MinireviewApplication of Positron Emission Tomography for Evaluation of Metabolism and Blood Flow in Human Brain: Normal Development, Aging, Dementia, and Stroke☆
References (67)
A critical period of brain development: Studies of cerebral glucose utilization with PET
Preventive Med
(1998)- et al.
Current concepts in the pathogenesis of Alzheimer's disease
American J Med
(1997) - et al.
The use of positron emission tomography in the clinical assessment of dementia
Semin Nucl Med
(1992) - et al.
Clinical value of neuroimaging in the diagnosis of dementia: Sensitivity and specificity of regional cerebral metabolic and other parameters for early identification of Alzheimer's disease
Clin Positron Imaging
(1999) - et al.
The neurometabolic landscape of cognitive decline: In vivo studies with positron emission tomography in Alzheimer's disease
Int J Psychophysiol
(2000) - et al.
Regional cerebral glucose metabolism in dementia with Lewy bodies and Alzheimer's disease: A comparative study using positron emission tomography
Neurosci Lett
(1997) - et al.
The [14C]deoxyglucose method for the measurement of local cerebral glucose utilization: Theory, procedure and normal values in the conscious and anesthesized albino rat
J Neurochem
(1977) - et al.
Noninvasive determination of local cerebral metabolic rate of glucose in man
Am J Physiol
(1980) - et al.
Mapping local metabolism and perfusion in normal and ischemic brain by emission computed tomography of 18FDG and 13NH3
Ann Neurol
(1980) - et al.
Tomographic mapping of human cerebral metabolism: Normal unstimulated state
Neurology
(1981)
Tomographic measurement of local cerebral glucose metabolic rate in humans with (F-18)2-fluoro-2-deoxyglucose: Validation of method
Ann Neurol
The [18F]fluorodeoxyglucose method for the measurement of local cerebral glucose utilization in man
Circ Res
Interpretation of metabolic abnormalities in Alzheimer's disease using three-dimensional stereotactic surface projections (3D-SSP) and normal database
J Nuclear Medicine.
The metabolic topography of normal aging
J Cereb Blood Flow Metabolism
Cerebral glucose metabolism in patients with frontotemporal dementia
J Nucl Med
Quantitation of regional cerebral blood flow corrected for partial volume effect using O-15 water and PET: II. Normal values and gray matter blood flow response to visual activation
J Cereb Blood Flow Metabolism
Quantitative measurement of local cerebral blood flow in humans by positron computed tomography and 15O-water
J Cereb Blood Flow Metab
Does cerebral blood flow decline in healthy aging?. A PET study with partial-volume correction
J Nucl Med
Maturational changes in cerebral function in infants determined by 18FDG positron emission tomography
Science
Positron emission tomography study of human brain functional development
Ann Neurol
Developmental changes of cerebral blood flow and oxygen metabolism in children
AJNR
Developmental changes in brain serotonin synthesis capacity in autistic and nonautistic children
Ann Neurol
Age-related changes in regional cerebral blood flow among young to mid-life adults
NeuroReport
Positron emission tomography studies of the Brain
Estimated prevalence of Alzheimer's disease in the US
Milbank Q
The U. S. economic and social costs of Alzheimer's disease revisited
Am J Public Health
The prevalence of dementia and Alzheimer's disease in Shanghai, China: Impact of age, gender, and education
Ann Neurol
Education and the prevalence of dementia and Alzheimer's disease
Neurology
Inverse relationship between education and parietotemporal perfusion deficit in Alzheimer's disease
Ann Neurol
Relationship between lifetime occupation and parietal flow: Implications for a reserve against Alzheimer's disease pathology
Neurology
Association of premorbid intellectual function with cerebral metabolism in Alzheimer's disease: Implications for the cognitive reserve hypothesis
Am J Psychiatry
Apolipoprotein E epsilon-4 and incidence of Alzheimer disease in a community population of older persons
J Am Med Assoc
Cited by (33)
Right Broca's area is hyperactive in right-handed subjects during meditation: Possible clinical implications?
2021, Medical HypothesesCitation Excerpt :The subjects were in fasting state for at least 3 h prior to the scanning procedure. After image reconstruction, a region of interest (ROI) was quantified with the help of ‘NeuroQ’ software Version 3.0 (University of California, Los Angeles), which aids in assessment of human brain scans through quantification of mean pixels values lying within standardized region of interest (ROI) [27–30]. The specific areas in brain which were hyperactive during meditation using 18FDG-PET have been published previously [24].
Amyloid imaging: Past, present and future perspectives
2016, Ageing Research ReviewsCitation Excerpt :The insight into the molecular mechanism of AD pathogenesis opened new avenues for the successful development of new neuroimaging approaches. ( Selkoe, 2000) Modern functional neuroimaging techniques such as positron emission tomography (PET), tend to be more sensitive than structural imaging modalities, identifying subtle pathophysiologic changes in the brain, before structural changes are present (Bobinski et al., 1999; de Leon et al., 1997; De Toledo-Morrell et al., 2000; Dickerson et al., 2001; Juottonen et al., 1998; Killiany et al., 2000; Xu et al., 2000), therefore possessing greater potential for accurate and early diagnosis, monitoring disease progression, and better treatment follow-up (Silverman and Phelps, 2001; Villemagne et al., 2005). PET is a sensitive molecular imaging technique that allows in vivo quantification of radiotracer concentrations in the picomolar range, where either the radiotracer bears the same biochemical structure, is an analog or a substrate of the chemical process being evaluated, allowing the in vivo assessment of the molecular process at their sites of action, (Phelps, 2000) permitting detection of disease processes at asymptomatic stages when there is no evidence of anatomic changes on CT and MRI.
Emerging trends in in vivo neurochemical monitoring by microdialysis
2013, Current Opinion in Chemical BiologyCitation Excerpt :Therefore analytical measurements must be compatible with ‘samples on legs’. Several techniques have been developed that allow in vivo neurotransmitter measurement including positron emission tomography (for reviews see [5–8]), cell based sensors [9], fluorescent tracers [10], implantable electrochemical sensors [11–15], and microdialysis sampling [16,17]). Although exciting advances have been made in all these areas recently, we will restrict our review to microdialysis sampling.
Carotid Artery Ultrasound and Echocardiography Testing to Lower the Prevalence of Alzheimer's Disease
2009, Journal of Stroke and Cerebrovascular DiseasesCitation Excerpt :Brain hypoperfusion may be present even before any cognitive symptoms appear. For example, it is well accepted that within a vascular territory, cerebral blood flow (CBF) is coupled to glucose uptake and both measures are practically linear.68 When 18fluoro-2-deoxy-D-glucose-positron emission tomography scans of cognitively healthy elderly individuals were analyzed, reduced glucose uptake in the hippocampus, a brain region linked to short-term memory, allowed significant prediction of which individuals would later convert to AD.69
Chapter 3 Cerebrovascular and Cardiovascular Pathology in Alzheimer's Disease
2009, International Review of NeurobiologyCitation Excerpt :Individuals at risk of AD but who do not express any cognitive deficits show local hypometabolic reductions of the cerebral metabolic rate of glucose after FDG in brain regions that will later develop atrophy and neurodegeneration (de Leon et al., 2001). Since measures of glucose metabolic rate and CBF are coupled (Silverman and Phelps, 2001), FDG‐PET studies are proof of concept that regional brain hypoperfusion precedes Alzheimer clinical symptoms, Aβ production, and neurodegenerative changes. FDG‐PET can also track AD progression (de Leon et al., 2001).
Imaginem oblivionis: The prospects of neuroimaging for early detection of Alzheimer's disease
2005, Journal of Clinical Neuroscience
- ☆
Supported by funds from the United States Department of Energy, Contract No. DE-FCO3-87ER60615, and the Los Angeles Alzheimer's Association, Turken Family Foundation Award.
- 2
To whom correspondence should be addressed at University of California, Los Angeles, School of Medicine, Ahmanson Biological Imaging Center, CHS AR-144, MC694215, Los Angeles, CA 90095-6942. E-mail: [email protected].