Dynamic FDG‐PET Study in Probable Alzheimer's Disease

Kawakami, Yasushi; Nagata, Ken; Sasaki, Hiroshi; Hatazawa, Jun

doi:10.1111/j.1749-6632.1997.tb48493.x

Cited by 7 publications

(7 citation statements)

References 4 publications

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“…Our dynamic PET study with 18 F‐fluorodeoxyglucose (FDG) in seven patients with probable AD demonstrated a profound reduction in the cerebral metabolic rate of glucose (CMRglu), which mainly represents anaerobic glycolysis, as compared with the control group consisting of seven normal volunteers 27 . The mean CMRglu was reduced to as low as 70% of the normal values in AD patients, and this reduction of CMRglu was greater than that of CMRO 2 as shown in the present results.…”

Section: Discussionsupporting

confidence: 66%

“…Utilizing the three‐compartment model, 28 kinetic parameters were also estimated in AD and control groups. The decreased k3 *, which designates phosphorylation of FDG by the hexokinase, may partly account for the reduced CMRglu in AD patients 27 . Another previous dynamic PET study suggested a significant decrease in K1 *, which designates forward FDG transport in AD patients 29 .…”

Section: Discussionmentioning

confidence: 92%

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Misery Perfusion with Preserved Vascular Reactivity in Alzheimer's Disease

Nagata

Buchan

Yokoyama

et al. 1997

Annals of the New York Academy of Sciences

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To elucidate the hemodynamic pathophysiology underlying Alzheimer's disease (AD), cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2) and oxygen extraction fraction (OEF) were measured with positron emission tomography in 10 patients with probable AD and in 20 age-matched normal volunteers. By the 15O intravenous bolus injection method, CBF was measured during resting state, CO2 inhalation (hypercapnia) and hyperventilation (hypocapnia), and the vascular reactivity (VR) was estimated by comparing the CBF changes (delta CBF%/PaCO2 mmHg) in the hyper- or hypocapnic to the resting state. By the 15O2 single-breath method or 15O steady-state method, CMRO2 and OEF were measured during resting state. Based on 26 regions of interest, local CBF, CMRO2 and OEF were compared statistically between the two groups. As compared with the control group, the mean CBF and CMRO2 decreased to as low as 77.0% and 88.4% of the normal values, respectively, while the mean OEF increased by 12.1% (p < 0.05) in AD patients. These changes were most pronounced in the supramarginal and superior temporal gyri. There was no focal change in VR in the AD group, and no significant difference was seen in VR to either hyper- or hypocapnia between AD and control groups. The results may suggest a vascular involvement, possibly at the capillary level, that might cause a relative misery perfusion syndrome accompanied by preserved vascular reactivity in AD.

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 92%

Misery Perfusion with Preserved Vascular Reactivity in Alzheimer's Disease

Nagata

Buchan

Yokoyama

et al. 1997

Annals of the New York Academy of Sciences

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“…Besides the larger cerebral vessels comprising penetrating arteries and arterioles with degenerative smooth muscle, [31][32][33] recent ultrastructural studies demonstrate characteristic angioarchitecural abnormalities in the capillaries and sites of the blood-brain barrier. [34][35][36][37] It was also speculated that the structural alterations of microvasculature can initiate interference with the fluid dynamics, hemorrhagic compromise resulting in the increased resistance, the increased blood viscosity, and changes in shear stress. [38][39][40] Extensive abnormalities in the capillaries and bloodbrain barrier may cause hemorrhagic and hemodynamic changes that will alter the delivery of energy nutrients to the brain.…”

Section: Discussionmentioning

confidence: 99%

Can PET Data Differentiate Alzheimer's Disease from Vascular Dementia?

Nagata

Maruya

Yuya

et al. 2000

Annals of the New York Academy of Sciences

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The present study endeavored to differentiate Alzheimer's disease (AD) from vascular dementia (VaD) by comparing the metabolic and hemodynamic parameters. Positron emission tomographic (PET) studies were carried out in 13 patients with probable AD and 20 patients with VaD. PET findings were not included in the diagnostic criteria of AD or VaD. Using oxygen-15 labeled compounds, cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), oxygen extraction fraction (OEF), cerebral blood volume, and vascular transit time (VTT) were measured quantitatively during the resting state. To evaluate vascular reactivity (VR), CBF was also measured during 7% CO2 inhalation. Regional CBF from the parietal cortex positively correlated with the neuropsychological scores in both AD and VaD groups. The typical parietotemporal pattern of hypoperfusion and hypometabolism was observed in the AD group, whereas the frontal lobe including the cingulate and superior frontal gyri were predominantly affected in the VaD group. The occipital cortex was preserved in both groups. A significant increase of the OEF was found in the parietotemporal areas in the AD group. No significant prolongation was seen with VTT. There was a marked difference in VR between the two groups: VR was depleted in the VaD group, whereas VR was normal in the AD group. The increased OEF with preserved vascular reserve seen in AD may implicate participation of a vascular factor in the pathogenesis of AD, possibly at the capillary level. Thus, PET provides important functional information in discriminating AD from VaD by comparing the patterns of hypoperfusion and/or hypometabolism, and in the understanding of the underlying hemodynamic pathophysiology.

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“…Together with the larger cerebral vessels comprising penetrating arteries and arterioles with degenerative smooth muscle [44,46], recent ultrastructural studies demonstrate characteristic angioarchitecural abnormalities in the capillaries and sites of the BBB [47,48]. It was also speculated that the structural alterations of microvasculature can initiate interference with the fluid dynamics, hemorrhagic compromise resulting in the increased resistance, the increased blood viscosity, and changes in shear stress [49,50].…”

Section: Differences Between Alzheimer's Disease and Vascular Dementimentioning

confidence: 98%

Primary Cerebral Blood Flow Deficiency and Alzheimer's Disease: Shadows and Lights

Mazza

Marano

Traversi

et al. 2011

JAD

110

108

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Alzheimer's disease (AD) is a degenerative disorder characterized by a decreased regional cerebral blood flow (CBF). It is most likely that a reduction in CBF could displace a pathway leading to AD genesis, in so far neuron death explains a sustained reduction in the supply of oxygen, glucose, and nutrients. Nevertheless, the concept of secondary CBF deficiency cannot explain the critical stages of early memory loss while, on the other hand, the picture of progressive ischemia due to primary CBF decline sheds light on the course of AD in a most persuasive manner. The concept of primary CBF deficiency is even more strengthened by the lack of correlation between degree of dementia and amount of CBF. Vascular abnormalities, frequently observed to co-occur with AD, might play a critical role in the initiation and aggravation of AD pathology given that the elimination of amyloid-β (Aβ) through a vascular route is an important brain Aβ clearance mechanism and its failure leads to formation of vascular amyloidosis and dense-core plaques. The goal of this review is to provide scientists comprehensive knowledge of the state-of the art influence vascular damage and reduced perfusion have on the final development of AD and to hopefully stimulate more research in this area of neuroscience.

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Dynamic FDG‐PET Study in Probable Alzheimer's Disease

Cited by 7 publications

References 4 publications

Misery Perfusion with Preserved Vascular Reactivity in Alzheimer's Disease

Misery Perfusion with Preserved Vascular Reactivity in Alzheimer's Disease

Can PET Data Differentiate Alzheimer's Disease from Vascular Dementia?

Primary Cerebral Blood Flow Deficiency and Alzheimer's Disease: Shadows and Lights

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