Glucose metabolism and rate constants in Alzheimer's disease examined with dynamic positron emission tomography scan

Fukuyama, Hidenao; Kameyama, Masakuni; Harada, Kiyoshi; Nishizawa, Sadahiko; Senda, Michio; Mukai, Takahiro; Yonekura, Yoshiharu; Torizuka, K

doi:10.1111/j.1600-0404.1989.tb03884.x

Cited by 23 publications

(12 citation statements)

References 20 publications

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“…Alteration of yATP peak in AD as also been reported by Pettegrew et al (1994), who observed that )'ATP was rather reduced in mildly affected subjects and, on the contrary, abnormally high in severely diseased patients. The right hippocampus lateralisation of the PDE and )'ATP observed draws attention, but it should be carefully considered because PET studies have shown that lateralisation of metabolic alterations in AD is not anatomically systematised and seems to essentially depend on the symptomatic variations of disease (Alavi et al, 1986;Haxby et al, 1988;Fukuyama et al, 1989;Rapofort, 1995).…”

Section: Discussionmentioning

confidence: 99%

In vivo hippocampal ³¹P NMR metabolites in Alzheimer's disease and ageing

et al. 1997

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Memory loss is the most common early symptom of Alzheimer's disease (AD). For this study, we chose the hippocampi as regions of interest. The hippocampus, which is closely associated with memory processing, is known to be vulnerable to damage in the early stage of AD. We considered both inter-group (patients vs controls) and intra-group (right vs left hippocampus) comparisons. We examined seven patients meeting the DSM-III-R criteria of senile dementia and the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association (NINCDS - ADRDA) criteria of probable AD, and II aged controls. This study focused on the measurement of phosphorus 31 ((31)P) Nuclear Magnetic Resonance (NMR) spectroscopy metabolites in each hippocampus. We found significant differences in phosphorus metabolites for both intra-group comparison (pH shifted towards relative alkalosis in the left hippocampus of patients) and inter-group consideration (reduced phosphodiesters [Pde]and elevated gamma adenosine triphosphate (ATP) in the right hippocampus, higher inorganic phosphate (pHi) in the left hippocampus for patients as compared to controls). We suggest energy failure and membrane functional breakdown in patients compared to aged controls.

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Section: Discussionmentioning

confidence: 99%

In vivo hippocampal ³¹P NMR metabolites in Alzheimer's disease and ageing

et al. 1997

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“…The rate constants K1* and k2* represent the forward and reverse FDG transport in the brain, respectively, and k3* represents the phosphorylation of FDG by the hexokinase. Previous reports using dynamic FDG‐PET showed that the reduced k3* is the most responsible for glucose hypometabolism in AD 2,3 . There was, however, no multiregional analysis of these rate constants in AD.…”

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confidence: 96%

Dynamic FDG‐PET Study in Probable Alzheimer's Disease

Kawakami

Nagata

Sasaki

et al. 1997

Annals of the New York Academy of Sciences

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“…The measurement of the CMR glc by Phelps' autoradiographic method is affected if changes in the rate constants and lumped constant values occur in persistent CCD. 23 In our preliminary analysis of the rate constants 24 in persistent CCD in some patients included in this study, the cerebellar CMR glc values obtained by the kinetic method had a tendency to be lower than those obtained by the autoradiographic method, which might lead to a further increase in the CMRO 2 /CMR glc ratio (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Uncoupling of Oxygen and Glucose Metabolism in Persistent Crossed Cerebellar Diaschisis

Fukuyama

Nagahama

Nishizawa

et al. 1999

Stroke

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Background and Purpose-The pathophysiology of deafferentation-induced changes after stroke remains unclear. Some supratentorial strokes cause persistent decreases in blood flow and metabolism in the contralateral cerebellum (persistent crossed cerebellar diaschisis [CCD]). Our previous study showed uncoupling of oxygen consumption and blood flow in this condition, which may reflect a characteristic change in brain metabolism caused by deafferentation. This uncoupling might be related to oxidation of some substrates other than blood-borne glucose, which could also lead to the uncoupling of oxygen consumption and glucose utilization. The purpose of this study was to investigate whether oxygen consumption is uncoupled from glucose utilization in persistent CCD. Methods-Using positron emission tomography in 10 unilateral supratentorial stroke patients, we evaluated regional blood flow, oxygen consumption, and glucose utilization in the cerebellar cortex in the chronic stage. Eight patients with a significant cerebellar blood flow asymmetry, defined as outside the 95% confidence limits predefined in 9 normal subjects, were selected as patients with persistent CCD. Results-In patients with CCD, the cerebellar cortex contralateral to the stroke showed significant decreases in both oxygen consumption and glucose utilization compared with the ipsilateral cerebellar cortex. The decrease in oxygen consumption was less than the decrease in glucose utilization, resulting in a significant increase in the oxygen consumption/glucose utilization ratio. Conclusions-Persistent CCD caused by stroke may induce uncoupling of oxygen consumption and glucose utilization, which may reflect a characteristic change in brain metabolism caused by deafferentation. (Stroke. 1999;30:1424-1428.)Key Words: cerebellum Ⅲ cerebral metabolism Ⅲ diaschisis Ⅲ tomography, emission computed I n cerebrovascular diseases, functional depression caused by a decrease in neural input tends to widely affect both cortical and subcortical structures, as a result of disconnection. 1,2 A decrease in neural input may have profound effects on postsynaptic neurons, including atrophy or death and synaptic reorganization. The avoidance of neuronal death and subsequent anatomic reorganization in the deafferented region may be one of the intrinsic mechanisms of functional recovery after stroke. 3,4 Thus, an understanding of the pathophysiology of deafferentation-induced changes may be important for designing therapies of functional deficits caused by stroke. In addition, it may give an insight into the pathophysiology of some neurodegenerative diseases in which deafferentation may contribute to the early metabolic changes in the regions without pathological changes. 5 However, the events at the cellular level underlying the effects of deafferentation remain unclear.One of the most consistent signs of transneuronal functional depression is crossed cerebellar diaschisis (CCD), which was first demonstrated by Baron and coworkers with positron emission tomography (PET) in 198...

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Glucose metabolism and rate constants in Alzheimer's disease examined with dynamic positron emission tomography scan

Cited by 23 publications

References 20 publications

In vivo hippocampal ³¹P NMR metabolites in Alzheimer's disease and ageing

In vivo hippocampal ³¹P NMR metabolites in Alzheimer's disease and ageing

Dynamic FDG‐PET Study in Probable Alzheimer's Disease

Uncoupling of Oxygen and Glucose Metabolism in Persistent Crossed Cerebellar Diaschisis

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Glucose metabolism and rate constants in Alzheimer's disease examined with dynamic positron emission tomography scan

Cited by 23 publications

References 20 publications

In vivo hippocampal 31P NMR metabolites in Alzheimer's disease and ageing

In vivo hippocampal 31P NMR metabolites in Alzheimer's disease and ageing

Dynamic FDG‐PET Study in Probable Alzheimer's Disease

Uncoupling of Oxygen and Glucose Metabolism in Persistent Crossed Cerebellar Diaschisis

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In vivo hippocampal ³¹P NMR metabolites in Alzheimer's disease and ageing

In vivo hippocampal ³¹P NMR metabolites in Alzheimer's disease and ageing