Blood-Based Kinase Assessments in Alzheimer’s Disease

Alzheimer’s disease (AD) is marked by memory disturbances followed by aphasia, apraxia and agnosia. Brain lesions include the accumulation of the amyloid peptide in extracellular plaques, neurofibrillary tangles with abnormally phosphorylated tau protein and synaptic and neuronal loss. New findings have suggested that brain lesions could occur one or two decades before the first clinical signs. This asymptomatic preclinical phase could be an opportunity to put in place a secondary prevention but the detection of these brain lesions can only be achieved so far by cerebrospinal fluid (CSF) evaluation or molecular amyloid and tau PET imaging. There is an urgent need to find out simple and easily accessible new biomarkers to set up an efficient screening in adult and aging population. Neuropathological and biochemical studies have revealed that abnormal accumulations of potentially toxic kinases are present in the brains of AD patients. Kinase activation leads to abnormal tau phosphorylation, amyloid production, apoptosis and neuroinflammation. Increased levels of these kinases are present in the CSF of mild cognitive impairment (MCI) and AD patients. Over the last years the search for abnormal kinase levels was performed in the blood of patients. Glycogen synthase kinase 3 (GSK 3), protein kinase R (PKR), mamalian target of rapamycin (mTOR), dual specificity tyrosine-phosphorylation-regulated kinase 1A (DIRK1A), c-Jun N-terminal kinase (JNK), protein 70 kD ribosomal protein S6 kinase (P70S6K), ERK2 and other kinase concentrations were evaluated and abnormal levels were found in many studies. For example, GSK3 levels are increased in MCI and AD patients. PKR levels are also augmented in peripheral blood mononuclear cells (PBMC) of AD patients. In the future, the assessment of several blood kinase levels in large cohorts of patients will be needed to confirm the usefulness of this test at an early phase of the disease. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Jacques Hugon [verfasserIn] François Mouton-Liger [verfasserIn] Emmanuel Cognat [verfasserIn] Julien Dumurgier [verfasserIn] Claire Paquet [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	Alzheimer kinase blood biomarkers diagnosis

Übergeordnetes Werk:	In: Frontiers in Aging Neuroscience - Frontiers Media S.A., 2010, 10(2018)
Übergeordnetes Werk:	volume:10 ; year:2018

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fnagi.2018.00338

Katalog-ID:	DOAJ049665928

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spelling	10.3389/fnagi.2018.00338 doi (DE-627)DOAJ049665928 (DE-599)DOAJ379187ef76e24a49a5a1af62138244b8 DE-627 ger DE-627 rakwb eng RC321-571 Jacques Hugon verfasserin aut Blood-Based Kinase Assessments in Alzheimer’s Disease 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Alzheimer’s disease (AD) is marked by memory disturbances followed by aphasia, apraxia and agnosia. Brain lesions include the accumulation of the amyloid peptide in extracellular plaques, neurofibrillary tangles with abnormally phosphorylated tau protein and synaptic and neuronal loss. New findings have suggested that brain lesions could occur one or two decades before the first clinical signs. This asymptomatic preclinical phase could be an opportunity to put in place a secondary prevention but the detection of these brain lesions can only be achieved so far by cerebrospinal fluid (CSF) evaluation or molecular amyloid and tau PET imaging. There is an urgent need to find out simple and easily accessible new biomarkers to set up an efficient screening in adult and aging population. Neuropathological and biochemical studies have revealed that abnormal accumulations of potentially toxic kinases are present in the brains of AD patients. Kinase activation leads to abnormal tau phosphorylation, amyloid production, apoptosis and neuroinflammation. Increased levels of these kinases are present in the CSF of mild cognitive impairment (MCI) and AD patients. Over the last years the search for abnormal kinase levels was performed in the blood of patients. Glycogen synthase kinase 3 (GSK 3), protein kinase R (PKR), mamalian target of rapamycin (mTOR), dual specificity tyrosine-phosphorylation-regulated kinase 1A (DIRK1A), c-Jun N-terminal kinase (JNK), protein 70 kD ribosomal protein S6 kinase (P70S6K), ERK2 and other kinase concentrations were evaluated and abnormal levels were found in many studies. For example, GSK3 levels are increased in MCI and AD patients. PKR levels are also augmented in peripheral blood mononuclear cells (PBMC) of AD patients. In the future, the assessment of several blood kinase levels in large cohorts of patients will be needed to confirm the usefulness of this test at an early phase of the disease. Alzheimer kinase blood biomarkers diagnosis Neurosciences. Biological psychiatry. Neuropsychiatry Jacques Hugon verfasserin aut François Mouton-Liger verfasserin aut François Mouton-Liger verfasserin aut Emmanuel Cognat verfasserin aut Emmanuel Cognat verfasserin aut Julien Dumurgier verfasserin aut Julien Dumurgier verfasserin aut Claire Paquet verfasserin aut Claire Paquet verfasserin aut In Frontiers in Aging Neuroscience Frontiers Media S.A., 2010 10(2018) (DE-627)629834350 (DE-600)2558898-9 16634365 nnns volume:10 year:2018 https://doi.org/10.3389/fnagi.2018.00338 kostenfrei https://doaj.org/article/379187ef76e24a49a5a1af62138244b8 kostenfrei https://www.frontiersin.org/article/10.3389/fnagi.2018.00338/full kostenfrei https://doaj.org/toc/1663-4365 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2018
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allfieldsGer	10.3389/fnagi.2018.00338 doi (DE-627)DOAJ049665928 (DE-599)DOAJ379187ef76e24a49a5a1af62138244b8 DE-627 ger DE-627 rakwb eng RC321-571 Jacques Hugon verfasserin aut Blood-Based Kinase Assessments in Alzheimer’s Disease 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Alzheimer’s disease (AD) is marked by memory disturbances followed by aphasia, apraxia and agnosia. Brain lesions include the accumulation of the amyloid peptide in extracellular plaques, neurofibrillary tangles with abnormally phosphorylated tau protein and synaptic and neuronal loss. New findings have suggested that brain lesions could occur one or two decades before the first clinical signs. This asymptomatic preclinical phase could be an opportunity to put in place a secondary prevention but the detection of these brain lesions can only be achieved so far by cerebrospinal fluid (CSF) evaluation or molecular amyloid and tau PET imaging. There is an urgent need to find out simple and easily accessible new biomarkers to set up an efficient screening in adult and aging population. Neuropathological and biochemical studies have revealed that abnormal accumulations of potentially toxic kinases are present in the brains of AD patients. Kinase activation leads to abnormal tau phosphorylation, amyloid production, apoptosis and neuroinflammation. Increased levels of these kinases are present in the CSF of mild cognitive impairment (MCI) and AD patients. Over the last years the search for abnormal kinase levels was performed in the blood of patients. Glycogen synthase kinase 3 (GSK 3), protein kinase R (PKR), mamalian target of rapamycin (mTOR), dual specificity tyrosine-phosphorylation-regulated kinase 1A (DIRK1A), c-Jun N-terminal kinase (JNK), protein 70 kD ribosomal protein S6 kinase (P70S6K), ERK2 and other kinase concentrations were evaluated and abnormal levels were found in many studies. For example, GSK3 levels are increased in MCI and AD patients. PKR levels are also augmented in peripheral blood mononuclear cells (PBMC) of AD patients. In the future, the assessment of several blood kinase levels in large cohorts of patients will be needed to confirm the usefulness of this test at an early phase of the disease. Alzheimer kinase blood biomarkers diagnosis Neurosciences. Biological psychiatry. Neuropsychiatry Jacques Hugon verfasserin aut François Mouton-Liger verfasserin aut François Mouton-Liger verfasserin aut Emmanuel Cognat verfasserin aut Emmanuel Cognat verfasserin aut Julien Dumurgier verfasserin aut Julien Dumurgier verfasserin aut Claire Paquet verfasserin aut Claire Paquet verfasserin aut In Frontiers in Aging Neuroscience Frontiers Media S.A., 2010 10(2018) (DE-627)629834350 (DE-600)2558898-9 16634365 nnns volume:10 year:2018 https://doi.org/10.3389/fnagi.2018.00338 kostenfrei https://doaj.org/article/379187ef76e24a49a5a1af62138244b8 kostenfrei https://www.frontiersin.org/article/10.3389/fnagi.2018.00338/full kostenfrei https://doaj.org/toc/1663-4365 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2018
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language	English
source	In Frontiers in Aging Neuroscience 10(2018) volume:10 year:2018
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title_full	Blood-Based Kinase Assessments in Alzheimer’s Disease
author_sort	Jacques Hugon
journal	Frontiers in Aging Neuroscience
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author_browse	Jacques Hugon François Mouton-Liger Emmanuel Cognat Julien Dumurgier Claire Paquet
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title_sort	blood-based kinase assessments in alzheimer’s disease
callnumber	RC321-571
title_auth	Blood-Based Kinase Assessments in Alzheimer’s Disease
abstract	Alzheimer’s disease (AD) is marked by memory disturbances followed by aphasia, apraxia and agnosia. Brain lesions include the accumulation of the amyloid peptide in extracellular plaques, neurofibrillary tangles with abnormally phosphorylated tau protein and synaptic and neuronal loss. New findings have suggested that brain lesions could occur one or two decades before the first clinical signs. This asymptomatic preclinical phase could be an opportunity to put in place a secondary prevention but the detection of these brain lesions can only be achieved so far by cerebrospinal fluid (CSF) evaluation or molecular amyloid and tau PET imaging. There is an urgent need to find out simple and easily accessible new biomarkers to set up an efficient screening in adult and aging population. Neuropathological and biochemical studies have revealed that abnormal accumulations of potentially toxic kinases are present in the brains of AD patients. Kinase activation leads to abnormal tau phosphorylation, amyloid production, apoptosis and neuroinflammation. Increased levels of these kinases are present in the CSF of mild cognitive impairment (MCI) and AD patients. Over the last years the search for abnormal kinase levels was performed in the blood of patients. Glycogen synthase kinase 3 (GSK 3), protein kinase R (PKR), mamalian target of rapamycin (mTOR), dual specificity tyrosine-phosphorylation-regulated kinase 1A (DIRK1A), c-Jun N-terminal kinase (JNK), protein 70 kD ribosomal protein S6 kinase (P70S6K), ERK2 and other kinase concentrations were evaluated and abnormal levels were found in many studies. For example, GSK3 levels are increased in MCI and AD patients. PKR levels are also augmented in peripheral blood mononuclear cells (PBMC) of AD patients. In the future, the assessment of several blood kinase levels in large cohorts of patients will be needed to confirm the usefulness of this test at an early phase of the disease.
abstractGer	Alzheimer’s disease (AD) is marked by memory disturbances followed by aphasia, apraxia and agnosia. Brain lesions include the accumulation of the amyloid peptide in extracellular plaques, neurofibrillary tangles with abnormally phosphorylated tau protein and synaptic and neuronal loss. New findings have suggested that brain lesions could occur one or two decades before the first clinical signs. This asymptomatic preclinical phase could be an opportunity to put in place a secondary prevention but the detection of these brain lesions can only be achieved so far by cerebrospinal fluid (CSF) evaluation or molecular amyloid and tau PET imaging. There is an urgent need to find out simple and easily accessible new biomarkers to set up an efficient screening in adult and aging population. Neuropathological and biochemical studies have revealed that abnormal accumulations of potentially toxic kinases are present in the brains of AD patients. Kinase activation leads to abnormal tau phosphorylation, amyloid production, apoptosis and neuroinflammation. Increased levels of these kinases are present in the CSF of mild cognitive impairment (MCI) and AD patients. Over the last years the search for abnormal kinase levels was performed in the blood of patients. Glycogen synthase kinase 3 (GSK 3), protein kinase R (PKR), mamalian target of rapamycin (mTOR), dual specificity tyrosine-phosphorylation-regulated kinase 1A (DIRK1A), c-Jun N-terminal kinase (JNK), protein 70 kD ribosomal protein S6 kinase (P70S6K), ERK2 and other kinase concentrations were evaluated and abnormal levels were found in many studies. For example, GSK3 levels are increased in MCI and AD patients. PKR levels are also augmented in peripheral blood mononuclear cells (PBMC) of AD patients. In the future, the assessment of several blood kinase levels in large cohorts of patients will be needed to confirm the usefulness of this test at an early phase of the disease.
abstract_unstemmed	Alzheimer’s disease (AD) is marked by memory disturbances followed by aphasia, apraxia and agnosia. Brain lesions include the accumulation of the amyloid peptide in extracellular plaques, neurofibrillary tangles with abnormally phosphorylated tau protein and synaptic and neuronal loss. New findings have suggested that brain lesions could occur one or two decades before the first clinical signs. This asymptomatic preclinical phase could be an opportunity to put in place a secondary prevention but the detection of these brain lesions can only be achieved so far by cerebrospinal fluid (CSF) evaluation or molecular amyloid and tau PET imaging. There is an urgent need to find out simple and easily accessible new biomarkers to set up an efficient screening in adult and aging population. Neuropathological and biochemical studies have revealed that abnormal accumulations of potentially toxic kinases are present in the brains of AD patients. Kinase activation leads to abnormal tau phosphorylation, amyloid production, apoptosis and neuroinflammation. Increased levels of these kinases are present in the CSF of mild cognitive impairment (MCI) and AD patients. Over the last years the search for abnormal kinase levels was performed in the blood of patients. Glycogen synthase kinase 3 (GSK 3), protein kinase R (PKR), mamalian target of rapamycin (mTOR), dual specificity tyrosine-phosphorylation-regulated kinase 1A (DIRK1A), c-Jun N-terminal kinase (JNK), protein 70 kD ribosomal protein S6 kinase (P70S6K), ERK2 and other kinase concentrations were evaluated and abnormal levels were found in many studies. For example, GSK3 levels are increased in MCI and AD patients. PKR levels are also augmented in peripheral blood mononuclear cells (PBMC) of AD patients. In the future, the assessment of several blood kinase levels in large cohorts of patients will be needed to confirm the usefulness of this test at an early phase of the disease.
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title_short	Blood-Based Kinase Assessments in Alzheimer’s Disease
url	https://doi.org/10.3389/fnagi.2018.00338 https://doaj.org/article/379187ef76e24a49a5a1af62138244b8 https://www.frontiersin.org/article/10.3389/fnagi.2018.00338/full https://doaj.org/toc/1663-4365
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author2	Jacques Hugon François Mouton-Liger Emmanuel Cognat Julien Dumurgier Claire Paquet
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up_date	2024-07-04T00:19:00.339Z
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