Cerebral Protein Turnover: Aspects and Problems

Lajtha, Ábel; Dunlop, David S.; Banay‐Schwartz, M.

doi:10.1007/978-94-011-1620-6_1

Cited by 5 publications

(3 citation statements)

References 42 publications

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“…Thus, admitting that the decrease of cortical ac cumulation rates of e lC]methionine reflects mainly neuronal loss and reduction of cytoplasmic RNA content (Lajtha, 1993;Mann et aI., 1988;Neary et aI., 1986), our in vivo data show that tissue loss is not sufficient to explain the cortical glucose hypo metabolism in AD. Neuronal protein synthesis is restricted to the perikarion, and peripheral trans port can hardly be important for the PET study time (Hammerschlag and Brady, 1989).…”

Section: Resultsmentioning

confidence: 66%

Combined Study of Cerebral Glucose Metabolism and [¹¹C]Methionine Accumulation in Probable Alzheimer's Disease Using Positron Emission Tomography

Salmon

Grégoire

Delfiore

et al. 1996

J Cereb Blood Flow Metab

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There is a characteristic decrease in glucose metabolism in associative frontal and temporo-parietal cortices of patients suffering from Alzheimer's disease (AD). The decrease in metabolism might result from local neuronal loss or from a decrease of synaptic activity. We measured in vivo [11C]methionine accumulation into proteins with positron emission tomography (PET) to assess cortical tissue loss in AD. Both global regional activity and compartmental analysis were used to express [11C]methionine accumulation into brain tissue. Glucose metabolism was measures with [18F]fluorodeoxyglucose and autoradiographic method. Combined studies were performed in 10 patients with probable AD, compared to age-matched healthy volunteers. There was a significant 45% decrease of temporo-parietal glucose metabolism in patients with AD, and frontal metabolism was lowered in most patients. Temporo-parietal metabolism correlated to dementia severity. [11C]methionine incorporation into temporo-parietal and frontal cortices was not significantly decreased in AD. There was no correlation with clinical symptoms. Data suggest that regional tissue loss, assessed by the decrease of [11C]methionine accumulation, is not sufficient to explain cortical glucose hypometabolism, which reflects, rather, reduced synaptic connectivity.

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Section: Resultsmentioning

confidence: 66%

Combined Study of Cerebral Glucose Metabolism and [¹¹C]Methionine Accumulation in Probable Alzheimer's Disease Using Positron Emission Tomography

Salmon

Grégoire

Delfiore

et al. 1996

J Cereb Blood Flow Metab

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“…The drinking water of ADX-chronic CORT rats contained ethanol vehicle. Ethanol has been reported to cause a small inhibition of brain protein synthesis (Lajtha et al, 1993). That such an inhibition may play a role in the observed metabolic process cannot be excluded, but it should be of slight importance, inasmuch as the acute replacement dose of CORT (i.e., stress physiological range) in ADX rats was sufficient to reduce apparent rates of protein synthesis to levels similar to control in most brain regions examined.…”

Section: Discussionmentioning

confidence: 94%

Adrenalectomy‐Induced Increase of Brain Protein Synthesis Is Antagonized by Corticosterone Replacements in Free‐Moving Rats

Grange¹,

Lepetit

Baubet

et al. 1994

Journal of Neurochemistry

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The autoradiographic method with l[35S]‐methionine was used to determine whether changes in glucocorticoid circulating levels were associated with changes in local rates of protein synthesis in rat brain. Chronic bilateral adrenalectomy induced an increase of me‐thionine incorporation rates into proteins in 60 of the 62 brain regions examined (mean effect, +50%). This effect was confirmed biochemically and quantified by correcting for the relative contribution of methionine derived from protein degradation to the precursor pool for protein synthesis in the whole brain. Acute or chronic administration of corticosterone, at doses that normalize basal levels of adrenocorticotrophic hormone, reversed or prevented the adrenalectomy‐induced increase of protein synthesis in most regions. However, in nearly all the regions studied (59 of 62), acute corticosterone administration to sham‐operated rats did not change the apparent rate of protein synthesis. These results demonstrate that glucocorticoids exert a generalized inhibitory action on brain protein synthesis, because the stimulatory and persistent effect of adrenalectomy on protein synthesis was antagonized by corticosterone replacements at physiological doses. Thus, the regulation of overall brain protein synthesis by glucocorticoids emphasizes the role of neuroendocrine events on long‐term neurochemical processes.

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“…For years, amino acids, the basic units of proteins, have been identified as a potential tool for the study of the in vivo cellular kinetics of protein synthesis [ 1 ]. In order to achieve this in humans, implementing nuclear medicine applications, researchers must make use of either radioactive forms of natural amino acids or radioactive analogues which can be incorporated into proteins.…”

Section: Introductionmentioning

confidence: 99%

Metabolism of no-carrier-added 2-[18F]fluoro-L-tyrosine in rats

et al. 2008

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Background: Several fluorine-18 labelled fluoroamino acids have been evaluated as tracers for the quantitative assessment of cerebral protein synthesis in vivo by positron emission tomography (PET). Among these, 2-[ 18 F]fluoro-L-tyrosine (2-[ 18 F]Tyr) has been studied in mice at a low specific activity. Its incorporation into proteins is fast and metabolism via other pathways is limited. The present in vivo study was carried out in normal awake rats using no-carrier-added 2-[ 18 F]Tyr. Under normal physiological conditions, we have studied the incorporation into proteins and the metabolism of the tracer in different brain areas.

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Cerebral Protein Turnover: Aspects and Problems

Cited by 5 publications

References 42 publications

Combined Study of Cerebral Glucose Metabolism and [¹¹C]Methionine Accumulation in Probable Alzheimer's Disease Using Positron Emission Tomography

Combined Study of Cerebral Glucose Metabolism and [¹¹C]Methionine Accumulation in Probable Alzheimer's Disease Using Positron Emission Tomography

Adrenalectomy‐Induced Increase of Brain Protein Synthesis Is Antagonized by Corticosterone Replacements in Free‐Moving Rats

Metabolism of no-carrier-added 2-[18F]fluoro-L-tyrosine in rats

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Cerebral Protein Turnover: Aspects and Problems

Cited by 5 publications

References 42 publications

Combined Study of Cerebral Glucose Metabolism and [11C]Methionine Accumulation in Probable Alzheimer's Disease Using Positron Emission Tomography

Combined Study of Cerebral Glucose Metabolism and [11C]Methionine Accumulation in Probable Alzheimer's Disease Using Positron Emission Tomography

Adrenalectomy‐Induced Increase of Brain Protein Synthesis Is Antagonized by Corticosterone Replacements in Free‐Moving Rats

Metabolism of no-carrier-added 2-[18F]fluoro-L-tyrosine in rats

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Combined Study of Cerebral Glucose Metabolism and [¹¹C]Methionine Accumulation in Probable Alzheimer's Disease Using Positron Emission Tomography

Combined Study of Cerebral Glucose Metabolism and [¹¹C]Methionine Accumulation in Probable Alzheimer's Disease Using Positron Emission Tomography