Positron emission tomography in Alzheimer's disease

Duara, Ranjan; Grady, Cheryl L.; Haxby, James V.; Sundaram, Magesh; Cutler, N.R.; Heston, Leonard L.; Moore, Alice E.; Schlageter, Nicholas L.; Larson, Steven M.; Rapoport, Stanley I.

doi:10.1212/wnl.36.7.879

Cited by 527 publications

(181 citation statements)

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“…Older adults with the ε4 allele who engaged in more physical activity had greater memory-related activation in posterior temporal and parietal regions than non ε4-carriers or those with lower physical activity. This result is particularly interesting as these areas are some of the first regions of cortex to show metabolic deficits in early AD [169][170][171] . This work shows interesting influences of both APOE genotype and physical activity on memory-related brain activation in cognitively intact but genetically at-risk older adults, but it is not clear if this increase is compensatory or protective against future cognitive decline.…”

Section: Risk Factors For Alzheimer's Disease: Apoementioning

confidence: 87%

The cognitive neuroscience of ageing

2012

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PrefaceThe availability of neuroimaging technology has spurred a marked increase in the human cognitive neuroscience literature, including the study of cognitive aging. Although there is a growing consensus that the aging brain retains considerable plasticity of function, currently measured primarily by means of functional magnetic resonance imaging, it is less clear how age differences in brain activity relate to cognitive performance. The field also is hampered by the complexity of the aging process itself and the large number of factors that are influenced by age. In this review, current trends and unresolved issues in the cognitive neuroscience of aging are discussed.

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Section: Risk Factors For Alzheimer's Disease: Apoementioning

confidence: 87%

The cognitive neuroscience of ageing

2012

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“…Marked declines in cerebral glucose metabolism are associated with Alzheimer's disease, especially in the parietal and temporal cortices (28,29,37,54). Initial studies by Kalaria and Harik (59) demonstrated a reduction in the 55-kDa form of GLUT1 in cerebral microvessels prepared from Alzheimer's patients compared with normal age-matched controls (60).…”

Section: Neuronal Glut3 and Cerebral Glucose Utilizationmentioning

confidence: 99%

The facilitative glucose transporter GLUT3: 20 years of distinction

Simpson

Dwyer

Malide

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

403

322

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Glucose metabolism is vital to most mammalian cells, and the passage of glucose across cell membranes is facilitated by a family of integral membrane transporter proteins, the GLUTs. There are currently 14 members of the SLC2 family of GLUTs, several of which have been the focus of this series of reviews. The subject of the present review is GLUT3, which, as implied by its name, was the third glucose transporter to be cloned (Kayano T, Fukumoto H, Eddy RL, Fan YS, Byers MG, Shows TB, Bell GI. J Biol Chem 263: [15245][15246][15247][15248] 1988) and was originally designated as the neuronal GLUT. The overriding question that drove the early work on GLUT3 was why would neurons need a separate glucose transporter isoform? What is it about GLUT3 that specifically suits the needs of the highly metabolic and oxidative neuron with its high glucose demand? More recently, GLUT3 has been studied in other cell types with quite specific requirements for glucose, including sperm, preimplantation embryos, circulating white blood cells, and an array of carcinoma cell lines. The last are sufficiently varied and numerous to warrant a review of their own and will not be discussed here. However, for each of these cases, the same questions apply. Thus, the objective of this review is to discuss the properties and tissue and cellular localization of GLUT3 as well as the features of expression, function, and regulation that distinguish it from the rest of its family and make it uniquely suited as the mediator of glucose delivery to these specific cells.neurons; sperm; preimplantation embryo; white blood cells GLUCOSE METABOLISM IS VITAL to most mammalian cells, and the passage of glucose across cell membranes is facilitated by a family of integral membrane transporter proteins, the GLUTs. There are currently 14 members of the SLC2 family of GLUTs, several of which have been the focus of this series of reviews. The subject of the present review is GLUT3 which, as implied by its name, was the third glucose transporter to be cloned (62) and was originally designated as the neuronal glucose transporter. Together with GLUT1, -2, and -4, it comprises the Class 1 group of transporters (For review see Refs. 15,81,121). With the cloning of GLUT3, it became apparent that the brain did not rely exclusively on GLUT1 and that GLUT3 was highly and specifically expressed by neurons. Thus, GLUT3 became the third facilitative glucose transporter isoform with unique characteristics suited for cell-specific expression and function. GLUT2 is ideally suited for expression in liver and pancreas due to its high K m for glucose; GLUT4 and its translocation from intracellular vesicles to the cell surface facilitates insulin-stimulated glucose uptake in insulin-sensitive cells: muscle and fat. The overriding question that drove the early work in GLUT3 in the brain was: why would neurons need a separate glucose transporter isoform; what is it about GLUT3 that specifically suits the needs of the highly metabolic and oxidative neuron with its high glucose demand?...

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“…Whereas there is general agreement that AD typi cally shows defects of perfusion and metabolism in the parietal cortex (Foster et aI., 1983;Duara et al , 1986;Deutsch and Tweedy, 1987;Jagust et aI., 1987), local alterations in metabolism and blood flow have not been consistently observed in PD. Since parkinsonism results from degeneration of the dopaminergic nigrostriatal neurons (Hornykiewicz, 1966), one would expect that dopamine depletion within the basal ganglia might result in consistent alterations of local functional activity and, conse quently, of rCMR and rCBF.…”

Section: S101mentioning

confidence: 99%

[^99mTc]-HM-PAO SPECT in Parkinson's Disease

Pizzolato

Dam

Borsato

et al. 1988

J Cereb Blood Flow Metab

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Thirty-six patients affected by Parkinson's disease were studied using single photon emission computed tomography (SPECT) and [99mTc]–HM-PAO as a tracer. The scanning procedure was performed 16–24 h after discontinuation of specific therapy. Tracer activity ratios were determined in 10 pairs of cerebellar, cortical, and subcortical regions. Data were compared with those of 10 age-matched controls. Most of the regions examined did not show any relevant change between parkinsonian and control subjects. Notably, mean activity in striatal regions were similar in the two groups. Increased activity in caudate–putamen was found in patients who were on chronic DOPA therapy. Side-to-side asymmetries in the basal ganglia increased with the severity of the disease. Significant reductions of tracer uptake, from control values, were observed bilaterally in the parietal cortex. These deficits were more pronounced in patients with mental deterioration and in subjects who had been chronically treated with anticholinergic drugs. Parietal perfusion deficits in parkinsonian patients resemble those described in Alzheimer's dementia. These findings suggest that the heterogeneous alterations of regional cerebral blood flow (rCBF) in parkinsonian patients reflect the multifactorial pathophysiology of the disease.

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Positron emission tomography in Alzheimer's disease

Cited by 527 publications

References 0 publications

The cognitive neuroscience of ageing

The cognitive neuroscience of ageing

The facilitative glucose transporter GLUT3: 20 years of distinction

[^99mTc]-HM-PAO SPECT in Parkinson's Disease

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Positron emission tomography in Alzheimer's disease

Cited by 527 publications

References 0 publications

The cognitive neuroscience of ageing

The cognitive neuroscience of ageing

The facilitative glucose transporter GLUT3: 20 years of distinction

[99mTc]-HM-PAO SPECT in Parkinson's Disease

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[^99mTc]-HM-PAO SPECT in Parkinson's Disease