Decrease in parietal cerebral hemoglobin oxygenation during performance of a verbal fluency task in patients with Alzheimer's disease monitored by means of near-infrared spectroscopy (NIRS) — correlation with simultaneous rCBF-PET measurements

Höck, Christoph; Villringer, Kersten; Müller‐Spahn, F.; Wenzel, Rüdiger; Heekeren, Hauke R.; Schuh‐Hofer, Sigrid; Hofmann, M.; Minoshima, Satoshi; Schwaiger, Markus; Dirnagl, Ulrich; Villringer, Arno

doi:10.1016/s0006-8993(97)00122-4

Cited by 347 publications

(216 citation statements)

References 34 publications

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“…Chronic brain hypoperfusion (Farkas and Luiten, 2001;Hirao et al, 2005;Bateman et al, 2006;Vicenzini et al, 2007;Claassen et al, 2009) and altered neurovascular coupling (Hock et al, 1997;Mentis et al, 1998;Rombouts et al, 2000;Machulda et al, 2003;Rosengarten et al, 2006) are prominent features of AD. Resting CBF in human is B50 ml/ 100 g brain per minute.…”

Section: Neurovascular Dysfunction In Alzheimer's Diseasementioning

confidence: 99%

Neurovascular function in Alzheimer's disease patients and experimental models

Nicolakakis

Hamel

2011

J Cereb Blood Flow Metab

133

118

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The ability of the brain to locally augment glucose delivery and blood flow during neuronal activation, termed neurometabolic and neurovascular coupling, respectively, is compromised in Alzheimer's disease (AD). Since perfusion deficits may hasten clinical deterioration and have been correlated with negative treatment outcome, strategies to improve the cerebral circulation should form an integral element of AD therapeutic efforts. These efforts have yielded several experimental models, some of which constitute AD models proper, others which specifically recapture the AD cerebrovascular pathology, characterized by anatomical alterations in brain vessel structure, as well as molecular changes within vascular smooth muscle cells and endothelial cells forming the bloodbrain barrier. The following paper will present the elements of AD neurovascular dysfunction and review the in vitro and in vivo model systems that have served to deepen our understanding of it. It will also critically evaluate selected groups of compounds, the FDA-approved cholinesterase inhibitors and thiazolidinediones, for their ability to correct neurovascular dysfunction in AD patients and models. These and several others are emerging as compounds with pleiotropic actions that may positively impact dysfunctional cerebrovascular, glial, and neuronal networks in AD.

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Section: Neurovascular Dysfunction In Alzheimer's Diseasementioning

confidence: 99%

Neurovascular function in Alzheimer's disease patients and experimental models

Nicolakakis

Hamel

2011

J Cereb Blood Flow Metab

133

118

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“…Converging lines of evidence suggest that cerebrovascular factors play a key role in the pathogenesis of AD (Iadecola, 2004). Cerebral blood flow (CBF) is reduced in the early stages of AD, and the reactivity of cerebral blood vessels is impaired (Prohovnik et al, 1988;Hock et al, 1997;Mentis et al, 1998;Jagust, 2000;de la Torre, 2004). AD and cerebrovascular diseases share common risk factors (Stewart et al, 1998;Breteler, 2000;Casserly and Topol, 2004), suggesting similarities in their pathogenic mechanisms.…”

Section: Introductionmentioning

confidence: 99%

NADPH Oxidase-Derived Reactive Oxygen Species Mediate the Cerebrovascular Dysfunction Induced by the Amyloid β Peptide

Park¹,

Anrather²,

Zhou³

et al. 2005

J. Neurosci.

223

229

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Overproduction of the amyloid ␤ (A␤) peptide is a key factor in the pathogenesis of Alzheimer's disease (AD), but the mechanisms of its pathogenic effects have not been defined. Patients with AD have cerebrovascular alterations attributable to the deleterious effects of A␤ on cerebral blood vessels. We report here that NADPH oxidase, the major source of free radicals in blood vessels, is responsible for the cerebrovascular dysregulation induced by A␤. Thus, the free-radical production and the associated alterations in vasoregulation induced by A␤ are abrogated by the NADPH oxidase peptide inhibitor gp91ds-tat and are not observed in mice lacking the catalytic subunit of NADPH oxidase (gp91 phox ). Furthermore, oxidative stress and cerebrovascular dysfunction do not occur in transgenic mice overexpressing the amyloid precursor protein but lacking gp91 phox . The mechanisms by which NADPH oxidase-derived radicals mediate the cerebrovascular dysfunction involve reduced bioavailability of nitric oxide. Thus, a gp91 phox -containing NADPH oxidase is the critical link between A␤ and cerebrovascular dysfunction, which may underlie the alteration in cerebral blood flow regulation observed in AD patients.

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“…This activation of single centers of the brain can be demonstrated with high temporal resolution. During cognitive tasks and visual simulation there are increases in cerebral tissue HbO 2 , often with corresponding decreases in Hb over the corresponding cortical areas (Heekeren et al, 1997;Villringer, et al, 1994Meek, et al, 1995). , Obrig, Valdueza, Dirnagl and Villringer, (1997) demonstrated increases in HbO 2 and decreases in Hb using optrodes placed over the left motor cortex during right hand movements but not with left hand movements.…”

Section: What Near-infrared Spectroscopy Can Tell Usmentioning

confidence: 96%

“…Simultaneous spectroscopy of both hemispheres can provide information on the asymmetry of cerebral activation during mental stimulus (Tamura, Hoshi & Okada, 1997). NIRS has also had application in psychiatric evaluation, demonstrating clear differences between cerebral function of schizophrenic and normal controls; and between patients with Alzheimer's dementia and healthy elderly subjects (Okada, Tokumitsu, Hoshi, & Tamura, 1994;Hock et al, 1997).…”

Section: What Near-infrared Spectroscopy Can Tell Usmentioning

confidence: 99%

Operator Functional State Assessment (L'evaluation de l'aptitude operationnelle de l'operateur humain)

2004

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Decrease in parietal cerebral hemoglobin oxygenation during performance of a verbal fluency task in patients with Alzheimer's disease monitored by means of near-infrared spectroscopy (NIRS) — correlation with simultaneous rCBF-PET measurements

Cited by 347 publications

References 34 publications

Neurovascular function in Alzheimer's disease patients and experimental models

Neurovascular function in Alzheimer's disease patients and experimental models

NADPH Oxidase-Derived Reactive Oxygen Species Mediate the Cerebrovascular Dysfunction Induced by the Amyloid β Peptide

Operator Functional State Assessment (L'evaluation de l'aptitude operationnelle de l'operateur humain)

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