313–21. http://dx.doi.org/10.1016/j.jep.2012.09.014.

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Rodriguez-Perez, Ana I., Antonio Dominguez-Meijide, Jose L. Lanciego, Maria J. Guerra et Jose L. Labandeira-Garcia. « Dopaminergic degeneration is enhanced by chronic brain hypoperfusion and inhibited by angiotensin receptor blockage ». AGE 35, n^o 5 (18 septembre 2012) : 1675–90. http://dx.doi.org/10.1007/s11357-012-9470-2.

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He, Xiao-Li, Yue-Hua Wang, Ming-Gang Bi et Guan-Hua Du. « Chrysin improves cognitive deficits and brain damage induced by chronic cerebral hypoperfusion in rats ». European Journal of Pharmacology 680, n^o 1-3 (avril 2012) : 41–48. http://dx.doi.org/10.1016/j.ejphar.2012.01.025.

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Tang, Li, et Yu Li. « Effects of Plant Compound Curcumin on Learning and Memory of Chronic Cerebral Hypoperfusion Rats ». Advanced Materials Research 1120-1121 (juillet 2015) : 853–56. http://dx.doi.org/10.4028/www.scientific.net/amr.1120-1121.853.

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Vascular dementia (VD) is the cognitive impairment clinical syndrome caused by various cerebrovascular diseases. At present the exact causes of VD are not clear, it is believed that ischemic cerebral vascular disease is one of the factors. Hypertension, hyperlipidemia, diabetes, tobacco and alcohol addiction are risk factors of VD. Most of them can be traced back to the youth. Curcumin has a neuroprotective effect in Alzheimer’s disease (AD) and other neurodegenerative diseases. But the effect of curcumin on brain injury caused by chronic cerebral hypoperfusion was unclear. In this study, chronic cerebral ischemia model was used to investigate the effect of curcumin on learning and memory ability of young and aged rats and to explore the mechanism of neuroprotective effect of Curcumin. The result showed that Curcumin can reduce the brain damage both in young and aged VD rats and improve learning and memory ability, and the effect was dose-dependent, without age difference. The pathological injury of the hippocampus might be one of the mechanisms of curcumin improving cognitive impairment of VD rats.

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Füchtemeier, Martina, Marie P. Brinckmann, Marco Foddis, Alexander Kunz, Chrystelle Po, Caterina Curato, Ulrich Dirnagl et Tracy D. Farr. « Vascular Change and Opposing Effects of the Angiotensin Type 2 Receptor in a Mouse Model of Vascular Cognitive Impairment ». Journal of Cerebral Blood Flow & ; Metabolism 35, n^o 3 (mars 2015) : 476–84. http://dx.doi.org/10.1038/jcbfm.2014.221.

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Our aims were to assess the spatiotemporal development of brain pathology in a mouse model of chronic hypoperfusion using magnetic resonance imaging (MRI), and to test whether the renin-angiotensin system (RAS) can offer therapeutic benefit. For the first time, different patterns of cerebral blood flow alterations were observed in hypoperfused mice that ranged from an immediate and dramatic to a delayed decrease in cerebral perfusion. Diffusion tensor imaging revealed increases in several quantitative parameters in different brain regions that are indicative of white-matter degeneration; this began around 3 weeks after induction of hypoperfusion. While this model may be more variable than previously reported, neuroimaging tools represent a promising way to identify surrogate markers of pathology. Vascular remodelling was observed in hypoperfused mice, particularly in the anterior part of the Circle of Willis. While the angiotensin II receptor type 2 agonist, Compound 21 (C21), did not influence this response, it did promote expansion of the basilar artery in microcoil animals. Furthermore, C21-treated animals exhibited increased brain lymphocyte infiltration, and importantly, C21 had opposing effects on spatial reference memory in hypoperfused and sham mice. These results suggest that the RAS may have a role in vascular cognitive impairment.

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de la Torre, Jack C. « Deciphering Alzheimer’s Disease Pathogenic Pathway : Role of Chronic Brain Hypoperfusion on p-Tau and mTOR ». Journal of Alzheimer's Disease 79, n^o 4 (16 février 2021) : 1381–96. http://dx.doi.org/10.3233/jad-201165.

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This review examines new biomolecular findings that lend support to the hemodynamic role played by chronic brain hypoperfusion (CBH) in driving a pathway to Alzheimer’s disease (AD). CBH is a common clinical feature of AD and the current topic of intense investigation in AD models. CBH is also the basis for the vascular hypothesis of AD which we originally proposed in 1993. New biomolecular findings reveal the interplay of CBH in increasing tau phosphorylation (p-Tau) in the hippocampus and cortex of AD mice, damaging fast axonal transport, increasing signaling of mammalian target of rapamycin (mTOR), impairing learning-memory function, and promoting the formation of neurofibrillary tangles, a neuropathologic hallmark of AD. These pathologic elements have been singularly linked with neurodegeneration and AD but their abnormal, collective participation during brain aging have not been fully examined. The format for this review will provide a consolidated analysis of each pathologic phase contributing to cognitive decline and AD onset, summarized in nine chronological steps. These steps galvanize each factor’s active participation and contribution in constructing a biomolecular pathway to AD onset generated by CBH.

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Yao, Zhao-Hui, Xiao-li Yao, Shao-feng Zhang, Ji-chang Hu et Yong Zhang. « Tripchlorolide May Improve Spatial Cognition Dysfunction and Synaptic Plasticity after Chronic Cerebral Hypoperfusion ». Neural Plasticity 2019 (24 février 2019) : 1–14. http://dx.doi.org/10.1155/2019/2158285.

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Chronic cerebral hypoperfusion (CCH) is a common pathophysiological mechanism that underlies cognitive decline and degenerative processes in dementia and other neurodegenerative diseases. Low cerebral blood flow (CBF) during CCH leads to disturbances in the homeostasis of hemodynamics and energy metabolism, which in turn results in oxidative stress, astroglia overactivation, and synaptic protein downregulation. These events contribute to synaptic plasticity and cognitive dysfunction after CCH. Tripchlorolide (TRC) is an herbal compound with potent neuroprotective effects. The potential of TRC to improve CCH-induced cognitive impairment has not yet been determined. In the current study, we employed behavioral techniques, electrophysiology, Western blotting, immunofluorescence, and Golgi staining to investigate the effect of TRC on spatial learning and memory impairment and on synaptic plasticity changes in rats after CCH. Our findings showed that TRC could rescue CCH-induced spatial learning and memory dysfunction and improve long-term potentiation (LTP) disorders. We also found that TRC could prevent CCH-induced reductions in N-methyl-D-aspartic acid receptor 2B, synapsin I, and postsynaptic density protein 95 levels. Moreover, TRC upregulated cAMP-response element binding protein, which is an important transcription factor for synaptic proteins. TRC also prevented the reduction in dendritic spine density that is caused by CCH. However, sham rats treated with TRC did not show any improvement in cognition. Because CCH causes disturbances in brain energy homeostasis, TRC therapy may resolve this instability by correcting a variety of cognitive-related signaling pathways. However, for the normal brain, TRC treatment led to neither disturbance nor improvement in neural plasticity. Additionally, this treatment neither impaired nor further improved cognition. In conclusion, we found that TRC can improve spatial learning and memory, enhance synaptic plasticity, upregulate the expression of some synaptic proteins, and increase the density of dendritic spines. Our findings suggest that TRC may be beneficial in the treatment of cognitive impairment induced by CCH.

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de la Torre, Jack C. « Cardiovascular Risk Factors Promote Brain Hypoperfusion Leading to Cognitive Decline and Dementia ». Cardiovascular Psychiatry and Neurology 2012 (3 décembre 2012) : 1–15. http://dx.doi.org/10.1155/2012/367516.

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Heart disease is the major leading cause of death and disability in the world. Mainly affecting the elderly population, heart disease and its main outcome, cardiovascular disease, have become an important risk factor in the development of cognitive decline and Alzheimer’s disease (AD). This paper examines the evidence linking chronic brain hypoperfusion induced by a variety of cardiovascular deficits in the development of cognitive impairment preceding AD. The evidence indicates a strong association between AD and cardiovascular risk factors, including ApoE4, atrial fibrillation, thrombotic events, hypertension, hypotension, heart failure, high serum markers of inflammation, coronary artery disease, low cardiac index, and valvular pathology. In elderly people whose cerebral perfusion is already diminished by their advanced age, additional reduction of cerebral blood flow stemming from abnormalities in the heart-brain vascular loop ostensibly increases the probability of developing AD. Evidence also suggests that a neuronal energy crisis brought on by relentless brain hypoperfusion may be responsible for protein synthesis abnormalities that later result in the classic neurodegenerative lesions involving the formation of amyloid-beta plaques and neurofibrillary tangles. Insight into how cardiovascular risk factors can induce progressive cognitive impairment offers an enhanced understanding of the multifactorial pathophysiology characterizing AD and ways at preventing or managing the cardiovascular precursors of this dementia.

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Ihara, Masafumi, et Hidekazu Tomimoto. « Lessons from a Mouse Model Characterizing Features of Vascular Cognitive Impairment with White Matter Changes ». Journal of Aging Research 2011 (2011) : 1–11. http://dx.doi.org/10.4061/2011/978761.

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With the demographic shift in age in advanced countries inexorably set to progress in the 21st century, dementia will become one of the most important health problems worldwide. Vascular cognitive impairment is the second most common type of dementia after Alzheimer's disease and is frequently responsible for the cognitive decline of the elderly. It is characterized by cerebrovascular white matter changes; thus, in order to investigate the underlying mechanisms involved in white matter changes, a mouse model of chronic cerebral hypoperfusion has been developed, which involves the narrowing of the bilateral common carotid arteries with newly designed microcoils. The purpose of this paper is to provide a comprehensive summary of the achievements made with the model that shows good reproducibility of the white matter changes characterized by blood-brain barrier disruption, glial activation, oxidative stress, and oligodendrocyte loss following chronic cerebral hypoperfusion. Detailed characterization of this model may help to decipher the substrates associated with impaired memory and move toward a more integrated therapy of vascular cognitive impairment.

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Ueno, Masaki, Hidekazu Tomimoto, Ichiro Akiguchi, Hideaki Wakita et Haruhiko Sakamoto. « Blood–Brain Barrier Disruption in White Matter Lesions in a Rat Model of Chronic Cerebral Hypoperfusion ». Journal of Cerebral Blood Flow & ; Metabolism 22, n^o 1 (janvier 2002) : 97–104. http://dx.doi.org/10.1097/00004647-200201000-00012.

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Blood–brain barrier damage has been implicated in the pathogenesis of cerebrovascular white matter lesions. This type of lesion is responsible for cognitive impairment in the elderly and can be induced by permanent ligation of the bilateral common carotid arteries in the rat. Because it is unclear whether the blood–brain barrier is impaired, we examined whether vascular permeability to horseradish peroxidase is altered using this model. According to light microscopic results, the reaction product of horseradish peroxidase was most intensely localized to the paramedian part of the corpus callosum in the brain, occurring to a small degree at 3 hours, day 1, markedly on day 3, but reduced on days 7 and 14. By electron microscopic study of the same area, the reaction product of horseradish peroxidase was localized to the plasmalemmal vesicles in the endothelial cells 3 hours after ligation, but appeared in the cytoplasm on days 1 and 3, suggesting a diffuse leakage of horseradish peroxidase. In addition, the reaction product was dispersed into the cytoplasm of glial cells in the perivascular regions on day 3. The luminal surface of the endothelial cell cytoplasm appeared irregular on day 7, suggesting a conformational change of the endothelial cells. Collagen fibrils proliferated in the thickened basal lamina and mitochondria degenerated in the pericyte on days 7 and 14. Perivascular glial endfeet were swollen throughout the survival period. In sham-operated rats, the reaction product of horseradish peroxidase was not observed at any time interval, except in vesicular structures. These findings indicate that chronic cerebral hypoperfusion induces blood–brain barrier damage with subsequent morphologic changes of the vascular structures in the corpus callosum. An extravasation of macromolecules, such as proteases and immunoglobulins, may contribute to the pathogenesis of white matter lesions.

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Damasceno, Benito P. « Relationship between cortical microinfarcts and cognitive impairment in Alzheimer's disease ». Dementia & ; Neuropsychologia 6, n^o 3 (septembre 2012) : 131–36. http://dx.doi.org/10.1590/s1980-57642012dn06030004.

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ABSTRACT Cerebrovascular disease and AD pathology co-exist in most dementia cases, and microinfarcts (MIs), particularly if cortical and multiple, play an additive and independent role in AD cognitive impairment. The main cause of cortical MIs is chronic cerebral hypoperfusion but occlusive vascular diseases, embolism and blood-brain barrier disruptions, isolated or combined, may also play a role. The precise mechanisms by which MIs cause cognitive impairment are not well known, but one plausible explanation is that they are widespread and accompanied by diffuse hypoperfusion, hypoxia, oxidative stress and inflammation, particularly in the watershed areas of the tertiary association cortex, and hence could damage cognition networks and explain many of AD's cognitive and behavioral disturbances. Therefore, it is crucial to control vascular risk factors and avoid uncontrolled use of the antihypertensives, neuroleptics and other sedative drugs frequently prescribed to AD patients.

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Poh, Luting, Vismitha Rajeev, Sharmelee Selvaraji, Mitchell K. P. Lai, Christopher Li-Hsian Chen, Thiruma V. Arumugam et David Y. Fann. « Intermittent fasting attenuates inflammasome-associated apoptotic and pyroptotic death in the brain following chronic hypoperfusion ». Neurochemistry International 148 (septembre 2021) : 105109. http://dx.doi.org/10.1016/j.neuint.2021.105109.

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Qu, Jie, Qiong Zhou, Ying Du, Wei Zhang, Miao Bai, Zhuo Zhang, Ye Xi, Zhuyi Li et Jianting Miao. « Retracted : Rutin protects against cognitive deficits and brain damage in rats with chronic cerebral hypoperfusion ». British Journal of Pharmacology 171, n^o 15 (17 juillet 2014) : 3702–15. http://dx.doi.org/10.1111/bph.12725.

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Gao, Minna, Li Liu, Linhui Wang, Gang Yu et Yu Li. « Chronic cerebral hypoperfusion induces UCP2 expression by decreasing mitochondrial respiratory activities in aging rat brain ». Molecular Neurodegeneration 7, Suppl 1 (2012) : O6. http://dx.doi.org/10.1186/1750-1326-7-s1-o6.

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