Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation

Alzheimer’s Disease (AD) contributes to most cases of dementia. Its prominent neuropathological features are the extracellular neuritic plaques and intercellular neurofibrillary tangles composed of aggregated β-amyloid (Aβ) and hyperphosphorylated tau protein, respectively. In the past few decades,...

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Bibliographic Details
Published inJournal of neuroinflammation Vol. 20; no. 1; pp. 165 - 21
Main Authors Chen, Yijun, Yu, Yang
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 14.07.2023
BioMed Central
BMC
Subjects
Age factors in disease
Alzheimer Disease - pathology
Alzheimer's disease
Amyloid beta-Peptides
Analysis
Brain
Care and treatment
Cell activation
Clinical trials
Cognitive ability
Dementia disorders
Diagnosis
Drug development
Glia
Glial cells
Humans
Inflammation
Inflammation - complications
Kinases
Neurodegeneration
Neurodegenerative diseases
Neurofibrillary tangles
Neuroinflammation
Neuroinflammatory Diseases
Neuronal-glial interactions
Neurophysiology
Pathology
Patient outcomes
Post-translation
Review
Senile plaques
Tau phosphorylation
Tau propagation
Tau protein
Tau proteins
tau Proteins - metabolism
Tauopathies
Tauopathies - pathology
Therapeutic applications
Therapeutic targets
Translation
β-Amyloid
China
Tau phosphorylation
Tauopathies
Alzheimer’s disease
Astrocytes
Neuroinflammation
Tau propagation
Glia
Microglia
Online AccessGet full text

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Abstract Alzheimer’s Disease (AD) contributes to most cases of dementia. Its prominent neuropathological features are the extracellular neuritic plaques and intercellular neurofibrillary tangles composed of aggregated β-amyloid (Aβ) and hyperphosphorylated tau protein, respectively. In the past few decades, disease-modifying therapy targeting Aβ has been the focus of AD drug development. Even though it is encouraging that two of these drugs have recently received accelerated US Food and Drug Administration approval for AD treatment, their efficacy or long-term safety is controversial. Tau has received increasing attention as a potential therapeutic target, since evidence indicates that tau pathology is more associated with cognitive dysfunction. Moreover, inflammation, especially neuroinflammation, accompanies AD pathological processes and is also linked to cognitive deficits. Accumulating evidence indicates that inflammation has a complex and tight interplay with tau pathology. Here, we review recent evidence on the interaction between tau pathology, focusing on tau post-translational modification and dissemination, and neuroinflammatory responses, including glial cell activation and inflammatory signaling pathways. Then, we summarize the latest clinical trials targeting tau and neuroinflammation. Sustained and increased inflammatory responses in glial cells and neurons are pivotal cellular drivers and regulators of the exacerbation of tau pathology, which further contributes to its worsening by aggravating inflammatory responses. Unraveling the precise mechanisms underlying the relationship between tau pathology and neuroinflammation will provide new insights into the discovery and clinical translation of therapeutic targets for AD and other tau-related diseases (tauopathies). Targeting multiple pathologies and precision therapy strategies will be the crucial direction for developing drugs for AD and other tauopathies.
AbstractList Alzheimer’s Disease (AD) contributes to most cases of dementia. Its prominent neuropathological features are the extracellular neuritic plaques and intercellular neurofibrillary tangles composed of aggregated β-amyloid (Aβ) and hyperphosphorylated tau protein, respectively. In the past few decades, disease-modifying therapy targeting Aβ has been the focus of AD drug development. Even though it is encouraging that two of these drugs have recently received accelerated US Food and Drug Administration approval for AD treatment, their efficacy or long-term safety is controversial. Tau has received increasing attention as a potential therapeutic target, since evidence indicates that tau pathology is more associated with cognitive dysfunction. Moreover, inflammation, especially neuroinflammation, accompanies AD pathological processes and is also linked to cognitive deficits. Accumulating evidence indicates that inflammation has a complex and tight interplay with tau pathology. Here, we review recent evidence on the interaction between tau pathology, focusing on tau post-translational modification and dissemination, and neuroinflammatory responses, including glial cell activation and inflammatory signaling pathways. Then, we summarize the latest clinical trials targeting tau and neuroinflammation. Sustained and increased inflammatory responses in glial cells and neurons are pivotal cellular drivers and regulators of the exacerbation of tau pathology, which further contributes to its worsening by aggravating inflammatory responses. Unraveling the precise mechanisms underlying the relationship between tau pathology and neuroinflammation will provide new insights into the discovery and clinical translation of therapeutic targets for AD and other tau-related diseases (tauopathies). Targeting multiple pathologies and precision therapy strategies will be the crucial direction for developing drugs for AD and other tauopathies.
Alzheimer's Disease (AD) contributes to most cases of dementia. Its prominent neuropathological features are the extracellular neuritic plaques and intercellular neurofibrillary tangles composed of aggregated β-amyloid (Aβ) and hyperphosphorylated tau protein, respectively. In the past few decades, disease-modifying therapy targeting Aβ has been the focus of AD drug development. Even though it is encouraging that two of these drugs have recently received accelerated US Food and Drug Administration approval for AD treatment, their efficacy or long-term safety is controversial. Tau has received increasing attention as a potential therapeutic target, since evidence indicates that tau pathology is more associated with cognitive dysfunction. Moreover, inflammation, especially neuroinflammation, accompanies AD pathological processes and is also linked to cognitive deficits. Accumulating evidence indicates that inflammation has a complex and tight interplay with tau pathology. Here, we review recent evidence on the interaction between tau pathology, focusing on tau post-translational modification and dissemination, and neuroinflammatory responses, including glial cell activation and inflammatory signaling pathways. Then, we summarize the latest clinical trials targeting tau and neuroinflammation. Sustained and increased inflammatory responses in glial cells and neurons are pivotal cellular drivers and regulators of the exacerbation of tau pathology, which further contributes to its worsening by aggravating inflammatory responses. Unraveling the precise mechanisms underlying the relationship between tau pathology and neuroinflammation will provide new insights into the discovery and clinical translation of therapeutic targets for AD and other tau-related diseases (tauopathies). Targeting multiple pathologies and precision therapy strategies will be the crucial direction for developing drugs for AD and other tauopathies.Alzheimer's Disease (AD) contributes to most cases of dementia. Its prominent neuropathological features are the extracellular neuritic plaques and intercellular neurofibrillary tangles composed of aggregated β-amyloid (Aβ) and hyperphosphorylated tau protein, respectively. In the past few decades, disease-modifying therapy targeting Aβ has been the focus of AD drug development. Even though it is encouraging that two of these drugs have recently received accelerated US Food and Drug Administration approval for AD treatment, their efficacy or long-term safety is controversial. Tau has received increasing attention as a potential therapeutic target, since evidence indicates that tau pathology is more associated with cognitive dysfunction. Moreover, inflammation, especially neuroinflammation, accompanies AD pathological processes and is also linked to cognitive deficits. Accumulating evidence indicates that inflammation has a complex and tight interplay with tau pathology. Here, we review recent evidence on the interaction between tau pathology, focusing on tau post-translational modification and dissemination, and neuroinflammatory responses, including glial cell activation and inflammatory signaling pathways. Then, we summarize the latest clinical trials targeting tau and neuroinflammation. Sustained and increased inflammatory responses in glial cells and neurons are pivotal cellular drivers and regulators of the exacerbation of tau pathology, which further contributes to its worsening by aggravating inflammatory responses. Unraveling the precise mechanisms underlying the relationship between tau pathology and neuroinflammation will provide new insights into the discovery and clinical translation of therapeutic targets for AD and other tau-related diseases (tauopathies). Targeting multiple pathologies and precision therapy strategies will be the crucial direction for developing drugs for AD and other tauopathies.
Alzheimer's Disease (AD) contributes to most cases of dementia. Its prominent neuropathological features are the extracellular neuritic plaques and intercellular neurofibrillary tangles composed of aggregated [beta]-amyloid (A[beta]) and hyperphosphorylated tau protein, respectively. In the past few decades, disease-modifying therapy targeting A[beta] has been the focus of AD drug development. Even though it is encouraging that two of these drugs have recently received accelerated US Food and Drug Administration approval for AD treatment, their efficacy or long-term safety is controversial. Tau has received increasing attention as a potential therapeutic target, since evidence indicates that tau pathology is more associated with cognitive dysfunction. Moreover, inflammation, especially neuroinflammation, accompanies AD pathological processes and is also linked to cognitive deficits. Accumulating evidence indicates that inflammation has a complex and tight interplay with tau pathology. Here, we review recent evidence on the interaction between tau pathology, focusing on tau post-translational modification and dissemination, and neuroinflammatory responses, including glial cell activation and inflammatory signaling pathways. Then, we summarize the latest clinical trials targeting tau and neuroinflammation. Sustained and increased inflammatory responses in glial cells and neurons are pivotal cellular drivers and regulators of the exacerbation of tau pathology, which further contributes to its worsening by aggravating inflammatory responses. Unraveling the precise mechanisms underlying the relationship between tau pathology and neuroinflammation will provide new insights into the discovery and clinical translation of therapeutic targets for AD and other tau-related diseases (tauopathies). Targeting multiple pathologies and precision therapy strategies will be the crucial direction for developing drugs for AD and other tauopathies.
Abstract Alzheimer’s Disease (AD) contributes to most cases of dementia. Its prominent neuropathological features are the extracellular neuritic plaques and intercellular neurofibrillary tangles composed of aggregated β-amyloid (Aβ) and hyperphosphorylated tau protein, respectively. In the past few decades, disease-modifying therapy targeting Aβ has been the focus of AD drug development. Even though it is encouraging that two of these drugs have recently received accelerated US Food and Drug Administration approval for AD treatment, their efficacy or long-term safety is controversial. Tau has received increasing attention as a potential therapeutic target, since evidence indicates that tau pathology is more associated with cognitive dysfunction. Moreover, inflammation, especially neuroinflammation, accompanies AD pathological processes and is also linked to cognitive deficits. Accumulating evidence indicates that inflammation has a complex and tight interplay with tau pathology. Here, we review recent evidence on the interaction between tau pathology, focusing on tau post-translational modification and dissemination, and neuroinflammatory responses, including glial cell activation and inflammatory signaling pathways. Then, we summarize the latest clinical trials targeting tau and neuroinflammation. Sustained and increased inflammatory responses in glial cells and neurons are pivotal cellular drivers and regulators of the exacerbation of tau pathology, which further contributes to its worsening by aggravating inflammatory responses. Unraveling the precise mechanisms underlying the relationship between tau pathology and neuroinflammation will provide new insights into the discovery and clinical translation of therapeutic targets for AD and other tau-related diseases (tauopathies). Targeting multiple pathologies and precision therapy strategies will be the crucial direction for developing drugs for AD and other tauopathies.
Alzheimer's Disease (AD) contributes to most cases of dementia. Its prominent neuropathological features are the extracellular neuritic plaques and intercellular neurofibrillary tangles composed of aggregated [beta]-amyloid (A[beta]) and hyperphosphorylated tau protein, respectively. In the past few decades, disease-modifying therapy targeting A[beta] has been the focus of AD drug development. Even though it is encouraging that two of these drugs have recently received accelerated US Food and Drug Administration approval for AD treatment, their efficacy or long-term safety is controversial. Tau has received increasing attention as a potential therapeutic target, since evidence indicates that tau pathology is more associated with cognitive dysfunction. Moreover, inflammation, especially neuroinflammation, accompanies AD pathological processes and is also linked to cognitive deficits. Accumulating evidence indicates that inflammation has a complex and tight interplay with tau pathology. Here, we review recent evidence on the interaction between tau pathology, focusing on tau post-translational modification and dissemination, and neuroinflammatory responses, including glial cell activation and inflammatory signaling pathways. Then, we summarize the latest clinical trials targeting tau and neuroinflammation. Sustained and increased inflammatory responses in glial cells and neurons are pivotal cellular drivers and regulators of the exacerbation of tau pathology, which further contributes to its worsening by aggravating inflammatory responses. Unraveling the precise mechanisms underlying the relationship between tau pathology and neuroinflammation will provide new insights into the discovery and clinical translation of therapeutic targets for AD and other tau-related diseases (tauopathies). Targeting multiple pathologies and precision therapy strategies will be the crucial direction for developing drugs for AD and other tauopathies. Keywords: Alzheimer's disease, Tauopathies, Tau phosphorylation, Tau propagation, Neuroinflammation, Glia, Microglia, Astrocytes
ArticleNumber 165
Audience Academic
Author Yu, Yang
Chen, Yijun
Author_xml – sequence: 1
  givenname: Yijun
  surname: Chen
  fullname: Chen, Yijun
– sequence: 2
  givenname: Yang
  surname: Yu
  fullname: Yu, Yang
BackLink https://www.ncbi.nlm.nih.gov/pubmed/37452321$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords Tau phosphorylation
Tauopathies
Alzheimer’s disease
Astrocytes
Neuroinflammation
Tau propagation
Glia
Microglia
Language English
License 2023. The Author(s).
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Snippet Alzheimer’s Disease (AD) contributes to most cases of dementia. Its prominent neuropathological features are the extracellular neuritic plaques and...
Alzheimer's Disease (AD) contributes to most cases of dementia. Its prominent neuropathological features are the extracellular neuritic plaques and...
Abstract Alzheimer’s Disease (AD) contributes to most cases of dementia. Its prominent neuropathological features are the extracellular neuritic plaques and...
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StartPage 165
SubjectTerms Age factors in disease
Alzheimer Disease - pathology
Alzheimer's disease
Amyloid beta-Peptides
Analysis
Brain
Care and treatment
Cell activation
Clinical trials
Cognitive ability
Dementia disorders
Diagnosis
Drug development
Glia
Glial cells
Humans
Inflammation
Inflammation - complications
Kinases
Neurodegeneration
Neurodegenerative diseases
Neurofibrillary tangles
Neuroinflammation
Neuroinflammatory Diseases
Neuronal-glial interactions
Neurophysiology
Pathology
Patient outcomes
Post-translation
Review
Senile plaques
Tau phosphorylation
Tau propagation
Tau protein
Tau proteins
tau Proteins - metabolism
Tauopathies
Tauopathies - pathology
Therapeutic applications
Therapeutic targets
Translation
β-Amyloid
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Title Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation
URI https://www.ncbi.nlm.nih.gov/pubmed/37452321
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