Total glutamine synthetase levels in cerebrospinal fluid of Alzheimer's disease patients are unchanged

Timmer, Nienke; Herbert, Megan K.; Claassen, Jurgen A.H.R.; Kuiperij, H. Bea; Verbeek, Marcel M.

doi:10.1016/j.neurobiolaging.2014.12.010

Cited by 16 publications

(13 citation statements)

References 7 publications

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“…However, there is a great overlap between patient groups and Ab42 (alone) seems not to be a valuable biomarker for the differential diagnosis of FTD and DLB. For Tau and pTau181, no (Timmer et al 2015) or only a marginal difference (Skillb€ ack et al 2015) between FTD and DLB patients was reported which is also in agreement with previous studies. Ab42, Tau, and pTau181 are not different between FTD and PDD (Skillb€ ack et al 2015).…”

Section: Differential Diagnosis Of Ftd To Other Dementiassupporting

confidence: 92%

“…Two recent studies reported lower (26-28%) Ab42 concentrations in CSF of DLB patients compared with FTD (Skillb€ ack et al 2015;Timmer et al 2015) and could confirm previous observations (Bibl et al 2007a;de Jong et al 2007). However, there is a great overlap between patient groups and Ab42 (alone) seems not to be a valuable biomarker for the differential diagnosis of FTD and DLB.…”

Section: Differential Diagnosis Of Ftd To Other Dementiassupporting

confidence: 82%

“…Skillb€ ack et al (2015) confirmed increased Tau and pTau181 and reduced Ab42 concentrations in AD in a large cohort of 5676 patients. Several other studies are in line with these observations (Alcolea et al 2014;Baldeiras et al 2015;Ewers et al 2015;Magdalinou et al 2015;Struyfs et al 2015b;Timmer et al 2015). The combination of Ab42 and pTau181 (ratio Ab42/pTau181) better differentiated AD and FTD patients (Skillb€ ack et al 2015).…”

Section: Differential Diagnosis Of Ftd To Other Dementiassupporting

confidence: 69%

“…; Timmer et al . ). The combination of Aβ42 and pTau181 (ratio Aβ42/pTau181) better differentiated AD and FTD patients (Skillbäck et al .…”

Section: Differential Diagnosis Of Ftd To Other Dementiasmentioning

confidence: 97%

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Neurochemical biomarkers in the diagnosis of frontotemporal lobar degeneration: an update

Oeckl

Steinacker

Feneberg

et al. 2016

Journal of Neurochemistry

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Frontotemporal lobar degeneration (FTLD) is a spectrum of rare neurodegenerative diseases with overlapping symptoms and neuropathology. It includes the behavioral variant of frontotemporal dementia (bvFTD), the semantic and non-fluent variant of primary progressive aphasia (svPPA and nfvPPA), FTD with motor neuron disease (FTD-MND), progressive supranuclear palsy, and corticobasal syndrome. The diagnosis of the FTLD spectrum of diseases is based on clinical symptoms which hampers the differentiation of the diseases among each other and with other disorders that show a similar clinical appearance resulting in a high rate of misdiagnoses.This highlights the need for objective and selective measures in the diagnostic criteria and there is extensive research on neurochemical biomarkers in FTLD as one option to address this unmet clinical need. Here, we review the advances in CSF biomarker research in FTLD in the last 2 years with regard to the validation of previously suggested and identification of new biomarker candidates for the differential diagnosis of FTLD. Keywords: biomarker, cerebrospinal fluid, corticobasal syndrome, frontotemporal dementia, frontotemporal lobar degeneration, progressive supranuclear palsy.This article is part of the Frontotemporal Dementia special issue.Frontotemporal lobar degeneration (FTLD) describes a group of neurodegenerative disorders with overlapping symptomatology and neuropathology. The common feature is the degeneration of the frontal and anterior temporal lobe, and at present, the following syndromes are assigned to the FTLD spectrum (Seltman and Matthews 2012): the three types of frontotemporal dementia (FTD) including the behavioral variant of frontotemporal dementia (bvFTD) and the semantic and non-fluent variant of primary progressive aphasia (svPPA and nfvPPA), FTD with motor neuron disease (FTD-MND), progressive supranuclear palsy (PSP), and corticobasal syndrome (CBS). These syndromes can further be classified as behavioral variant (bvFTD), language variant (svPPA and nfvPPA), and motor variant (FTD-MND, PSP and CBS) of FTLD.FTD is the third most common subtype of neurodegenerative dementia after Alzheimer 0 s disease (AD) and dementia with Lewy bodies (DLB) with an estimated prevalence of 1-26 cases per 100 000 persons and bvFTD accounts for most cases (50-70%) (Bang et al. 2015). The prevalence of PSP is estimated to 4-9 cases per 100 000 persons in the age-group > 60 years (Savica et al. 2013).

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Section: Differential Diagnosis Of Ftd To Other Dementiassupporting

confidence: 92%

Section: Differential Diagnosis Of Ftd To Other Dementiassupporting

confidence: 82%

Section: Differential Diagnosis Of Ftd To Other Dementiassupporting

confidence: 69%

“…; Timmer et al . ). The combination of Aβ42 and pTau181 (ratio Aβ42/pTau181) better differentiated AD and FTD patients (Skillbäck et al .…”

Section: Differential Diagnosis Of Ftd To Other Dementiasmentioning

confidence: 97%

See 2 more Smart Citations

Neurochemical biomarkers in the diagnosis of frontotemporal lobar degeneration: an update

Oeckl

Steinacker

Feneberg

et al. 2016

Journal of Neurochemistry

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show abstract

“…Aβ42 was shown in previous studies to be slightly decreased in DLB compared with FTD (123, 124) although not always significant (125). Two recent studies reported lower (26-28%) Aβ42 concentrations in the CSF of DLB patients compared with FTD (120,126) and this could confirm previous observations (123,124). Tau, pTau181 and Aβ42 are not different between FTD and PD with dementia (PDD) (120).…”

Section: Ratio Aβ42/ptau181supporting

confidence: 84%

Precision medicine of frontotemporal dementia from genotype to phenotype

et al. 2018

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Frontotemporal dementia (FTD) is the second most common neurodegenerative cause of early-onset dementia. FTD has an important genetic component contributing to its pathogenic mechanisms. Currently, extensive research on neuroimaging biomarkers and neurochemical biomarkers in FTD is being conducted to address the clinical need for a sensitive and specific diagnostic marker. Here, we review the advances in genetics, biomarkers and treatment of FTD and how this may represent a shift towards precision medicine. To advance the clinical use of precision medicine, big data cohort for genotype/phenotype research and multidisciplinary team approaches are necessary.

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High‐resolution metabolomic profiling of Alzheimer’s disease in plasma

Niedzwiecki

Walker

Howell

et al. 2019

Ann Clin Transl Neurol

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BackgroundAlzheimer’s disease (AD) is a complex neurological disorder with contributions from genetic and environmental factors. High‐resolution metabolomics (HRM) has the potential to identify novel endogenous and environmental factors involved in AD. Previous metabolomics studies have identified circulating metabolites linked to AD, but lack of replication and inconsistent diagnostic algorithms have hindered the generalizability of these findings. Here we applied HRM to identify plasma metabolic and environmental factors associated with AD in two study samples, with cerebrospinal fluid (CSF) biomarkers of AD incorporated to achieve high diagnostic accuracy.MethodsLiquid chromatography‐mass spectrometry (LC–MS)‐based HRM was used to identify plasma and CSF metabolites associated with AD diagnosis and CSF AD biomarkers in two studies of prevalent AD (Study 1: 43 AD cases, 45 mild cognitive impairment [MCI] cases, 41 controls; Study 2: 50 AD cases, 18 controls). AD‐associated metabolites were identified using a metabolome‐wide association study (MWAS) framework.ResultsAn MWAS meta‐analysis identified three non‐medication AD‐associated metabolites in plasma, including elevated levels of glutamine and an unknown halogenated compound and lower levels of piperine, a dietary alkaloid. The non‐medication metabolites were correlated with CSF AD biomarkers, and glutamine and the unknown halogenated compound were also detected in CSF. Furthermore, in Study 1, the unknown compound and piperine were altered in MCI patients in the same direction as AD dementia.ConclusionsIn plasma, AD was reproducibly associated with elevated levels of glutamine and a halogen‐containing compound and reduced levels of piperine. These findings provide further evidence that exposures and behavior may modify AD risks.

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Total glutamine synthetase levels in cerebrospinal fluid of Alzheimer's disease patients are unchanged

Cited by 16 publications

References 7 publications

Neurochemical biomarkers in the diagnosis of frontotemporal lobar degeneration: an update

Neurochemical biomarkers in the diagnosis of frontotemporal lobar degeneration: an update

Precision medicine of frontotemporal dementia from genotype to phenotype

High‐resolution metabolomic profiling of Alzheimer’s disease in plasma

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