Chronic Ischemia and Neurocognition

Chmayssani, Mohamad; Festa, Joanne R.; Marshall, Randolph S.

doi:10.1016/j.nic.2007.03.002

Cited by 27 publications

(19 citation statements)

References 137 publications

(170 reference statements)

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“…Brain chronic hypoperfusion, caused by partial carotid occlusion during aging, represents a chronic, dynamic process that causes multiple progressive alterations, and eventually leads to neurodegeneration (Ozacmak et al 2007;Farkas et al 2007) and vascular dementia (Chmayssani et al 2007). 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).…”

Section: Discussionmentioning

confidence: 99%

“…Chronic ischemia is a progressive neurodegenerative process caused by cerebral hypoperfusion that may manifest with cognitive impairment (Sarti et al 2002b;Melani et al 2010;Schmidt-Kastner et al 2005;Lana et al 2013). Indeed, chronic hypoperfusion of the brain, secondary to vascular pathology, is a prominent risk factor for neurodegenerative diseases (Naritomi 1991) such as vascular dementia (Chmayssani et al 2007). In aging humans, cerebrovascular stenosis caused by arteriosclerosis decreases brain blood flow with consequent cerebral hypoperfusion.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

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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“…A link between chronic cerebral hypoperfusion and reversible neuronal dysfunction is supported by reports of revascularization resulting in increased cerebral blood flow and improvements in cognition [6]. In a case of moyamoya with preoperative bilateral hemispheral hypoperfusion on perfusion MR, extracranial-intracranial arterial bypass to the right cerebral hemisphere increased MR perfusion to normal levels in both hemispheres and resulted in improvements in right hemisphere neurocognitive functions [13].…”

Section: Discussionmentioning

confidence: 99%

Neurocognitive dysfunction in adult moyamoya disease

et al. 2009

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We wanted to determine the neurocognitive profile of adult patients with moyamoya disease prior to neurosurgical intervention. The experience of three United States medical centers, Columbia University, University of Illinois at Chicago, and the University of Texas Southwestern Medical Center at Dallas, were combined. Clinical data from adult patients (N = 29) referred for neuropsychological evaluation from 1996 to 2008 were reviewed. Neurocognitive functioning was assessed using standardized neuropsychological tests and all data were converted to z-scores. Memory, attention, processing speed, verbal memory, visuo-spatial, language, and executive functions were examined. Cognitive dysfunction was defined as performance in two or more cognitive domains 1.5 standard deviations below age-corrected normative means OR one or more cognitive domains two standard deviations below age-corrected normative means. Manual strength and dexterity, as well as depressive symptoms, were also assessed. Two-thirds of patients demonstrated neurocognitive dysfunction. A large proportion of patients were found to have pronounced cognitive dysfunction (>2 SD below the mean) on tests of processing speed (29%), verbal memory (31%), verbal fluency (26%) and executive function (25%). Manual strength and dexterity were also affected in many patients, with impairment found in 36-58% of patients. Twenty-eight percent of patients reported moderate to severe depression, but depressive symptoms did not correlate with neurocognitive findings. A large proportion of adults with moyamoya disease demonstrate disruption of neurocognition in a broad range of functions, particularly those mediated by subcortical and frontal regions. The pattern of deficits suggests a mechanism of diffuse small vessel disease possibly caused by chronic hypoperfusion.

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“…As Ab formation and eventual deposition represents a key feature and possibly the triggering mechanism of AD, hypothesis was made that highexpression of BACE1 and Ab from CCH was a potential factor for the vascular pathogenesis of AD. Chronic cerebral hypoperfusion which is usually observed in carotid arteriosclerosis and stroke leads to neuronal injury and cognitive impairment [31][32][33]. The development of ischemic white matter lesions under chronic hypoperfusion induces cognitive impairment through oxditive stress and inflammatory reaction [34,35].…”

Section: Discussionmentioning

confidence: 99%

Upregulation of BACE1 and β-Amyloid Protein Mediated by Chronic Cerebral Hypoperfusion Contributes to Cognitive Impairment and Pathogenesis of Alzheimer’s Disease

et al. 2009

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Chronic cerebral hypoperfusion (CCH) increases the risk of Alzheimer disease (AD) through several biologically plausible pathways, but the relationship between CCH and the development of AD remains uncertain. To investigate expression of APP, BACE1 and A beta in the hippocampus of BCCAO rats and study pathophysiological mechanism of AD from CCH. CCH rat model was established by chronic bilateral common carotid artery occlusion (BCCAO). Behavior was evaluated after BCCAO with Morris water maze and open-field task. Expression of A beta was measured by enzyme linked immunosorbent assay (ELISA). beta-Amyloid precursor protein cleavage enzyme 1 (BACE1) and beta-amyloid precursor protein (APP) were tested by ELISA, Western blotting and RT-PCR. Cognitive impairment occurred with CCH by Morris water maze test and open-field task. The BACE1 and A beta level in BCCAO rats was more increased than sham-operation control rats (P < 0.01) but APP had no difference(P > 0.05). The expression of BACE1 and A beta has no inter-group difference in BCCAO rats (P > 0.05). The level of BACE1 and A beta had positive correlation with cognitive impairment (P < 0.01) while no correlation was observed between APP and cognitive impairment. Chronic cerebral ischemia contributes to cognitive impairment and vascular pathogenesis of Alzheimer's disease that chronic cerebral hypoperfusion increases BACE1 and A beta level in brain.

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Chronic Ischemia and Neurocognition

Cited by 27 publications

References 137 publications

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

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

Neurocognitive dysfunction in adult moyamoya disease

Upregulation of BACE1 and β-Amyloid Protein Mediated by Chronic Cerebral Hypoperfusion Contributes to Cognitive Impairment and Pathogenesis of Alzheimer’s Disease

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