The metabolic signature of C9ORF72-related ALS: FDG PET comparison with nonmutated patients (Q59901143)

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title

The metabolic signature of C9ORF72-related ALS: FDG PET comparison with nonmutated patients (English)

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amyotrophic lateral sclerosis

5 March 2020

main subject

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1

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Andrea Calvo

4

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Cristina Moglia

5

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Flavio Nobili

10

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Adriano Chiò

15

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9

Bryan J Traynor

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author name string

Marco Pagani

2

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Anna Montuschi

3

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Antonio Canosa

6

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Giovanna Carrara

11

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Piercarlo Fania

12

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Gabriella Restagno

7

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Maura Brunetti

8

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Leonardo Lopiano

13

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M Consuelo Valentini

14

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publication date

21 January 2014

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European Journal of Nuclear Medicine and Molecular Imaging

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published in

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volume

41

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issue

5

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page(s)

844-852

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https://scigraph.springernature.com/pub.10.1007/s00259-013-2667-5

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exact match

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12 December 2020

Neuroimaging signatures of frontotemporal dementia genetics: C9ORF72, tau, progranulin and sporadics

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Early and phasic cortical metabolic changes in vestibular neuritis onset

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Characterization of frontotemporal dementia and/or amyotrophic lateral sclerosis associated with the GGGGCC repeat expansion in C9ORF72

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Summary metrics to assess Alzheimer disease-related hypometabolic pattern with 18F-FDG PET: head-to-head comparison

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Glutamate uptake into astrocytes stimulates aerobic glycolysis: a mechanism coupling neuronal activity to glucose utilization

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Brain hypermetabolism in amyotrophic lateral sclerosis: a FDG PET study in ALS of spinal and bulbar onset.

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SOD1, ANG, TARDBP and FUS mutations in amyotrophic lateral sclerosis: A United States clinical testing lab experience

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Clinico-pathological features in amyotrophic lateral sclerosis with expansions in C9ORF72.

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Regional glucose metabolic abnormalities are not the result of atrophy in Alzheimer's disease.

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Clinical, neuroimaging and neuropathological features of a new chromosome 9p-linked FTD-ALS family

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El Escorial revisited: revised criteria for the diagnosis of amyotrophic lateral sclerosis

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C9orf72 repeat expansions are a rare genetic cause of parkinsonism

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Expanded GGGGCC hexanucleotide repeat in noncoding region of C9ORF72 causes chromosome 9p-linked FTD and ALS

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Evidence for astrocytosis in ALS demonstrated by [11C](L)-deprenyl-D2 PET.

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1H-MRS evidence of neurodegeneration and excess glutamate + glutamine in ALS medulla.

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Frequency of the C9orf72 hexanucleotide repeat expansion in patients with amyotrophic lateral sclerosis and frontotemporal dementia: a cross-sectional study

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Clinical characteristics of patients with familial amyotrophic lateral sclerosis carrying the pathogenic GGGGCC hexanucleotide repeat expansion of C9ORF72.

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Evidence of widespread cerebral microglial activation in amyotrophic lateral sclerosis: an [11C](R)-PK11195 positron emission tomography study.

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A hexanucleotide repeat expansion in C9ORF72 is the cause of chromosome 9p21-linked ALS-FTD

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Cognitive and clinical characteristics of patients with amyotrophic lateral sclerosis carrying a C9orf72 repeat expansion: a population-based cohort study

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EANM procedure guidelines for PET brain imaging using [18F]FDG, version 2.

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Unawareness of memory deficit in amnestic MCI: FDG-PET findings

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The anterior cingulate cortex. The evolution of an interface between emotion and cognition

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Multiparametric MRI study of ALS stratified for the C9orf72 genotype

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MCI patients declining and not-declining at mid-term follow-up: FDG-PET findings.

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Frontotemporal dementia with the C9ORF72 hexanucleotide repeat expansion: clinical, neuroanatomical and neuropathological features

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C9ORF72 hexanucleotide repeat expansions in the Italian sporadic ALS population

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10.1007/S00259-013-2667-5

Identifiers

DOI

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5 March 2020

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